A class of protein components which can be found in several lipoproteins including HIGH-DENSITY LIPOPROTEINS; VERY-LOW-DENSITY LIPOPROTEINS; and CHYLOMICRONS. Synthesized in most organs, Apo E is important in the global transport of lipids and cholesterol throughout the body. Apo E is also a ligand for LDL receptors (RECEPTORS, LDL) that mediates the binding, internalization, and catabolism of lipoprotein particles in cells. There are several allelic isoforms (such as E2, E3, and E4). Deficiency or defects in Apo E are causes of HYPERLIPOPROTEINEMIA TYPE III.
A major and the second most common isoform of apolipoprotein E. In humans, Apo E4 differs from APOLIPOPROTEIN E3 at only one residue 112 (cysteine is replaced by arginine), and exhibits a lower resistance to denaturation and greater propensity to form folded intermediates. Apo E4 is a risk factor for ALZHEIMER DISEASE and CARDIOVASCULAR DISEASES.
A 34-kDa glycosylated protein. A major and most common isoform of apolipoprotein E. Therefore, it is also known as apolipoprotein E (ApoE). In human, Apo E3 is a 299-amino acid protein with a cysteine at the 112 and an arginine at the 158 position. It is involved with the transport of TRIGLYCERIDES; PHOSPHOLIPIDS; CHOLESTEROL; and CHOLESTERYL ESTERS in and out of the cells.
One of three major isoforms of apolipoprotein E. In humans, Apo E2 differs from APOLIPOPROTEIN E3 at one residue 158 where arginine is replaced by cysteine (R158--C). In contrast to Apo E3, Apo E2 displays extremely low binding affinity for LDL receptors (RECEPTORS, LDL) which mediate the internalization and catabolism of lipoprotein particles in liver cells. ApoE2 allelic homozygosity is associated with HYPERLIPOPROTEINEMIA TYPE III.
The most abundant protein component of HIGH DENSITY LIPOPROTEINS or HDL. This protein serves as an acceptor for CHOLESTEROL released from cells thus promoting efflux of cholesterol to HDL then to the LIVER for excretion from the body (reverse cholesterol transport). It also acts as a cofactor for LECITHIN CHOLESTEROL ACYLTRANSFERASE that forms CHOLESTEROL ESTERS on the HDL particles. Mutations of this gene APOA1 cause HDL deficiency, such as in FAMILIAL ALPHA LIPOPROTEIN DEFICIENCY DISEASE and in some patients with TANGIER DISEASE.
A 513-kDa protein synthesized in the LIVER. It serves as the major structural protein of low-density lipoproteins (LIPOPROTEINS, LDL; LIPOPROTEINS, VLDL). It is the ligand for the LDL receptor (RECEPTORS, LDL) that promotes cellular binding and internalization of LDL particles.
Major structural proteins of triacylglycerol-rich LIPOPROTEINS. There are two forms, apolipoprotein B-100 and apolipoprotein B-48, both derived from a single gene. ApoB-100 expressed in the liver is found in low-density lipoproteins (LIPOPROTEINS, LDL; LIPOPROTEINS, VLDL). ApoB-48 expressed in the intestine is found in CHYLOMICRONS. They are important in the biosynthesis, transport, and metabolism of triacylglycerol-rich lipoproteins. Plasma Apo-B levels are high in atherosclerotic patients but non-detectable in ABETALIPOPROTEINEMIA.
Protein components on the surface of LIPOPROTEINS. They form a layer surrounding the hydrophobic lipid core. There are several classes of apolipoproteins with each playing a different role in lipid transport and LIPID METABOLISM. These proteins are synthesized mainly in the LIVER and the INTESTINES.
A 9-kDa protein component of VERY-LOW-DENSITY LIPOPROTEINS and CHYLOMICRON REMNANTS. Apo C-III, synthesized in the liver, is an inhibitor of LIPOPROTEIN LIPASE. Apo C-III modulates the binding of chylomicron remnants and VLDL to receptors (RECEPTORS, LDL) thus decreases the uptake of triglyceride-rich particles by the liver cells and subsequent degradation. The normal Apo C-III is glycosylated. There are several polymorphic forms with varying amounts of SIALIC ACID (Apo C-III-0, Apo C-III-1, and Apo C-III-2).
A 6.6-kDa protein component of VERY-LOW-DENSITY LIPOPROTEINS; INTERMEDIATE-DENSITY LIPOPROTEINS; and HIGH-DENSITY LIPOPROTEINS. Apo C-I displaces APO E from lipoproteins, modulate their binding to receptors (RECEPTORS, LDL), and thereby decrease their clearance from plasma. Elevated Apo C-I levels are associated with HYPERLIPOPROTEINEMIA and ATHEROSCLEROSIS.
The second most abundant protein component of HIGH DENSITY LIPOPROTEINS or HDL. It has a high lipid affinity and is known to displace APOLIPOPROTEIN A-I from HDL particles and generates a stable HDL complex. ApoA-II can modulate the activation of LECITHIN CHOLESTEROL ACYLTRANSFERASE in the presence of APOLIPOPROTEIN A-I, thus affecting HDL metabolism.
A 9-kDa protein component of VERY-LOW-DENSITY LIPOPROTEINS. It contains a cofactor for LIPOPROTEIN LIPASE and activates several triacylglycerol lipases. The association of Apo C-II with plasma CHYLOMICRONS; VLDL, and HIGH-DENSITY LIPOPROTEINS is reversible and changes rapidly as a function of triglyceride metabolism. Clinically, Apo C-II deficiency is similar to lipoprotein lipase deficiency (HYPERLIPOPROTEINEMIA TYPE I) and is therefore called hyperlipoproteinemia type IB.
Structural proteins of the alpha-lipoproteins (HIGH DENSITY LIPOPROTEINS), including APOLIPOPROTEIN A-I and APOLIPOPROTEIN A-II. They can modulate the activity of LECITHIN CHOLESTEROL ACYLTRANSFERASE. These apolipoproteins are low in atherosclerotic patients. They are either absent or present in extremely low plasma concentration in TANGIER DISEASE.
A 241-kDa protein synthesized only in the INTESTINES. It serves as a structural protein of CHYLOMICRONS. Its exclusive association with chylomicron particles provides an indicator of intestinally derived lipoproteins in circulation. Apo B-48 is a shortened form of apo B-100 and lacks the LDL-receptor region.
The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils.
A group of apolipoproteins that can readily exchange among the various classes of lipoproteins (HDL; VLDL; CHYLOMICRONS). After lipolysis of TRIGLYCERIDES on VLDL and chylomicrons, Apo-C proteins are normally transferred to HDL. The subtypes can modulate remnant binding to receptors, LECITHIN CHOLESTEROL ACYLTRANSFERASE, or LIPOPROTEIN LIPASE.
A class of lipoproteins of very light (0.93-1.006 g/ml) large size (30-80 nm) particles with a core composed mainly of TRIGLYCERIDES and a surface monolayer of PHOSPHOLIPIDS and CHOLESTEROL into which are imbedded the apolipoproteins B, E, and C. VLDL facilitates the transport of endogenously made triglycerides to extrahepatic tissues. As triglycerides and Apo C are removed, VLDL is converted to INTERMEDIATE-DENSITY LIPOPROTEINS, then to LOW-DENSITY LIPOPROTEINS from which cholesterol is delivered to the extrahepatic tissues.
Lipid-protein complexes involved in the transportation and metabolism of lipids in the body. They are spherical particles consisting of a hydrophobic core of TRIGLYCERIDES and CHOLESTEROL ESTERS surrounded by a layer of hydrophilic free CHOLESTEROL; PHOSPHOLIPIDS; and APOLIPOPROTEINS. Lipoproteins are classified by their varying buoyant density and sizes.
A class of lipoproteins of small size (4-13 nm) and dense (greater than 1.063 g/ml) particles. HDL lipoproteins, synthesized in the liver without a lipid core, accumulate cholesterol esters from peripheral tissues and transport them to the liver for re-utilization or elimination from the body (the reverse cholesterol transport). Their major protein component is APOLIPOPROTEIN A-I. HDL also shuttle APOLIPOPROTEINS C and APOLIPOPROTEINS E to and from triglyceride-rich lipoproteins during their catabolism. HDL plasma level has been inversely correlated with the risk of cardiovascular diseases.
Receptors on the plasma membrane of nonhepatic cells that specifically bind LDL. The receptors are localized in specialized regions called coated pits. Hypercholesteremia is caused by an allelic genetic defect of three types: 1, receptors do not bind to LDL; 2, there is reduced binding of LDL; and 3, there is normal binding but no internalization of LDL. In consequence, entry of cholesterol esters into the cell is impaired and the intracellular feedback by cholesterol on 3-hydroxy-3-methylglutaryl CoA reductase is lacking.
A degenerative disease of the BRAIN characterized by the insidious onset of DEMENTIA. Impairment of MEMORY, judgment, attention span, and problem solving skills are followed by severe APRAXIAS and a global loss of cognitive abilities. The condition primarily occurs after age 60, and is marked pathologically by severe cortical atrophy and the triad of SENILE PLAQUES; NEUROFIBRILLARY TANGLES; and NEUROPIL THREADS. (From Adams et al., Principles of Neurology, 6th ed, pp1049-57)
An autosomal recessively inherited disorder characterized by the accumulation of intermediate-density lipoprotein (IDL or broad-beta-lipoprotein). IDL has a CHOLESTEROL to TRIGLYCERIDES ratio greater than that of VERY-LOW-DENSITY LIPOPROTEINS. This disorder is due to mutation of APOLIPOPROTEINS E, a receptor-binding component of VLDL and CHYLOMICRONS, resulting in their reduced clearance and high plasma levels of both cholesterol and triglycerides.
The genetic constitution of the individual, comprising the ALLELES present at each GENETIC LOCUS.
A generic term for fats and lipoids, the alcohol-ether-soluble constituents of protoplasm, which are insoluble in water. They comprise the fats, fatty oils, essential oils, waxes, phospholipids, glycolipids, sulfolipids, aminolipids, chromolipids (lipochromes), and fatty acids. (Grant & Hackh's Chemical Dictionary, 5th ed)
A thickening and loss of elasticity of the walls of ARTERIES that occurs with formation of ATHEROSCLEROTIC PLAQUES within the ARTERIAL INTIMA.
Variant forms of the same gene, occupying the same locus on homologous CHROMOSOMES, and governing the variants in production of the same gene product.
Thickening and loss of elasticity of the walls of ARTERIES of all sizes. There are many forms classified by the types of lesions and arteries involved, such as ATHEROSCLEROSIS with fatty lesions in the ARTERIAL INTIMA of medium and large muscular arteries.
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
A large and highly glycosylated protein constituent of LIPOPROTEIN (A). It has very little affinity for lipids but forms disulfide-linkage to APOLIPOPROTEIN B-100. Apoprotein(a) has SERINE PROTEINASE activity and can be of varying sizes from 400- to 800-kDa. It is homologous to PLASMINOGEN and is known to modulate THROMBOSIS and FIBRINOLYSIS.
A class of lipoproteins of small size (18-25 nm) and light (1.019-1.063 g/ml) particles with a core composed mainly of CHOLESTEROL ESTERS and smaller amounts of TRIGLYCERIDES. The surface monolayer consists mostly of PHOSPHOLIPIDS, a single copy of APOLIPOPROTEIN B-100, and free cholesterol molecules. The main LDL function is to transport cholesterol and cholesterol esters to extrahepatic tissues.
Conditions with abnormally elevated levels of LIPOPROTEINS in the blood. They may be inherited, acquired, primary, or secondary. Hyperlipoproteinemias are classified according to the pattern of lipoproteins on electrophoresis or ultracentrifugation.
Cell surface proteins that bind lipoproteins with high affinity. Lipoprotein receptors in the liver and peripheral tissues mediate the regulation of plasma and cellular cholesterol metabolism and concentration. The receptors generally recognize the apolipoproteins of the lipoprotein complex, and binding is often a trigger for endocytosis.
The regular and simultaneous occurrence in a single interbreeding population of two or more discontinuous genotypes. The concept includes differences in genotypes ranging in size from a single nucleotide site (POLYMORPHISM, SINGLE NUCLEOTIDE) to large nucleotide sequences visible at a chromosomal level.
A lipoprotein that resembles the LOW-DENSITY LIPOPROTEINS but with an extra protein moiety, APOPROTEIN (A) also known as APOLIPOPROTEIN (A), linked to APOLIPOPROTEIN B-100 on the LDL by one or two disulfide bonds. High plasma level of lipoprotein (a) is associated with increased risk of atherosclerotic cardiovascular disease.
A family of proteins that share sequence similarity with the low density lipoprotein receptor (RECEPTORS, LDL).
A glycoprotein component of HIGH-DENSITY LIPOPROTEINS that transports small hydrophobic ligands including CHOLESTEROL and STEROLS. It occurs in the macromolecular complex with LECITHIN CHOLESTEROL ACYLTRANSFERASE. Apo D is expressed in and secreted from a variety of tissues such as liver, placenta, brain tissue and others.
Cholesterol which is contained in or bound to high-density lipoproteins (HDL), including CHOLESTEROL ESTERS and free cholesterol.
A LDL-receptor related protein involved in clearance of chylomicron remnants and of activated ALPHA-MACROGLOBULINS from plasma.
A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.
Conditions with excess LIPIDS in the blood.
Peptides generated from AMYLOID BETA-PEPTIDES PRECURSOR. An amyloid fibrillar form of these peptides is the major component of amyloid plaques found in individuals with Alzheimer's disease and in aged individuals with trisomy 21 (DOWN SYNDROME). The peptide is found predominantly in the nervous system, but there have been reports of its presence in non-neural tissue.
Cholesterol which is contained in or bound to low density lipoproteins (LDL), including CHOLESTEROL ESTERS and free cholesterol.
Physiological processes in biosynthesis (anabolism) and degradation (catabolism) of LIPIDS.
A superfamily of large integral ATP-binding cassette membrane proteins whose expression pattern is consistent with a role in lipid (cholesterol) efflux. It is implicated in TANGIER DISEASE characterized by accumulation of cholesteryl ester in various tissues.
The proportion of one particular in the total of all ALLELES for one genetic locus in a breeding POPULATION.
The main trunk of the systemic arteries.
A class of lipoproteins that carry dietary CHOLESTEROL and TRIGLYCERIDES from the SMALL INTESTINE to the tissues. Their density (0.93-1.006 g/ml) is the same as that of VERY-LOW-DENSITY LIPOPROTEINS.
A diet that contributes to the development and acceleration of ATHEROGENESIS.
A condition with abnormally high levels of CHOLESTEROL in the blood. It is defined as a cholesterol value exceeding the 95th percentile for the population.
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
An enzyme of the hydrolase class that catalyzes the reaction of triacylglycerol and water to yield diacylglycerol and a fatty acid anion. The enzyme hydrolyzes triacylglycerols in chylomicrons, very-low-density lipoproteins, low-density lipoproteins, and diacylglycerols. It occurs on capillary endothelial surfaces, especially in mammary, muscle, and adipose tissue. Genetic deficiency of the enzyme causes familial hyperlipoproteinemia Type I. (Dorland, 27th ed) EC
Fatty acid esters of cholesterol which constitute about two-thirds of the cholesterol in the plasma. The accumulation of cholesterol esters in the arterial intima is a characteristic feature of atherosclerosis.
Cholesterol which is contained in or bound to very low density lipoproteins (VLDL). High circulating levels of VLDL cholesterol are found in HYPERLIPOPROTEINEMIA TYPE IIB. The cholesterol on the VLDL is eventually delivered by LOW-DENSITY LIPOPROTEINS to the tissues after the catabolism of VLDL to INTERMEDIATE-DENSITY LIPOPROTEINS, then to LDL.
An individual having different alleles at one or more loci regarding a specific character.
An enzyme secreted from the liver into the plasma of many mammalian species. It catalyzes the esterification of the hydroxyl group of lipoprotein cholesterol by the transfer of a fatty acid from the C-2 position of lecithin. In familial lecithin:cholesterol acyltransferase deficiency disease, the absence of the enzyme results in an excess of unesterified cholesterol in plasma. EC
The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.
Electrophoresis in which a pH gradient is established in a gel medium and proteins migrate until they reach the site (or focus) at which the pH is equal to their isoelectric point.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
A group of familial disorders characterized by elevated circulating cholesterol contained in either LOW-DENSITY LIPOPROTEINS alone or also in VERY-LOW-DENSITY LIPOPROTEINS (pre-beta lipoproteins).
The relatively long-lived phagocytic cell of mammalian tissues that are derived from blood MONOCYTES. Main types are PERITONEAL MACROPHAGES; ALVEOLAR MACROPHAGES; HISTIOCYTES; KUPFFER CELLS of the liver; and OSTEOCLASTS. They may further differentiate within chronic inflammatory lesions to EPITHELIOID CELLS or may fuse to form FOREIGN BODY GIANT CELLS or LANGHANS GIANT CELLS. (from The Dictionary of Cell Biology, Lackie and Dow, 3rd ed.)
A condition of elevated levels of TRIGLYCERIDES in the blood.
A mixture of very-low-density lipoproteins (VLDL), particularly the triglyceride-poor VLDL, with slow diffuse electrophoretic mobilities in the beta and alpha2 regions which are similar to that of beta-lipoproteins (LDL) or alpha-lipoproteins (HDL). They can be intermediate (remnant) lipoproteins in the de-lipidation process, or remnants of mutant CHYLOMICRONS and VERY-LOW-DENSITY LIPOPROTEINS which cannot be metabolized completely as seen in FAMILIAL DYSBETALIPOPROTEINEMIA.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
Conditions with abnormally low levels of LIPOPROTEINS in the blood. This may involve any of the lipoprotein subclasses, including ALPHA-LIPOPROTEINS (high-density lipoproteins); BETA-LIPOPROTEINS (low-density lipoproteins); and PREBETA-LIPOPROTEINS (very-low-density lipoproteins).
A latent susceptibility to disease at the genetic level, which may be activated under certain conditions.
An individual in which both alleles at a given locus are identical.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
Pathological processes involving any part of the AORTA.
The part of CENTRAL NERVOUS SYSTEM that is contained within the skull (CRANIUM). Arising from the NEURAL TUBE, the embryonic brain is comprised of three major parts including PROSENCEPHALON (the forebrain); MESENCEPHALON (the midbrain); and RHOMBENCEPHALON (the hindbrain). The developed brain consists of CEREBRUM; CEREBELLUM; and other structures in the BRAIN STEM.
Fats present in food, especially in animal products such as meat, meat products, butter, ghee. They are present in lower amounts in nuts, seeds, and avocados.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
Cholesterol present in food, especially in animal products.
Lipid-laden macrophages originating from monocytes or from smooth muscle cells.
A highly conserved heterodimeric glycoprotein that is differentially expressed during many severe physiological disturbance states such as CANCER; APOPTOSIS; and various NEUROLOGICAL DISORDERS. Clusterin is ubiquitously expressed and appears to function as a secreted MOLECULAR CHAPERONE.
A synthetic phospholipid used in liposomes and lipid bilayers for the study of biological membranes.
A severe type of hyperlipidemia, sometimes familial, that is characterized by the elevation of both plasma CHYLOMICRONS and TRIGLYCERIDES contained in VERY-LOW-DENSITY LIPOPROTEINS. Type V hyperlipoproteinemia is often associated with DIABETES MELLITUS and is not caused by reduced LIPOPROTEIN LIPASE activity as in HYPERLIPOPROTEINEMIA TYPE I .
Different forms of a protein that may be produced from different GENES, or from the same gene by ALTERNATIVE SPLICING.
An aspect of personal behavior or lifestyle, environmental exposure, or inborn or inherited characteristic, which, on the basis of epidemiologic evidence, is known to be associated with a health-related condition considered important to prevent.
A heterogeneous group of sporadic or familial disorders characterized by AMYLOID deposits in the walls of small and medium sized blood vessels of CEREBRAL CORTEX and MENINGES. Clinical features include multiple, small lobar CEREBRAL HEMORRHAGE; cerebral ischemia (BRAIN ISCHEMIA); and CEREBRAL INFARCTION. Cerebral amyloid angiopathy is unrelated to generalized AMYLOIDOSIS. Amyloidogenic peptides in this condition are nearly always the same ones found in ALZHEIMER DISEASE. (from Kumar: Robbins and Cotran: Pathologic Basis of Disease, 7th ed., 2005)
Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.
A hypertriglyceridemia disorder, often with autosomal dominant inheritance. It is characterized by the persistent elevations of plasma TRIGLYCERIDES, endogenously synthesized and contained predominantly in VERY-LOW-DENSITY LIPOPROTEINS (pre-beta lipoproteins). In contrast, the plasma CHOLESTEROL and PHOSPHOLIPIDS usually remain within normal limits.
A family of MEMBRANE TRANSPORT PROTEINS that require ATP hydrolysis for the transport of substrates across membranes. The protein family derives its name from the ATP-binding domain found on the protein.
Lipids containing one or more phosphate groups, particularly those derived from either glycerol (phosphoglycerides see GLYCEROPHOSPHOLIPIDS) or sphingosine (SPHINGOLIPIDS). They are polar lipids that are of great importance for the structure and function of cell membranes and are the most abundant of membrane lipids, although not stored in large amounts in the system.
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
Electrophoresis in which a polyacrylamide gel is used as the diffusion medium.
The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific protein-binding measures are often used as assays in diagnostic assessments.
Conditions with abnormally low levels of BETA-LIPOPROTEINS (low density lipoproteins or LDL) in the blood. It is defined as LDL values equal to or less than the 5th percentile for the population. They include the autosomal dominant form involving mutation of the APOLIPOPROTEINS B gene, and the autosomal recessive form involving mutation of the microsomal triglyceride transfer protein. All are characterized by low LDL and dietary fat malabsorption.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.
The first and largest artery branching from the aortic arch. It distributes blood to the right side of the head and neck and to the right arm.
The rate dynamics in chemical or physical systems.
Disturbances in mental processes related to learning, thinking, reasoning, and judgment.
Lesions formed within the walls of ARTERIES.
An enzyme of the hydrolase class that catalyzes the reaction of triacylglycerol and water to yield diacylglycerol and a fatty acid anion. It is produced by glands on the tongue and by the pancreas and initiates the digestion of dietary fats. (From Dorland, 27th ed) EC
An acquired organic mental disorder with loss of intellectual abilities of sufficient severity to interfere with social or occupational functioning. The dysfunction is multifaceted and involves memory, behavior, personality, judgment, attention, spatial relations, language, abstract thought, and other executive functions. The intellectual decline is usually progressive, and initially spares the level of consciousness.
Accumulations of extracellularly deposited AMYLOID FIBRILS within tissues.
The age, developmental stage, or period of life at which a disease or the initial symptoms or manifestations of a disease appear in an individual.
Intermediate-density subclass of the high-density lipoproteins, with particle sizes between 7 to 8 nm. As the larger lighter HDL2 lipoprotein, HDL3 lipoprotein is lipid-rich.
The range or frequency distribution of a measurement in a population (of organisms, organs or things) that has not been selected for the presence of disease or abnormality.
Abnormal structures located in various parts of the brain and composed of dense arrays of paired helical filaments (neurofilaments and microtubules). These double helical stacks of transverse subunits are twisted into left-handed ribbon-like filaments that likely incorporate the following proteins: (1) the intermediate filaments: medium- and high-molecular-weight neurofilaments; (2) the microtubule-associated proteins map-2 and tau; (3) actin; and (4) UBIQUITINS. As one of the hallmarks of ALZHEIMER DISEASE, the neurofibrillary tangles eventually occupy the whole of the cytoplasm in certain classes of cell in the neocortex, hippocampus, brain stem, and diencephalon. The number of these tangles, as seen in post mortem histology, correlates with the degree of dementia during life. Some studies suggest that tangle antigens leak into the systemic circulation both in the course of normal aging and in cases of Alzheimer disease.
A family of scavenger receptors that are predominately localized to CAVEOLAE of the PLASMA MEMBRANE and bind HIGH DENSITY LIPOPROTEINS.
A single-pass type I membrane protein. It is cleaved by AMYLOID PRECURSOR PROTEIN SECRETASES to produce peptides of varying amino acid lengths. A 39-42 amino acid peptide, AMYLOID BETA-PEPTIDES is a principal component of the extracellular amyloid in SENILE PLAQUES.
Established cell cultures that have the potential to propagate indefinitely.
Triple-looped protein domains linked by disulfide bonds. These common structural domains, so-named for their resemblance to Danish pastries known as kringlers, play a role in binding membranes, proteins, and phospholipids as well as in regulating proteolysis. Kringles are also present in coagulation-related and fibrinolytic proteins and other plasma proteinases.
Tests designed to assess neurological function associated with certain behaviors. They are used in diagnosing brain dysfunction or damage and central nervous system disorders or injury.
The gradual irreversible changes in structure and function of an organism that occur as a result of the passage of time.
Elements of limited time intervals, contributing to particular results or situations.
A deoxyribonucleotide polymer that is the primary genetic material of all cells. Eukaryotic and prokaryotic organisms normally contain DNA in a double-stranded state, yet several important biological processes transiently involve single-stranded regions. DNA, which consists of a polysugar-phosphate backbone possessing projections of purines (adenine and guanine) and pyrimidines (thymine and cytosine), forms a double helix that is held together by hydrogen bonds between these purines and pyrimidines (adenine to thymine and guanine to cytosine).
Relating to the size of solids.
Centrifugation with a centrifuge that develops centrifugal fields of more than 100,000 times gravity. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)
Studies which start with the identification of persons with a disease of interest and a control (comparison, referent) group without the disease. The relationship of an attribute to the disease is examined by comparing diseased and non-diseased persons with regard to the frequency or levels of the attribute in each group.
In vitro method for producing large amounts of specific DNA or RNA fragments of defined length and sequence from small amounts of short oligonucleotide flanking sequences (primers). The essential steps include thermal denaturation of the double-stranded target molecules, annealing of the primers to their complementary sequences, and extension of the annealed primers by enzymatic synthesis with DNA polymerase. The reaction is efficient, specific, and extremely sensitive. Uses for the reaction include disease diagnosis, detection of difficult-to-isolate pathogens, mutation analysis, genetic testing, DNA sequencing, and analyzing evolutionary relationships.
The dilatation of the aortic wall behind each of the cusps of the aortic valve.
An autosomal recessively inherited disorder caused by mutation of ATP-BINDING CASSETTE TRANSPORTERS involved in cellular cholesterol removal (reverse-cholesterol transport). It is characterized by near absence of ALPHA-LIPOPROTEINS (high-density lipoproteins) in blood. The massive tissue deposition of cholesterol esters results in HEPATOMEGALY; SPLENOMEGALY; RETINITIS PIGMENTOSA; large orange tonsils; and often sensory POLYNEUROPATHY. The disorder was first found among inhabitants of Tangier Island in the Chesapeake Bay, MD.
Genotypic differences observed among individuals in a population.
A type of familial lipid metabolism disorder characterized by a variable pattern of elevated plasma CHOLESTEROL and/or TRIGLYCERIDES. Multiple genes on different chromosomes may be involved, such as the major late transcription factor (UPSTREAM STIMULATORY FACTORS) on CHROMOSOME 1.
An imprecise term referring to dementia associated with CEREBROVASCULAR DISORDERS, including CEREBRAL INFARCTION (single or multiple), and conditions associated with chronic BRAIN ISCHEMIA. Diffuse, cortical, and subcortical subtypes have been described. (From Gerontol Geriatr 1998 Feb;31(1):36-44)
Proteins prepared by recombinant DNA technology.
An ACUTE PHASE REACTION protein present in low concentrations in normal sera, but found at higher concentrations in sera of older persons and in patients with AMYLOIDOSIS. It is the circulating precusor of amyloid A protein, which is found deposited in AA type AMYLOID FIBRILS.
Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.
Variation occurring within a species in the presence or length of DNA fragment generated by a specific endonuclease at a specific site in the genome. Such variations are generated by mutations that create or abolish recognition sites for these enzymes or change the length of the fragment.
A large group of structurally diverse cell surface receptors that mediate endocytic uptake of modified LIPOPROTEINS. Scavenger receptors are expressed by MYELOID CELLS and some ENDOTHELIAL CELLS, and were originally characterized based on their ability to bind acetylated LOW-DENSITY LIPOPROTEINS. They can also bind a variety of other polyanionic ligand. Certain scavenger receptors can internalize micro-organisms as well as apoptotic cells.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
Mononuclear phagocytes derived from bone marrow precursors but resident in the peritoneum.
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
Transport proteins that carry specific substances in the blood or across cell membranes.
Measurable and quantifiable biological parameters (e.g., specific enzyme concentration, specific hormone concentration, specific gene phenotype distribution in a population, presence of biological substances) which serve as indices for health- and physiology-related assessments, such as disease risk, psychiatric disorders, environmental exposure and its effects, disease diagnosis, metabolic processes, substance abuse, pregnancy, cell line development, epidemiologic studies, etc.
Substances used to lower plasma CHOLESTEROL levels.
(Z)-9-Octadecenoic acid 1,2,3-propanetriyl ester.
Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.
A mercaptoethylamine compound that is endogenously derived from the COENZYME A degradative pathway. The fact that cysteamine is readily transported into LYSOSOMES where it reacts with CYSTINE to form cysteine-cysteamine disulfide and CYSTEINE has led to its use in CYSTINE DEPLETING AGENTS for the treatment of CYSTINOSIS.
The metabolic process of breaking down LIPIDS to release FREE FATTY ACIDS, the major oxidative fuel for the body. Lipolysis may involve dietary lipids in the DIGESTIVE TRACT, circulating lipids in the BLOOD, and stored lipids in the ADIPOSE TISSUE or the LIVER. A number of enzymes are involved in such lipid hydrolysis, such as LIPASE and LIPOPROTEIN LIPASE from various tissues.
A highly dense subclass of the high-density lipoproteins, with particle sizes below 7 nm. They are also known as nascent HDL, composed of a few APOLIPOPROTEIN A-I molecules which are complexed with PHOSPHOLIPIDS. The lipid-poor pre-beta-HDL particles serve as progenitors of HDL3 and then HDL2 after absorption of free cholesterol from cell membranes, cholesterol esterification, and acquisition of apolipoproteins A-II, Cs, and E. Pre-beta-HDL initiate the reverse cholesterol transport process from cells to liver.
An enzyme of the isomerase class that catalyzes the eliminative cleavage of polysaccharides containing 1,4-linked D-glucuronate or L-iduronate residues and 1,4-alpha-linked 2-sulfoamino-2-deoxy-6-sulfo-D-glucose residues to give oligosaccharides with terminal 4-deoxy-alpha-D-gluc-4-enuronosyl groups at their non-reducing ends. (From Enzyme Nomenclature, 1992) EC
An enzyme which catalyzes the hydrolysis of an aryl-dialkyl phosphate to form dialkyl phosphate and an aryl alcohol. It can hydrolyze a broad spectrum of organophosphate substrates and a number of aromatic carboxylic acid esters. It may also mediate an enzymatic protection of LOW DENSITY LIPOPROTEINS against oxidative modification and the consequent series of events leading to ATHEROMA formation. The enzyme was previously regarded to be identical with Arylesterase (EC
Electrophoresis in which agar or agarose gel is used as the diffusion medium.
The worsening of a disease over time. This concept is most often used for chronic and incurable diseases where the stage of the disease is an important determinant of therapy and prognosis.
Derivatives of phosphatidic acids in which the phosphoric acid is bound in ester linkage to a choline moiety. Complete hydrolysis yields 1 mole of glycerol, phosphoric acid and choline and 2 moles of fatty acids.
The movement of materials (including biochemical substances and drugs) through a biological system at the cellular level. The transport can be across cell membranes and epithelial layers. It also can occur within intracellular compartments and extracellular compartments.
Substances that lower the levels of certain LIPIDS in the BLOOD. They are used to treat HYPERLIPIDEMIAS.
Microtubule-associated proteins that are mainly expressed in neurons. Tau proteins constitute several isoforms and play an important role in the assembly of tubulin monomers into microtubules and in maintaining the cytoskeleton and axonal transport. Aggregation of specific sets of tau proteins in filamentous inclusions is the common feature of intraneuronal and glial fibrillar lesions (NEUROFIBRILLARY TANGLES; NEUROPIL THREADS) in numerous neurodegenerative disorders (ALZHEIMER DISEASE; TAUOPATHIES).
Metabolic products of chylomicron particles in which TRIGLYCERIDES have been selectively removed by the LIPOPROTEIN LIPASE. These remnants carry dietary lipids in the blood and are cholesterol-rich. Their interactions with MACROPHAGES; ENDOTHELIAL CELLS; and SMOOTH MUSCLE CELLS in the artery wall can lead to ATHEROSCLEROSIS.
The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.
An enzyme that catalyzes the deamination of cytidine, forming uridine. EC
Conjugated protein-carbohydrate compounds including mucins, mucoid, and amyloid glycoproteins.
Abnormalities in the serum levels of LIPIDS, including overproduction or deficiency. Abnormal serum lipid profiles may include high total CHOLESTEROL, high TRIGLYCERIDES, low HIGH DENSITY LIPOPROTEIN CHOLESTEROL, and elevated LOW DENSITY LIPOPROTEIN CHOLESTEROL.
A highly acidic mucopolysaccharide formed of equal parts of sulfated D-glucosamine and D-glucuronic acid with sulfaminic bridges. The molecular weight ranges from six to twenty thousand. Heparin occurs in and is obtained from liver, lung, mast cells, etc., of vertebrates. Its function is unknown, but it is used to prevent blood clotting in vivo and vitro, in the form of many different salts.
An imbalance between myocardial functional requirements and the capacity of the CORONARY VESSELS to supply sufficient blood flow. It is a form of MYOCARDIAL ISCHEMIA (insufficient blood supply to the heart muscle) caused by a decreased capacity of the coronary vessels.
An autosomal recessive disorder of lipid metabolism. It is caused by mutation of the microsomal triglyceride transfer protein that catalyzes the transport of lipids (TRIGLYCERIDES; CHOLESTEROL ESTERS; PHOSPHOLIPIDS) and is required in the secretion of BETA-LIPOPROTEINS (low density lipoproteins or LDL). Features include defective intestinal lipid absorption, very low serum cholesterol level, and near absent LDL.
The level of protein structure in which regular hydrogen-bond interactions within contiguous stretches of polypeptide chain give rise to alpha helices, beta strands (which align to form beta sheets) or other types of coils. This is the first folding level of protein conformation.
A fibrous protein complex that consists of proteins folded into a specific cross beta-pleated sheet structure. This fibrillar structure has been found as an alternative folding pattern for a variety of functional proteins. Deposits of amyloid in the form of AMYLOID PLAQUES are associated with a variety of degenerative diseases. The amyloid structure has also been found in a number of functional proteins that are unrelated to disease.
Leukocyte differentiation antigens and major platelet membrane glycoproteins present on MONOCYTES; ENDOTHELIAL CELLS; PLATELETS; and mammary EPITHELIAL CELLS. They play major roles in CELL ADHESION; SIGNAL TRANSDUCTION; and regulation of angiogenesis. CD36 is a receptor for THROMBOSPONDINS and can act as a scavenger receptor that recognizes and transports oxidized LIPOPROTEINS and FATTY ACIDS.
A change from planar to elliptic polarization when an initially plane-polarized light wave traverses an optically active medium. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)
Mice bearing mutant genes which are phenotypically expressed in the animals.
Colloids formed by the combination of two immiscible liquids such as oil and water. Lipid-in-water emulsions are usually liquid, like milk or lotion. Water-in-lipid emulsions tend to be creams. The formation of emulsions may be aided by amphiphatic molecules that surround one component of the system to form MICELLES.
A process that changes the nucleotide sequence of mRNA from that of the DNA template encoding it. Some major classes of RNA editing are as follows: 1, the conversion of cytosine to uracil in mRNA; 2, the addition of variable number of guanines at pre-determined sites; and 3, the addition and deletion of uracils, templated by guide-RNAs (RNA, GUIDE).
Immunologic method used for detecting or quantifying immunoreactive substances. The substance is identified by first immobilizing it by blotting onto a membrane and then tagging it with labeled antibodies.
Identification of genetic carriers for a given trait.
The characteristic 3-dimensional shape of a protein, including the secondary, supersecondary (motifs), tertiary (domains) and quaternary structure of the peptide chain. PROTEIN STRUCTURE, QUATERNARY describes the conformation assumed by multimeric proteins (aggregates of more than one polypeptide chain).
The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.
A prodromal phase of cognitive decline that may precede the emergence of ALZHEIMER DISEASE and other dementias. It may include impairment of cognition, such as impairments in language, visuospatial awareness, ATTENTION and MEMORY.
Age as a constituent element or influence contributing to the production of a result. It may be applicable to the cause or the effect of a circumstance. It is used with human or animal concepts but should be differentiated from AGING, a physiological process, and TIME FACTORS which refers only to the passage of time.
Cell surface molecules on cells of the immune system that specifically bind surface molecules or messenger molecules and trigger changes in the behavior of cells. Although these receptors were first identified in the immune system, many have important functions elsewhere.
The interaction of two or more substrates or ligands with the same binding site. The displacement of one by the other is used in quantitative and selective affinity measurements.
Either of the two principal arteries on both sides of the neck that supply blood to the head and neck; each divides into two branches, the internal carotid artery and the external carotid artery.
Cytokine-induced cell adhesion molecule present on activated endothelial cells, tissue macrophages, dendritic cells, bone marrow fibroblasts, myoblasts, and myotubes. It is important for the recruitment of leukocytes to sites of inflammation. (From Pigott & Power, The Adhesion Molecule FactsBook, 1993, p154)
The time frame after a meal or FOOD INTAKE.
The record of descent or ancestry, particularly of a particular condition or trait, indicating individual family members, their relationships, and their status with respect to the trait or condition.
An enzyme that catalyzes the formation of cholesterol esters by the direct transfer of the fatty acid group from a fatty acyl CoA derivative. This enzyme has been found in the adrenal gland, gonads, liver, intestinal mucosa, and aorta of many mammalian species. EC
Chemical analysis based on the phenomenon whereby light, passing through a medium with dispersed particles of a different refractive index from that of the medium, is attenuated in intensity by scattering. In turbidimetry, the intensity of light transmitted through the medium, the unscattered light, is measured. In nephelometry, the intensity of the scattered light is measured, usually, but not necessarily, at right angles to the incident light beam.
Detection of a MUTATION; GENOTYPE; KARYOTYPE; or specific ALLELES associated with genetic traits, heritable diseases, or predisposition to a disease, or that may lead to the disease in descendants. It includes prenatal genetic testing.
Intellectual or mental process whereby an organism obtains knowledge.
Regular course of eating and drinking adopted by a person or animal.
A statistical technique that isolates and assesses the contributions of categorical independent variables to variation in the mean of a continuous dependent variable.
A condition marked by the development of widespread xanthomas, yellow tumor-like structures filled with lipid deposits. Xanthomas can be found in a variety of tissues including the SKIN; TENDONS; joints of KNEES and ELBOWS. Xanthomatosis is associated with disturbance of LIPID METABOLISM and formation of FOAM CELLS.
Microscopy using an electron beam, instead of light, to visualize the sample, thereby allowing much greater magnification. The interactions of ELECTRONS with specimens are used to provide information about the fine structure of that specimen. In TRANSMISSION ELECTRON MICROSCOPY the reactions of the electrons that are transmitted through the specimen are imaged. In SCANNING ELECTRON MICROSCOPY an electron beam falls at a non-normal angle on the specimen and the image is derived from the reactions occurring above the plane of the specimen.
An immunoassay utilizing an antibody labeled with an enzyme marker such as horseradish peroxidase. While either the enzyme or the antibody is bound to an immunosorbent substrate, they both retain their biologic activity; the change in enzyme activity as a result of the enzyme-antibody-antigen reaction is proportional to the concentration of the antigen and can be measured spectrophotometrically or with the naked eye. Many variations of the method have been developed.
An autosomal recessively inherited disorder caused by mutation of LECITHIN CHOLESTEROL ACYLTRANSFERASE that facilitates the esterification of lipoprotein cholesterol and subsequent removal from peripheral tissues to the liver. This defect results in low HDL-cholesterol level in blood and accumulation of free cholesterol in tissue leading to a triad of CORNEAL OPACITY, hemolytic anemia (ANEMIA, HEMOLYTIC), and PROTEINURIA.
Studies in which subsets of a defined population are identified. These groups may or may not be exposed to factors hypothesized to influence the probability of the occurrence of a particular disease or other outcome. Cohorts are defined populations which, as a whole, are followed in an attempt to determine distinguishing subgroup characteristics.
Maleness or femaleness as a constituent element or influence contributing to the production of a result. It may be applicable to the cause or effect of a circumstance. It is used with human or animal concepts but should be differentiated from SEX CHARACTERISTICS, anatomical or physiological manifestations of sex, and from SEX DISTRIBUTION, the number of males and females in given circumstances.
A class of large neuroglial (macroglial) cells in the central nervous system - the largest and most numerous neuroglial cells in the brain and spinal cord. Astrocytes (from "star" cells) are irregularly shaped with many long processes, including those with "end feet" which form the glial (limiting) membrane and directly and indirectly contribute to the BLOOD-BRAIN BARRIER. They regulate the extracellular ionic and chemical environment, and "reactive astrocytes" (along with MICROGLIA) respond to injury.
A single nucleotide variation in a genetic sequence that occurs at appreciable frequency in the population.
Abstaining from all food.
A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function.
Chromatography on non-ionic gels without regard to the mechanism of solute discrimination.
A drug used to lower LDL and HDL cholesterol yet has little effect on serum-triglyceride or VLDL cholesterol. (From Martindale, The Extra Pharmacopoeia, 30th ed, p993).
The innermost layer of an artery or vein, made up of one layer of endothelial cells and supported by an internal elastic lamina.
Surface ligands that mediate cell-to-cell adhesion and function in the assembly and interconnection of the vertebrate nervous system. These molecules promote cell adhesion via a homophilic mechanism. These are not to be confused with NEURAL CELL ADHESION MOLECULES, now known to be expressed in a variety of tissues and cell types in addition to nervous tissue.
The portion of the descending aorta proceeding from the arch of the aorta and extending to the DIAPHRAGM, eventually connecting to the ABDOMINAL AORTA.
Diseases in which there is a familial pattern of AMYLOIDOSIS.
Large, phagocytic mononuclear leukocytes produced in the vertebrate BONE MARROW and released into the BLOOD; contain a large, oval or somewhat indented nucleus surrounded by voluminous cytoplasm and numerous organelles.
The main structural component of the LIVER. They are specialized EPITHELIAL CELLS that are organized into interconnected plates called lobules.
Short sequences (generally about 10 base pairs) of DNA that are complementary to sequences of messenger RNA and allow reverse transcriptases to start copying the adjacent sequences of mRNA. Primers are used extensively in genetic and molecular biology techniques.
Techniques used to add in exogenous gene sequence such as mutated genes; REPORTER GENES, to study mechanisms of gene expression; or regulatory control sequences, to study effects of temporal changes to GENE EXPRESSION.
Those characteristics that distinguish one SEX from the other. The primary sex characteristics are the OVARIES and TESTES and their related hormones. Secondary sex characteristics are those which are masculine or feminine but not directly related to reproduction.
The parts of a macromolecule that directly participate in its specific combination with another molecule.
Members of the class of compounds composed of AMINO ACIDS joined together by peptide bonds between adjacent amino acids into linear, branched or cyclical structures. OLIGOPEPTIDES are composed of approximately 2-12 amino acids. Polypeptides are composed of approximately 13 or more amino acids. PROTEINS are linear polypeptides that are normally synthesized on RIBOSOMES.
DNA sequences which are recognized (directly or indirectly) and bound by a DNA-dependent RNA polymerase during the initiation of transcription. Highly conserved sequences within the promoter include the Pribnow box in bacteria and the TATA BOX in eukaryotes.
An unsaturated fatty acid that is the most widely distributed and abundant fatty acid in nature. It is used commercially in the preparation of oleates and lotions, and as a pharmaceutical solvent. (Stedman, 26th ed)

Apo E phenotype and changes in serum lipids in adult patients during growth hormone replacement. (1/855)

OBJECTIVE: To determine whether apo E phenotype influences changes in lipid profiles induced by growth hormone replacement in growth hormone (GH)-deficient adults. DESIGNS: Patients were treated for 6 months with recombinant human GH (hGH), given in a dose of 0.125 U/kg per week for 4 weeks followed by 0.25 U/kg per week thereafter. The effects on serum lipids and the influence of apo E phenotype were examined. METHODS: Thirty patients (aged 35.1+/-11.8 years: mean +/- S.D.) with adult growth hormone deficiency with included in the study. Fasting serum samples were analysed for apo E phenotype total cholesterol, high-density lipoprotein (HDL)-cholesterol, triglycerides, lipoprotein (a) (Lp(a)) and IGF-I. Low-density lipoprotein (LDL)-cholesterol was calculated using the Friedwald formula. RESULTS: Six months of replacement treatment with hGH resulted in a reduction in HDL-cholesterol from 0.90+/-0.10 to 0.68+/-0.08 mmol/l (P<0.01), and a small, non-significant reduction in total cholesterol from 6.14+/-0.40 to 5.99+/-0.35 mmol/l (P = 0.06). There was no significant change in the other lipid parameters. The decrease in HDL-cholesterol concentration was greater in patients carrying the apo E2 allele (0.40+/-0.07 mmol/l, P<0.05) than in patients homozygous for the apo E3 allele (0.23+/-0.04 mmol/l) and patients carrying the apo E4 allele (0.15+/-0.36 mmol/l). Patients with the apo E4 allele had lower baseline cholesterol concentrations than patients lacking the apo E4 allele, and this persisted after treatment with hGH (P<0.05). CONCLUSIONS: Apo E phenotype may be a determining factor in the response of HDL-cholesterol to hGH in GH-deficient adults.  (+info)

Comparison of the LDL-receptor binding of VLDL and LDL from apoE4 and apoE3 homozygotes. (2/855)

Compared with apolipoprotein E3 (apoE3), apoE2 is less effective in mediating the binding of lipoproteins to the low-density lipoprotein (LDL) receptor. The influence of the E4 isoform, which is associated with adverse effects on plasma lipids and coronary heart disease, is less clear. We compared the ability of very low density lipoprotein (VLDL) and LDL from paired E4/4 and E3/3 subjects to compete against 125I-labeled LDL for binding with the LDL receptor on cultured fibroblasts and Hep G2 cells. The concentrations of VLDL or LDL required to inhibit binding of 125I-LDL by 50% (IC50, microgram apoB/ml) were determined, and results were assessed in terms of an IC50 ratio, E4/4 IC50 relative to E3/3 IC50, to reduce the influence of interassay variability. In Hep G2 cells, E4/4 VLDL was more effective than E3/3 VLDL in competing for the LDL receptor, the IC50 ratio being lower than unity (0.73 +/- 0.31, P < 0.05, two-tailed t-test). IC50 values themselves were marginally lower in E4/4 than E3/3 subjects (3.7 +/- 1.3 vs. 6.1 +/- 3.7, P < 0.08). However, there was no difference between E4/4 and E3/3 VLDL in competing for the LDL receptor on fibroblasts or between E4/4 and E3/3 LDL in competing for the LDL receptor on either cell type. These results suggest that inheritance of apoE4 is associated with an increased affinity of VLDL particles for LDL receptors on hepatocytes and may partly explain the influence of the E4 isoform on lipid metabolism.  (+info)

Synergistic effects of prothrombotic polymorphisms and atherogenic factors on the risk of myocardial infarction in young males. (3/855)

Several recent studies evaluated a possible effect of the prothrombotic polymorphisms such as 5,10 methylenetetrahydrofolate reductase (MTHFR) nt 677C --> T, factor V (F V) nt 1691G --> A (F V Leiden), and factor II (F II) nt 20210 G --> A on the risk of myocardial infarction. In the present study, we analyzed the effect of these prothrombotic polymorphisms, as well as apolipoprotein (Apo) E4, smoking, hypertension, diabetes mellitus, and hypercholesterolemia, on the risk of myocardial infarction in young males. We conducted a case-control study of 112 young males with first acute myocardial infarction (AMI) before the age of 52 and 187 healthy controls of similar age. The prevalences of heterozygotes for F V G1691A and F II G20210A were not significantly different between cases and controls (6.3% v 6.4% and 5.9% v 3.4% among cases and controls, respectively). In contrast, the prevalence of MTHFR 677T homozygosity and the allele frequency of Apo E4 were significantly higher among patients (24.1% v 10.7% and 9.4% v 5.3% among cases and controls, respectively). Concomitant presence of hypertension, hypercholesterolemia, or diabetes and one or more of the four examined polymorphisms increased the risk by almost ninefold (odds ratio [OR] = 8.66; 95% confidence interval [CI], 3.49 to 21.5) and concomitant smoking by almost 18-fold (OR = 17.6; 95% CI, 6.30 to 48.9). When all atherogenic risk factors were analyzed simultaneously by a logistic model, the combination of prothrombotic and Apo E4 polymorphisms with current smoking increased the risk 25-fold (OR = 24.7; 95% CI, 7.17 to 84.9). The presented data suggest a synergistic effect between atherogenic and thrombogenic risk factors in the pathogenesis of AMI, as was recently found in a similar cohort of women.  (+info)

Apolipoprotein E4, cholinergic integrity and the pharmacogenetics of Alzheimer's disease. (4/855)

Recent evidence indicates that apolipoprotein E (apoE) plays a central role in the brain's response to injury. The coordinated expression of apoE and its receptors (the so-called LDL [low density lipoprotein] receptor family) appears to regulate the transport and internalization of cholesterol and phospholipids during the early phase of the re-innervation process in the adult brain. During dendritic remodelling and synaptogenesis, neurons progressively repress the synthesis of cholesterol in favour of cholesterol internalization through the apoE/LDL receptor pathway. The discovery a few years ago, that the apolipoprotein epsilon 4 allele found in 15% of the normal population is strongly linked to both sporadic and familial late-onset Alzheimer's disease (AD), raises the possibility that a dysfunction of the lipid transport system associated with compensatory sprouting and synaptic remodelling could be central to the AD process. The role of apoE in the central nervous system is particularly important in relation to the cholinergic system, which relies to a certain extent on the integrity of phospholipid homeostasis in neurons. Recent evidence obtained by 4 independent research teams indicates that apo epsilon 4 allele directly affects cholinergic activity in the brain of AD subjects. It was also shown to modulate the drug efficacy profile of several cholinomimetic and noncholinomimetic drugs used for the treatment of AD patients.  (+info)

Effects of a frequent apolipoprotein E isoform, ApoE4Freiburg (Leu28-->Pro), on lipoproteins and the prevalence of coronary artery disease in whites. (5/855)

Different isoforms of apoE modulate the concentrations of plasma lipoproteins and the risk for atherosclerosis. A novel apoE isoform, apoE4Freiburg, was detected in plasma by isoelectric focusing because its isoelectric point is slightly more acidic than that of apoE4. ApoE4Freiburg results from a base exchange in the APOE4 gene that causes the replacement of a leucine by a proline at position 28. Analysis of the allelic frequencies in whites in southwestern Germany revealed that this isoform is frequent among control subjects (10:4264 alleles) and is even more frequent in patients with coronary artery disease (21:2874 alleles; P=0.004; adjusted odds ratio, 3.09; 95% confidence interval, 1.20 to 7.97). ApoE4Freiburg affects serum lipoproteins by lowering cholesterol, apoB, and apoA-I compared with apoE4 (P<0.05). Our 4 apoE4Freiburg homozygotes suffered from various phenotypes of hyperlipoproteinemia (types IIa, IIb, IV, and V). In vitro binding studies excluded a binding defect of apoE4Freiburg, and in vivo studies excluded an abnormal accumulation of chylomicron remnants. ApoE4Freiburg and apoE4 accumulated to a similar extent in triglyceride-rich lipoproteins. HDLs, however, contained about 40% less apoE4Freiburg than apoE4. In conclusion, our data indicate that apoE4Freiburg exerts its possible atherogenic properties by affecting the metabolism of triglyceride-rich lipoproteins and HDL.  (+info)

Apo E structure determines VLDL clearance and atherosclerosis risk in mice. (6/855)

We have generated mice expressing the human apo E4 isoform in place of the endogenous murine apo E protein and have compared them with mice expressing the human apo E3 isoform. Plasma lipid and apolipoprotein levels in the mice expressing only the apo E4 isoform (4/4) did not differ significantly from those in mice with the apo E3 isoform (3/3) on chow and were equally elevated in response to increased lipid and cholesterol in their diet. However, on all diets tested, the 4/4 mice had approximately twice the amount of cholesterol, apo E, and apo B-48 in their VLDL as did 3/3 mice. The 4/4 VLDL competed with human LDL for binding to the human LDL receptor slightly better than 3/3 VLDL, but the VLDL clearance rate in 4/4 mice was half that in 3/3 mice. On an atherogenic diet, there was a trend toward greater atherosclerotic plaque size in 4/4 mice compared with 3/3 mice. These data, together with our earlier observations in wild-type and human APOE*2-replacement mice, demonstrate a direct and highly significant correlation between VLDL clearance rate and mean atherosclerotic plaque size. Therefore, differences solely in apo E protein structure are sufficient to cause alterations in VLDL residence time and atherosclerosis risk in mice.  (+info)

Expression of human apolipoprotein E3 or E4 in the brains of Apoe-/- mice: isoform-specific effects on neurodegeneration. (7/855)

Apolipoprotein (apo) E isoforms are key determinants of susceptibility to Alzheimer's disease. The apoE4 isoform is the major known genetic risk factor for this disease and is also associated with poor outcome after acute head trauma or stroke. To test the hypothesis that apoE3, but not apoE4, protects against age-related and excitotoxin-induced neurodegeneration, we analyzed apoE knockout (Apoe-/-) mice expressing similar levels of human apoE3 or apoE4 in the brain under control of the neuron-specific enolase promoter. Neuronal apoE expression was widespread in the brains of these mice. Kainic acid-challenged wild-type or Apoe-/- mice had a significant loss of synaptophysin-positive presynaptic terminals and microtubule-associated protein 2-positive neuronal dendrites in the neocortex and hippocampus, and a disruption of neurofilament-positive axons in the hippocampus. Expression of apoE3, but not of apoE4, protected against this excitotoxin-induced neuronal damage. ApoE3, but not apoE4, also protected against the age-dependent neurodegeneration seen in Apoe-/- mice. These differences in the effects of apoE isoforms on neuronal integrity may relate to the increased risk of Alzheimer's disease and to the poor outcome after head trauma and stroke associated with apoE4 in humans.  (+info)

Failure to confirm a synergistic effect between the K-variant of the butyrylcholinesterase gene and the epsilon4 allele of the apolipoprotein gene in Japanese patients with Alzheimer's disease. (8/855)

To confirm a synergistic effect between the polymorphic K variant of the butyrylcholinesterase (BChE-K) gene and the epsilon4 allele of the apolipoprotein E (APOE) gene in Alzheimer's disease, the frequency of the BChE-K allele was re-examined in a large series of Japanese patients with Alzheimer's disease and controls. Two hundred and three patients with Alzheimer's disease and 288 age and sex matched controls were genotyped by polymerase chain reaction and restriction fragment length polymorphism for BChE-K and APOE. No changes were found in the frequency of BChE-K, either in the Alzheimer's disease group as a whole (0.17 v 0.14; p=0.36) or in early (0.16 v 0.16; p=0.98) or late (0.17 v 0.13; p=0.24) onset patients compared with age matched controls. The study failed to confirm the findings of a previous study which found a significantly higher incidence of BChE-K in patients with Alzheimer's disease with APOE epsilon4 allele than in controls. In the Japanese population studied here, there was no association between BChE-K and Alzheimer's disease, nor an interaction between BChE-K and APOE epsilon4 allele.  (+info)

TY - JOUR. T1 - Influence of APOE status on lexical-semantic skills in mild cognitive impairment. AU - Biundo, Roberta. AU - Gardini, Simona. AU - Caffarra, Paolo. AU - Concari, Letizia. AU - Martorana, Davide. AU - Neri, Tauro Maria. AU - Shanks, Michael F.. AU - Venneri, Annalena. PY - 2011/5. Y1 - 2011/5. N2 - This study characterized the relationship between apolipoprotein E (APOE) status and residual semantic abilities in amnestic mild cognitive impairment (MCI). APOE status (ε4 carrier/non ε4 carrier) was determined in 30 amnestic MCIs and in 22 healthy matched non ε4 carrier controls. The lexical characteristics (age of acquisition, typicality, familiarity) of words produced in a category fluency task were determined. MCIs produced fewer words than controls and these were also earlier acquired and more familiar. The words produced by MCI ε4 carriers were earlier acquired than those of non ε4 carriers. Analyses limited to the first 10 words produced by patients and controls showed ...
By 2050, individuals over the age of 60 years are likely to make up about 30% of the population in developed countries.1 The number of people with cognitive impairment is rising in the same way and the next 30 years will see an anticipated threefold increase in Alzheimers disease (AD) sufferers in the US alone.2 These changes are likely to put healthcare budgets under significant strain, especially with regard to the provision of nursing care.3 Half of all patients diagnosed will need help with personal care, and one third will eventually be institutionalised.4,5. Intensive research into the pathophysiology of dementia has failed to identify disease modifying therapeutic agents; however, greater understanding of the components of dementia that finally necessitate admission to residential or nursing home care is also very necessary. Older dementia sufferers living alone, or those with greater functional disability seem more at risk.6,7 Carer provision and coping skills are also important.8-10 ...
Results from two small studies, involving a total of only 174 cases, have suggested that the increased risk of coronary heart disease conferred by cigarette smoking is substantially affected by genotype at the apolipoprotein E (APOE) epsilon2/epsilon3/epsilon4 polymorphism. We have established APOE genotypes in 4484 patients with acute myocardial infarction diagnosed before the age of 55 years for male and 65 years for female patients, and in 5757 controls with no history of cardiovascular disease. On average, the hazard ratio for myocardial infarction was 1.17 (95% CI 1.09-1.25; p|0.00001) per stepwise change from epsilon3/2 to epsilon3/3 to epsilon3/4 genotype. Among individuals in this study with known cigarette smoking status, the hazard ratio for myocardial infarction in smokers versus non-smokers was 4.6 (4.2-5.1). There was, however, no significant difference between the smoker/non-smoker hazard ratios for those with different APOE genotypes (chi2(2)=0.69; p=0.7). When differences in risk between
Alzheimer disease is the most common form of dementia in Western countries and the leading cause of disability in the over-65 population. Apolipoprotein E (APOE) is a multifunctional protein implied in lipid metabolism and neurobiology. Polymorphisms of the APOE gene have been associated with a vari …
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An excel sheet containing data for the 2 APOE SNPs (rs429358 and rs7412), translation rules for the SNPs, failures by individual, failures by rs number, and genotyping errors (the last 3 only if applicable). It is very important to note that these results are only to be used for research purposes. This test is not approved for clinical use and therefore the data cannot be returned to subjects. ...
A well-known result, due to Ostrowski, states that if $\Vert P-Q \Vert_2< \varepsilon$, then the roots $(x_j)$ of $P$ and $(y_j)$ of $Q$ satisfy $,x_j -y_j,\le C n \varepsilon^{1/n}$, where $n$ is the degree of $P$ and $Q$. Though there are cases where this estimate is sharp, it can still be made more precise in general, in two ways: first by using Bombieris norm instead of the classical $l_1$ or $l_2$ norms, and second by taking into account the multiplicity of each root. For instance, if $x$ is a simple root of $P$, we show that $,x-y,< C \varepsilon$ instead of $\varepsilon^{1/n}$. The proof uses the properties of Bombieris scalar product and Walsh Contraction Principle ...
Despite apolipoprotein Es important role in cholesterol transport and metabolism in the brain as well as its influence on Alzheimers disease, the impact of the human APOE genotype on cholesterol metabolism in brain has not been fully examined. This study was carried out to investigate APOE genotype effects on oxysterols measured. In this study the measurement of cholesterol and several oxysterols in the brains of human APOE ε2, ε3 and ε4 knock-in mice at 8 weeks and 1 year of age using gas chromatography mass spectrometry (GC-MS) demonstrated no APOE genotype or age effect on total brain cholesterol and the oxysterol 24-hydroxycholesterol. The level of 27-hydroxycholesterol was elevated in 1 year old animals for all APOE genotypes. Interestingly, lathosterol an indicator of cholesterol synthesis was significantly reduced in the 1 year old animals for all APOE genotypes. APOE ε4 expressing mice exhibited statistically lower levels of lathosterol compared to APOE ε2 in both the young and ...
OBJECTIVE:To investigate the association between the apolipoprotein E (APOE) genotypes and dementia in patients with stroke, defined as either vascular dementia (VaD) or Alzheimer disease with cerebrovascular disease (AD with CVD). DESIGN AND SETTING:Population-based, case-control study from Rotterdam, the Netherlands, and New York City. PARTICIPANTS:A total of 187 patients with dementia and stroke were compared with 507 controls similar in age and ethnic group. MAIN OUTCOME MEASURES:The APOE allele frequencies in patients and controls; the odds ratio of dementia with stroke, VaD, and AD with CVD, adjusted for age, sex, residency, and education; and the percent attributable risk related to the APOE epsilon4 allele. RESULTS:Overall, patients with dementia and stroke had a higher APOE epsilon4 allele frequency than controls. Compared with APOE epsilon3 homozygote individuals, APOE epsilon4 homozygotes had a 7-fold increased risk of dementia with stroke (OR=6.9; 95% CI, 1.6-29.4), while APOE epsilon4
Human apolipoprotein E4 targeted replacement mice show increased prevalence of intracerebral hemorrhage associated with vascular amyloid deposition.
Short-term adverse effects of the apolipoprotein E e4 allele over language function and executive function in healthy older adults Wei Li,1,2,* Qi Qiu,1,2,* Lin Sun,1,2,* Xia Li1,2, Shifu Xiao1,21Department of Geriatric Psychiatry, Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China; 2Alzheimers Disease and Related Disorders Center, Shanghai Jiao Tong University, Shanghai, China*These authors contributed equally to this workBackground: The 4 allele of the apolipoprotein E (APOE) gene is known as a risk factor for cognitive impairment. How APOE ϵ polymorphism affects the language and executive functions of healthy aging subjects remains less clear.Purpose: In this follow-up study, the relationship between APOE status and cognitive performance across various cognitive domains in healthy individuals (without dementia or mild cognitive impairment (MCI)) over 60 years old was investigated.Patients and methods: Based on multiplex amplification refractory mutation
APOE epsilon4 is the best-established genetic risk factor for sporadic Alzheimers disease (AD). However, while homozygotes show greater disease susceptibility and earlier age of onset than heterozygotes, they may not show faster rates of clinical progression. We hypothesize that there are differential APOE epsilon4 allele-load dependent influences on neuropathology across the brain. Our aim was to define the relationship between APOE epsilon4 allele load and regionally-specific brain cortical atrophy in Alzheimers Disease (AD). For this reason voxel-based morphometry (VBM) was performed using T1-weighted MR images from 83 AD patients, contrasting regional cortical grey matter by APOE epsilon4 load according to either dominant or genotypic models. Patients fulfilled NINCDS-ADRDA criteria and were genotyped for APOE epsilon4 (15 epsilon4/epsilon4, 39 epsilon4/- and 29-/-). We observed that grey matter volume (GMV) decreased additively with increasing allele load in the medial (MTL) and anterior temporal
Associations between apolipoprotein E genotypes and serum levels of glucose, cholesterol, and triglycerides in a cognitively normal aging Han Chinese population Qing-Qing Tao,1,* Yan Chen,2,3,* Zhi-Jun Liu,1 Yi-Min Sun,1 Ping Yang,1 Shen-Ji Lu,1 Miao Xu,1 Qin-Yun Dong,1 Jia-Jun Yang,2 Zhi-Ying Wu11Department of Neurology and Institute of Neurology, Huashan Hospital, Shanghai Medical College, Fudan University, 2Department of Neurology, Sixth People’s Hospital Affiliated to Shanghai Jiao Tong University, 3Department of Medicine, Shanghai Fengxian District Central Hospital, Shanghai, People’s Republic of China*These authors contributed equally to this workPurpose: To determine the associations between apolipoprotein E (APOE) genotypes and serum levels of glucose, total cholesterol, and triglycerides in a cognitively normal aging Han Chinese population.Methods: There were 1,003 cognitively normal aging subjects included in this study. APOE genotypes were analyzed and biochemical
Apolipoprotein (apo) E isoforms are key determinants of susceptibility to Alzheimers disease. The apoE4 isoform is the major known genetic risk factor for this disease and is also associated with poor outcome after acute head trauma or stroke. To test the hypothesis that apoE3, but not apoE4, prote …
TY - JOUR. T1 - Functional connectivity in autosomal dominant and late-onset Alzheimer disease. AU - Thomas, Jewell B.. AU - Brier, Matthew R.. AU - Bateman, Randall J.. AU - Snyder, Abraham Z.. AU - Benzinger, Tammie L.. AU - Xiong, Chengjie. AU - Raichle, Marcus. AU - Holtzman, David M.. AU - Sperling, Reisa A.. AU - Mayeux, Richard. AU - Ghetti, Bernardino. AU - Ringman, John M.. AU - Salloway, Stephen. AU - McDade, Eric. AU - Rossor, Martin N.. AU - Ourselin, Sebastien. AU - Schofield, Peter R.. AU - Masters, Colin L.. AU - Martins, Ralph N.. AU - Weiner, Michael W.. AU - Thompson, Paul M.. AU - Fox, Nick C.. AU - Koeppe, Robert A.. AU - Jack, Clifford R.. AU - Mathis, Chester A.. AU - Oliver, Angela. AU - Blazey, Tyler M.. AU - Moulder, Krista. AU - Buckles, Virginia. AU - Hornbeck, Russ. AU - Chhatwal, Jasmeer. AU - Schultz, Aaron P.. AU - Goate, Alison M.. AU - Fagan, Anne M.. AU - Cairns, Nigel J.. AU - Marcus, Daniel S.. AU - Morris, John C.. AU - Ances, Beau M.. N1 - Publisher ...
Strong evidence of linkage to late-onset Alzheimer disease (LOAD) has been observed on chromosome 10, which implicates a wide region and at least one disease-susceptibility locus. Although significant associations with several biological candidate genes on chromosome 10 have been reported, these findings have not been consistently replicated, and they remain controversial. We performed a chromosome 10-specific association study with 1,412 gene-based single-nucleotide polymorphisms (SNPs), to identify susceptibility genes for developing LOAD. The scan included SNPs in 677 of 1,270 known or predicted genes; each gene contained one or more markers, about half (48%) of which represented putative functional mutations. In general, the initial testing was performed in a white case-control sample from the St. Louis area, with 419 LOAD cases and 377 age-matched controls. Markers that showed significant association in the exploratory analysis were followed up in several other white case-control sample sets to
Researchers at the University of Glasgows Institute of Health and Wellbeing have announced they have found people with genetic risk of Alzheimers disease exhibiting clear differences in certain biomarkers.. It supports a link between a major genetic risk factor and blood cholesterol levels. The risk factor APOE e4, which is present in a quarter of the population and triples the risk of. dementia, could possibly be the key to future early diagnosis and treatment. The 2% of the. population with a double copy have a 15 times higher risk of developing the disease.. The team investigated associations between common blood biomarkers and apolipoprotein E (APOE), a known genetic risk factor for Alzheimers disease, to improve understanding of disease mechanisms and risk. The study reviewed anonymised data from nearly 400,000 White European participants of the UK Biobank, a public health database, including lifestyle data in their analysis to account for the impact of environmental factors. Using a ...
TY - JOUR. T1 - Apolipoprotein e metabolism and functions in brain and its role in Alzheimers disease. AU - Liao, Fan. AU - Yoon, Hyejin. AU - Kim, Jungsu. PY - 2017. Y1 - 2017. N2 - Purpose of review APOE4 genotype is the strongest genetic risk factor for Alzheimers disease. Prevailing evidence suggests that amyloid βa plays a critical role in Alzheimers disease. The objective of this article is to review the recent findings about the metabolism of apolipoprotein E (ApoE) and amyloid β and other possible mechanisms by which ApoE contributes to the pathogenesis of Alzheimers disease. Recent findings ApoE isoforms have differential effects on amyloid b metabolism. Recent studies demonstrated that ApoE-interacting proteins, such as ATP-binding cassette A1 (ABCA1) and LDL receptor, may be promising therapeutic targets for Alzheimers disease treatment. Activation of liver X receptor and retinoid X receptor pathway induces ABCA1 and other genes, leading to amyloid b clearance. Inhibition of ...
TY - JOUR. T1 - Effect of APOE genotype on gray matter density in patients with Parkinsons disease. AU - Chung, Seok Jong. AU - Lee, Ji Eun. AU - Hong, Jin Yong. AU - Lim, Soohwan. AU - Kim, Myong Hwan. AU - Sohn, Young H.. AU - Lee, Phil Hyu. PY - 2013/1. Y1 - 2013/1. UR - http://www.scopus.com/inward/record.url?scp=84871523413&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=84871523413&partnerID=8YFLogxK. U2 - 10.1016/j.parkreldis.2012.06.001. DO - 10.1016/j.parkreldis.2012.06.001. M3 - Letter. C2 - 22784692. AN - SCOPUS:84871523413. VL - 19. SP - 138. EP - 140. JO - Parkinsonism and Related Disorders. JF - Parkinsonism and Related Disorders. SN - 1353-8020. IS - 1. ER - ...
Background: Apolipoprotein E4 (ApoE4) is the major genetic risk factor of Alzheimer’s disease (AD). ApoE4 carriers have cerebral hypometabolism which is thought as a harbinger of AD. Our previous studies indicated ketones improved mitochondria energy metabolism via sirtuin 3 (Sirt3). However, it is unclear whether ketones upregulate Sirt3 and improve ApoE4-related learning and memory deficits.Results: Ketones improved learning and memory abilities of ApoE4 mice but not ApoE3 mice. Sirt3, synaptic proteins, the NAD+/ NADH ratio, and ATP production were significantly increased in the hippocampus and the cortex from ketone treatment.Methods: Human ApoE3 and ApoE4 transgenic mice (9-month-old) were treated with either ketones or normal saline by daily subcutaneous injections for 3 months (ketones, beta-hydroxybutyrate (BHB): 600 mg/kg/day; acetoacetate (ACA): 150 mg/kg/day). Learning and memory ability of these mice were assessed. Sirt3 protein, synaptic proteins (PSD95, Synaptophysin),
PURPOSE: To investigate the possible effect of the APOE epsilon4 allele on age-related regional volume loss within the corpus callosum (CC) in healthy epsilon4 allele carriers compared with noncarriers. MATERIALS AND METHODS: A total of 211 subjects, ages 27 to 83 years, 51 epsilon4 carriers and 160 noncarriers underwent T1-weighted MRI scan. All subjects had normal MRI scan and performed within normal range on a neuropsychological battery of tests. CC was segmented into seven functionally relevant regions using a previously published probabilistic map of the CC connectivity. We measured the volumes of the CC and its subregions. We used a regression model (with volumes as dependent and age as independent variables) and compared the slopes between carriers and noncarriers using an analysis of covariance model. We also carried out voxel-based-morphometry analysis to investigate the possible effect of the APOE epsilon4 gene on the gray matter. RESULTS: We found that the volume of the CC and all subregions
Sporadic, late-onset Alzheimers disease has no known cause and shows no obvious inheritance pattern. However, in some families, clusters of cases are seen. Although a specific gene has not been identified as the cause of late-onset Alzheimers, genetic factors do appear to play a role in the development of this form.. Two risk factor genes have been linked to Alzheimers diseases so far. Researchers have identified an increased risk of developing late-onset Alzheimers related to the apolipoprotein E (APOE) gene found on chromosome 19. The APOE gene comes in several different forms, but three occur most frequently: APOE e2, APOE e3, and APOE e4. People inherit one APOE from each parent. Having the e4 form is a risk factor for Alzheimers disease, but it does not mean that Alzheimers disease will necessarily develop. The e3 form is the most common form found in the general population and may play a neutral role in AD. The rarer e2 form appears to be associated with a lower risk of AD.. The ...
...The apolipoprotein E gene ε4 allele is considered a negative fact......,A,non-invasive,,rapid,screening,method,for,Alzheimers,disease,biological,biology news articles,biology news today,latest biology news,current biology news,biology newsletters
January 15, 2006. In a scientific paper published today a team of scientists from deCODE genetics (Nasdaq:DCGN) and colleagues report the discovery of a variant in a gene on chromosome 10 that represents the most significant genetic risk factor for type 2 diabetes (T2D) found to date. More than one third of individuals in the populations studied carry one copy of the at-risk variant and are at an approximately 45% increased risk of the disease compared to controls; 7% carry two copies and are at a 141% greater risk. The original finding was made in Iceland and was subsequently confirmed in studies in Denmark and the United States. The paper is published today in the online edition of Nature Genetics at www.nature.com/ng, and will appear in the journals February print edition.. This is a milestone in human genetics. A common gene variant conferring elevated risk of T2D has been earnestly sought by the genetics community for many years. We have found such a variant, which we estimate accounts ...
Authors: Blautzik, Janusch , Kotz, Sebastian , Brendel, Matthias , Sauerbeck, Julia , Vettermann, Franziska , Winter, Yaroslav , Bartenstein, Peter , Ishii, Kazunari , Rominger, Axel Article Type: Research Article Abstract: Body weight loss in late-life is known to occur at a very early stage of Alzheimers disease (AD). Apolipoprotein E4 (ApoE4) represents a major genetic risk factor for AD and is linked to an increased cortical amyloid-β (Aβ) accumulation. Since the relationship between body weight, ApoE4, and AD pathology is poorly investigated, we aimed to evaluate whether ApoE4 allelic status modifies the association of body mass index (BMI) with markers of AD pathology. A total of 368 Aβ-positive cognitively healthy or mild cognitive impaired subjects had undergone [18 F]-AV45-PET, [18 F]-FDG-PET, and T1w-MRI examinations. Composite cortical [18 F]-AV45 uptake and …[18 F]-FDG uptake in posterior cingulate cortex were calculated as surrogates of cortical Aβ load and glucose ...
Lipnicki DM; Crawford JD; Dutta R; Thalamuthu A; Kochan NA; Andrews G; Fernanda Lima-Costa M; Castro-Costa E; Brayne C; Matthews FE, 2017, Age-related cognitive decline and associations with sex, education and apolipoprotein E genotype across ethnocultural groups and geographic regions: a collaborative cohort study, PLOS ONE, vol. 12, http://dx.doi.org/10.1371/journal.pmed.1002261. Opel N; Redlich R; Kaehler C; Grotegerd D; Dohm K; Heindel W; Kugel H; Thalamuthu A; Koutsouleris N; Arolt V, 2017, Prefrontal gray matter volume mediates genetic risks for obesity, Molecular Psychiatry, vol. 22, pp. 703 - 710, http://dx.doi.org/10.1038/mp.2017.51. Lipnicki DM; Crawford JD; Dutta R; Thalamuthu A; Kochan NA; Andrews G; Lima-Costa MF; Castro-Costa E; Brayne C; Matthews FE, 2017, Age-related cognitive decline and associations with sex, education and apolipoprotein E genotype across ethnocultural groups and geographic regions: a collaborative cohort study, PLoS Medicine, vol. 14, ...
Background Epilepsy is associated with precocious development of Alzheimer-type neuropathological changes, including appearance of senile plaques, neuronal loss and glial activation. As inheritance of ...
Suppose you have 8 observations ($i=1,...,8$) from three different states (A, B, C) and you also know that observations for $i=1,2$ are from state A, for $i=3,4,5$ are from state B and for $i=6,7,8$ are from state C. You are trying to estimate parameters with a linear regression model where $\varepsilon_i$ is the error term. The assumptions on this error term are that: $E[\varepsilon_i]=0$, $V[\varepsilon]=\sigma^2$ and:. $$Cov[\varepsilon_i, \varepsilon_j]=\begin{cases} \sigma^2 \rho & \text{ if observation i comes from the same state of observation j} \\ 0 & \text{otherwise} \end{cases}$$. Now you have that:. $$\overline{\varepsilon_h}=\frac{1}{n_h} \sum_{i \in h} \varepsilon_i$$. where $h=A,B,C$. Im asked to compute the variance-covariance matrix of $\overline{\varepsilon}$ (notated $V[\overline{\varepsilon}]$) so Ive started to compute variances and covariances of $\overline{\varepsilon}$ for $h=A, \ B, \ C$.. ...
This SNP, located in the fourth exon of the ApoE gene, affects the amino acid at position 130 of the resulting protein. The more common rs429358 allele is (T). If the allele is (C) and the same chromosome also harbors the rs7412(C) allele, the combination is known as an APOE-ε4 allele. The APOE-ε4 allele has a strong influence on the risk of Alzheimers disease. Many studies have estimated the level of risk, and it varies depending on age, sex, ethnicity, and other factors. One meta-analysis estimated the odds ratios for homozygous rs429358(C;C) individuals compared to the more common ApoE3/ApoE3 homozygotes to be 12x for late-onset Alzheimers and 61x for early-onset disease. [PMID 10325447] Meta-analyses have also supported the association between the APOE-ε4 allele and somewhat increased risk for heart disease, with an odds ratio of 1.42 (CI: 1.26 - 1.61).[15488874?dopt=Abstract PMID 15488874] Note: Although ApoE status is technically defined by these two SNPs, rs429358 and rs7412, a SNP ...
A recent article in this month s Archives of General Psychiatry underscores all this hoopla about the Apo E4 alleles. Apolipoprotein E Genotype and Age-Related Mylein Breakdown in Healthy Individuals by George Bartzokis M.D. et al. These authors discuss that In addition to genotype-phenotype associations with vascular disease, the alleles and isoforms of Apo E4 have been related to dementias, most commonly Alzheimer s disease. Apolipoprotein E (APOE) genotype is the most influential Alzheimer disease (AD) risk factor after advanced age. The APOE4 alleles decrease and the APOE2 alleles increase age at onset of AD. Human and nonhuman primate data suggest that in midlife, the structural integrity of myelin sheaths begins breaking down, with an accelerating age-related trajectory most evident in the brains later-myelinating association regions. This may result in a progressive disconnection of widely distributed neural networks that may underlie the age risk factor for AD. The authors of this ...
Sept. 25, 2013 - Researchers have identified and validated two rare gene mutations that appear to cause the common form of Alzheimers disease (AD) that strikes after the age of 60. The two mutations occur in a gene called ADAM10 coding for an enzyme involved in processing the amyloid precursor protein which now becomes the second pathologically-confirmed gene for late-onset AD and the fifth AD gene overall.
Alleles of the apolipoprotein E (ApoE) gene are known to modulate the genetic risk for developing late-onset Alzheimers disease (AD) and have been associated with hippocampal volume differences in AD. However, the effect of these alleles on hippocam
Buy anti-APOE antibody, anti-Mouse Apolipoprotein E (Apo E) Polyclonal Antibody-P02649.1 (MBS315478) product datasheet at MyBioSource, Primary Antibodies. Application: DD, IEP, RID, Western Blot
Kozan, Ö.; Özcan, E.E.; Sancaktar, O.; Kabakci, G.; Sözcüer, A.H.; Kerpeten, A.; Delice, A.; Içli, A.; Sökmen, A.; Gürlek, A.; Abaci, A.; Bayram, A.; Köşüş, A.; Çamsari, A.; Sakalli, A.; Sert, A.; Temizhan, A.; Yilmaz, A.; Daver, A.; Aydinlar, A.; Ergin, A.; Kiliçoǧlu, A.E.; Birdane, A.; Aribaş, A.; Lazoǧlu, A.; Özdemir, A.; Fiskeci, A.; Çelik, A.; Bitigen, A.; Keskin, A.; Yavuz, A.; Akyüz, A.; Karanfil, A.; Ünsal, A.; Sinci, A.; Gülmez, A.U.; Irmak, A.; Vural, A.; Güven, A.; Ilerigelen, B.; Erol, B.; Polat, B.; Tosun, B.; Aǧçal, C.; Genç, C.; Kirdar, C.; Rezzagil, C.; Köz, C.; Nazli, C.; Ceyhan, C.; Örem, C.; Uyan, C.; Türkoǧlu, C.; Gaffari, D.; Aytekin, D.; Ural, D.; Yeşilbursa, D.; Aras, D.; Semiz, E.; Koçak, E.; Atalar, E.; Varol, E.; Onrat, E.; Şensoy, E.; Acartürk, E.; Akarca, E.; Aygün, E.; Ertaş, F.S.; Koca, F.; Özmen, F.; Ulusoy, F.V.; Özerkan, F.; Inceer, F.K.; Dönmez, G.; Topkara, G.; Daş, G.; Bozkurt, H.; Kültürsay, H.; Tikiz, H.; Akgöz, H.; ...
Effective immediately, SpectraCell Laboratories now offers apolipoprotein E genotyping. This test determines a persons genetic risk for heart disease associated with the commonly
TY - JOUR. T1 - Variations in apolipoprotein e frequency with age in a pooled analysis of a large group of older people. AU - McKay, Gareth J.. AU - Silvestri, Giuliana. AU - Chakravarthy, Usha. AU - Dasari, Shilpa. AU - Fritsche, Lars G.. AU - Weber, Bernhard H.. AU - Keilhauer, Claudia N.. AU - Klein, Michael L.. AU - Francis, Peter J.. AU - Klaver, Caroline C.. AU - Vingerling, Johannes R.. AU - Ho, Lintje. AU - De Jong, Paulus T.D.V.. AU - Dean, Michael. AU - Sawitzke, Julie. AU - Baird, Paul N.. AU - Guymer, Robyn H.. AU - Stambolian, Dwight. AU - Orlin, Anton. AU - Seddon, Johanna M.. AU - Peter, Inga. AU - Wright, Alan F.. AU - Hayward, Caroline. AU - Lotery, Andrew J.. AU - Ennis, Sarah. AU - Gorin, Michael B.. AU - Weeks, Daniel E.. AU - Kuo, Chia Ling. AU - Hingorani, Aroon D.. AU - Sofat, Reecha. AU - Cipriani, Valentina. AU - Swaroop, Anand. AU - Othman, Mohammad. AU - Kanda, Atsuhiro. AU - Chen, Wei. AU - Abecasis, Goncalo R.. AU - Yates, John R.. AU - Webster, Andrew R.. AU - ...
Mice purchased from the Citrix Store or an authorized Distributor have a 90-day warranty. Mice obtained as part of the Citrix Synergy X1 Mouse giveaway do not qualify for a warranty. If an issue with a purchased Citrix X1 Mouse occurs, customers should follow the diagnostics instructions on the Citrix X1 Mouse website to troubleshoot their issue. If the issue persists, customers should obtain their Order Number and enter a request for a replacement mouse. Once you submit a request for a return, Citrix operations will review your request and respond within 10 days.. ...
In 2 massive studies involving thousands of DNA samples, scientists from around the world identified a number of new genes and confirmed several others that may be risk factors for late-onset Alzheimers disease.
Daw EW, Payami H, Nemens EJ, Nochlin D, Bird TD, Schellenberg GD, Wijsman EM. The number of trait loci in late-onset Alzheimer disease ...
Blood donors of the Madrid area show a 6% frequency of apolipoprotein E genotype carrying allele epsilon 4. This frequency is smaller than other populations of Caucasian origin. This proportion decreases to 4% in a selected sample of healthy individuals of ages | 60 years. The frequency (34%) of the allele epsilon 4 was significantly increased in patients of late onset Alzheimers disease, similarly to other populations. An earlier age of onset of the dementia is observed in the patients of late-onset Alzheimers disease carrying the allele epsilon 4. No increased frequency in allele epsilon 4 frequency was found in patients of early-onset Alzheimers disease. Patients of Parkinsons disease do not show any differences in the frequency of the alleles of apolipoprotein E when compared with healthy individuals.
article{50e72dbd-9a4a-4abf-ad00-0ae9efb2dd9e, abstract = {,p,Introduction: Apolipoprotein E (APOE) ε4 is the major genetic risk factor for Alzheimers disease (AD), but its prevalence is unclear because earlier studies did not require biomarker evidence of amyloid β (Aβ) pathology. Methods: We included 3451 Aβ+ subjects (853 AD-type dementia, 1810 mild cognitive impairment, and 788 cognitively normal). Generalized estimating equation models were used to assess APOE ε4 prevalence in relation to age, sex, education, and geographical location. Results: The APOE ε4 prevalence was 66% in AD-type dementia, 64% in mild cognitive impairment, and 51% in cognitively normal, and it decreased with advancing age in Aβ+ cognitively normal and Aβ+ mild cognitive impairment (P <.05) but not in Aβ+ AD dementia (P =.66). The prevalence was highest in Northern Europe but did not vary by sex or education. Discussion: The APOE ε4 prevalence in AD was higher than that in previous studies, which did not ...
Effect of Dietary Fat on LDL Size Influenced by Apolipoprotein E Genotype in Healthy Subjects - posted in Lifestyle: Any thoughts? I read this laymans article here which explains how smaller LDL particle size is a better predictor for increased risk of heart disease, and how high carbohydrate diets decrease the size of LDL particles.The paper below claims the opposite if you are ApoE3/4. Im ApoE3/4, and Ive discussed this topic on longecity before, so I guess Ill contin...
This is a pre-registration of an experimental plan to examine the effect of APOE genotype on microglial-mediated synapse loss in Alzheimers disease. There is now extensive literature covering synapse loss in AD and mouse studies have shown microglia are key players in aberrantly clearing synapses during AD. From this pilot study, we expect to establish the effect size of engulfed synaptic elements inside microglial cells, and investigate if having AD, and particularly being an APOE4 carrier, affects this process. As APOE4 carriers are more likely to develop AD and have an earlier AD onset, we postulate that microglia are activated and primed for synapse phagocytosis, with e4 individuals microglia internalizing more synapses and amyloid beta. We also hypothesize that microglia around plaques, being more reactive, will phagocytose synapses more than microglia away from plaques ...
Meckes, C., Moyna, N., Tsongalis, G., Miles, M. (2001). Apolipoprotein E Genotype Does Not Affect the Changes in Serum Lipids with Exercise Training. Circulation, 104(17), 343-343 ...
The human APOE gene, which codes for apolipoprotein E (apoE), has three major polymorphic alleles: ε2, ε3, and ε4 that give rise to amino acid substitutions. APOE-ε4 is a strong risk factor of sporadic Alzheimers disease (AD) but the reason why is still unknown despite intense research for more than 20 years. The aim of the study was to investigate if the concentrations of total apoE and the specific apoE isoforms in cerebrospinal fluid (CSF) differ between various neurodegenerative diseases and control individuals, as well as among the APOE genotypes. Quantification of total apoE and specific apoE isoforms (E2, E3, and E4) in CSF was performed using high-resolution parallel reaction monitoring mass spectrometry. In total, 1820 individuals were involved in the study including clinically diagnosed AD patients (n = 228), cognitively unimpaired (CU) patients (n = 896), and patients with other neurodegenerative disorders (n = 696). Follow-up data was available for 100 individuals, assessed at two time
The APOE e4 allele polymorphism is associated with the increased risk of behavioral and psychological signs and symptoms of dementia. Treatment strategies based on APOE genotypes are being developed. In this study, we aimed to assess the frequencies of APOE4 alleles in patients with Alzheimers disease (AD) and vascular dementia (VaD) in different ethnic and geographic groups, and compare them with our results. Method: We determined APOE polymorphisms in patients with VaD, AD, and in controls. For comparison, the literature was searched systematically. Out of 80 papers, 42 papers were assessed for APOE genotype and allele frequencies from several regions of America, Asia and Europe. Results: There were marked variations in the APOE allele and genotype frequencies in all groups. The strength of association between AD and APOE e4 allele carrying was found significant [OR:2.905 (95%CI: 1.237-6.823)]. APOE e4 allele frequencies (%) showed gradual increase from controls to the AD patients (Control: ...
In this study, we examined Abca1 gene dose effect on the phenotype of APP transgenic mice expressing human ApoE3 or ApoE4 isoforms. Surprisingly, our results demonstrate that the lack of one copy of Abca1 significantly aggravates memory deficits and amyloid pathology in APP/E4 but not in APP/E3 mice. An important finding of the study was that Aβ clearance from the brain was decreased by Abca1 deficiency in APP/E4/Abca1−/+ but not in APP/E3/Abca1−/+ mice. In contrast, Abca1 deficiency did not affect cognition, amyloid phenotype, and Aβ clearance in APP mice expressing ApoE3. Interestingly, the correlation between plasma HDL and brain amyloid load (Fig. 7) suggests that there may be a causative connection between peripheral lipoproteins and Aβ load in the CNS.. Previous studies demonstrated that ABCA1 affects amyloid deposition and memory deficits in experimental animals (Hirsch-Reinshagen et al., 2005; Koldamova et al., 2005b; Wahrle et al., 2005; Lefterov et al., 2009). Furthermore, ...
BACKGROUND: Compared to the epsilon 2 or epsilon 3 alleles, the epsilon 4 allele of apolipoprotein E (ApoE4) is associated with twice the prevalence of late-onset Alzheimers disease (AD). Epidemiological studies show that risk of AD varies inversely with consumption of omega-3 fatty acids from fish and seafood. Despite apparently lower fish intake in AD, pooled analysis of the literature shows that plasma and brain docosahexaenoic acid (DHA) is actually the same in AD as in healthy age-matched controls. Fish oil trials in AD are also not convincing. We recently shown that ApoE4 carriers have 41% higher fasting plasma EPA and DHA compared to non-carriers, but the plasma EPA and DHA response to fish oil in ApoE4 carriers was half that seen in non-carriers.. HYPOTHESES: (i) Carriers of ApoE4 have altered metabolism of carbon-13 (13C)-DHA as well as EPA and DHA provided in a dietary supplement. (ii) A dietary supplement of EPA+DHA will improve cognitive performance but only in non-carriers of ...
TY - JOUR. T1 - Changes in subcortical structures in early- versus late-onset Alzheimers disease. AU - Cho, Hanna. AU - Seo, Sang Won. AU - Kim, Jeong Hun. AU - Kim, Changsoo. AU - Ye, Byoung Seok. AU - Kim, Geon Ha. AU - Noh, Young. AU - Kim, Hee Jin. AU - Yoon, Cindy W.. AU - Seong, Joon Kyung. AU - Kim, Chang Hun. AU - Kang, Sue J.. AU - Chin, Juhee. AU - Kim, Sung Tae. AU - Lee, Kyung Han. AU - Na, Duk L.. N1 - Funding Information: This study was supported by a grant of the Korea Healthcare Technology R&D Project, Ministry of Health and Welfare , Republic of Korea ( A102065 ), a Korean Science and Engineering Foundation (KOSEF) NRL program grant funded by the Korean government (MEST; 2011- 0028333 ), a Samsung Medical Center Clinical Research Development Program grants (CRL- 108011 , and CRS 110-14-1), and the Converging Research Center Program through the Ministry of Education, Science and Technology (2010 K001054 ). PY - 2013/7. Y1 - 2013/7. N2 - Patients with early-onset Alzheimers ...
Accumulation of β-amyloid (Aβ) in the brain is essential to Alzheimers disease (AD) pathogenesis. Carriers of the apolipoprotein E (APOE) ε4 allele demonstrate greatly increased AD risk and enhanced brain Aβ deposition. In contrast, APOE ε2 allele carries show reduced AD risk, later age of disease onset, and lesser Aβ accumulation. However, it remains elusive whether the apoE2 isoform exerts truly protective effect against Aβ pathology or apoE2 plays deleterious role albeit less pronounced than the apoE4 isoform. Here, we characterized APPSW/PS1dE9/APOE ε2-TR (APP/E2) and APPSW/PS1dE9/APOE ε4-TR (APP/E4) mice, with targeted replacement (TR) of the murine Apoe for human ε2 or ε4 alleles, and used these models to investigate effects of pharmacological inhibition of the apoE/Aβ interaction on Aβ deposition and neuritic degeneration. APP/E2 and APP/E4 mice replicate differential effect of human apoE isoforms on Aβ pathology with APP/E4 mice showing a several-fold greater load of Aβ plaques,
OBJECT: The presence of the apolipoprotein E-epsilon4 (APOE-epsilon4) allele is reported to be associated with poor outcome after traumatic brain injury (TBI). This study was performed to determine if the presence of the APOE-epsilon4 allele influenced outcome in a cohort of black patients with TBI
ABSTRACT. Alzheimer disease (AD) is a progressive and irreversible neurodegenerative disorder that is characterized by cognitive decline, memory loss and confusion. The E4 allele of the apolipoprotein E gene (APOE) is associated with AD and it is the main genetic risk factor for disease. Although the exact physiological function is unknown, bleomycin hydrolase (BLMH) may also be associated with AD development, although previous immunohistochemical findings have been inconsistent. Therefore, the purpose of this study was to evaluate the genotypic and allele frequencies of the APOE gene and BLMH 1450 G > A polymorphism and assess BLMH expression using PCR-RFLP and RT-qPCR analyses of blood samples from patients with Alzheimer disease (AD), healthy elderly adults (EC) and healthy young subjects (YC). BLMH expression was significantly different among groups (p = 0.015) and there was substantial reduction with age and with AD. The APOE and BLMH genotype frequency did not diverge from the ...
The apolipoprotein E (APOE) gene exists in three isoforms in humans: APOE2, APOE3 and APOE4. APOE4 causes structural and functional alterations in normal brains, and is the strongest genetic risk factor of the sporadic form of Alzheimers disease (LOAD). Research on APOE4 has mainly focused on the neuronal damage caused by defective cholesterol transport and exacerbated amyloid-β and Tau pathology. The impact of APOE4 on non-neuronal cell functions has been overlooked. Astrocytes, the main producers of ApoE in the healthy brain, are building blocks of neural circuits, and Ca2+ signaling is the basis of their excitability. Because APOE4 modifies membrane-lipid composition, and lipids regulate Ca2+ channels, we determined whether APOE4 dysregulates Ca2+signaling in astrocytes. Ca2+ signals were recorded in astrocytes in hippocampal slices from APOE3 and APOE4 gene targeted replacement male and female mice using Ca2+ imaging. Mechanistic analyses were performed in immortalized astrocytes. Ca2+ fluxes were
FITC偶联Apolipoprotein E 抗体(ab27613)可与人样本反应并经ICC/IF实验严格验证,实验条件参看说明书。Abcam对所有产品均提供质保服务和专属技术支持,中国75%以上现货。
The PREVENT Research Programme has established a cohort of individuals to explore differences in the brain and cognitive function in healthy people in mid-life (aged 40-59). People are grouped into high, mid and low risk based on their family history and APOE status (a well-known risk gene for Alzheimers disease). Participants are assessed on biological indicators including markers in blood, saliva, urine and spinal fluid as well as direct imaging of the brains structure and function. Changes in all of these markers will be monitored at 2 years to work out if risks that predict these changes. One of the main aims of the study is to identify the earliest signs of changes in the brain whilst people are still in good health ...
environmental toxins (especially heavy metals and mycotoxins), vitamin D, and gluten sensitivity, plus a comprehensive nutritional analysis, microbiome assessment, genome sequencing (especially for ApoE status), brain MRI with volumetric assessment, and cognitive performance tests (using an online system like BrainHQ).. By synthesizing this information, skilled clinicians can determine which of the many contributors predominate, and then work to eliminate the triggers, clear existing b-amyloid buildup, and finally rebuild and restore synapses.. The multifactorial, aggravated assault on the brain goes on for 15 to 20 years before someone notices symptoms that warrant medical attention. That means there is a very wide window for early intervention, says Bredesen.. What follows are excerpts of our extensive interview with Dr. Bredesen on April 30, 2018. We touched on the role of prescription drugs in triggering dementia, the risks and benefits of cannabis, the connection between depression and ...
TMEM106B has a strong association with brain pathology and was discovered as a risk allele in diseases on the ALS/FTLD spectrum. But indeed, the main impact of TDP-43 proteinopathy on public health is on LATE, which is ,100-fold more common than ALS/FTLD conditions (~1:3 lifetime risk versus ,1:1000 lifetime risk). Its interesting that the rare variant of TMEM106B is actually protective.. This new contribution by Yang and colleagues and the Rush University group is significant, and focused on LATE. This paper shows evidence of pathways that both TMEM106B and APOE contribute to, and there has been published evidence (including from Rush) that both TMEM106B and APOE status are associated with risk for TDP-43 proteinopathy in advanced age. One question that I had was whether or not other pathways associated with LATE show signals. GRN is only mentioned somewhat tangentially, whereas ABCC9 and KCNMB2 are not discussed.. ...
Published on 10/1/2017. Neu SC, Pa J, Kukull W, Beekly D, Kuzma A, Gangadharan P, Wang LS, Romero K, Arneric SP, Redolfi A, Orlandi D, Frisoni GB, Au R, Devine S, Auerbach S, Espinosa A, Boada M, Ruiz A, Johnson SC, Koscik R, Wang JJ, Hsu WC, Chen YL, Toga AW. Apolipoprotein E Genotype and Sex Risk Factors for Alzheimer Disease: A Meta-analysis. JAMA Neurol. 2017 Oct 01; 74(10):1178-1189. PMID: 28846757.. Read at: PubMed ...
Common variants of the ApoE gene are strongly associated with the risk of developing late-onset Alzheimers disease, but the genes role in the disease has been unclear. Now, researchers funded by the National Institutes ...
Amino Acid SequenceMHHHHHHKVE QAVETEPEPE LRQQTEWQSG QRWELALGRF WDYLRWVQTL SEQVQEELLS SQVTQELRAL MDETMKELKA YKSELEEQLT PVAEETRARL SKELQAAQAR LGADMEDVRG RLVQYRGEVQ AMLGQSTEEL RVRLASHLRK LRKRLLRDAD DLQKRLAVYQ AGAREGAERG LSAIRERLGP LVEQGRVRAA TVGSLAGQPL QERAQAWGER LRARMEEMGS RTRDRLDEVK EQVAEVRAKL EEQAQQIRLQ AEAFQARLKS WFEPLVEDMQ RQWAGLVEKV QAAVGTSAAP VPSDNH.DescriptionApolipoprotein E4 Human Recombinant produced in E.coli is a single, non-glycosylated polypeptide chain containing a total of 306 amino acids including a His Tag at N-terminus and having a molecular mass of 35.2kDa. The Accession # is P02649 VAR_000652.FormulationLyophilized from a sterile (0.2µm) filtered aqueous solution containing 10mM sodium phosphate, pH 7.5.Physical AppearanceSterile Filtered White lyophilized (freeze-dried) powder.PurityGreater than 90% as determined by SDS-PAGE.SolubilityIt is recommended to reconstitute the lyophilized APOE4 in sterile 18M-cm H2O not less than 100µg/ml, which can then be further diluted to other
Mouse Monoclonal Anti-Apolipoprotein E/ApoE Antibody (WUE-4) [DyLight 650]. Validated: WB, ELISA, Flow, ICC/IF, IHC. Tested Reactivity: Human, Mouse. 100% Guaranteed.
Researchers have identified a protein called apolipoprotein E (ApoE) which affects your chances of developing Alzheimers disease. There are three forms of ApoE: ApoE2, ApoE3 and ApoE4.. Having one or two copies of ApoE4 increases someones chance of developing the disease, but does not make it certain. Some researchers think that ApoE4 does not affect whether a person will get the disease but, rather, when they get it, causing people with ApoE4 to develop the disease before people with ApoE2.. ...
rs911541 increases susceptibility to late-onset Alzheimers disease 1.58 times for heterozygotes (A;G) and 1.48 times for homozygotes (G;G,) based on a case-control study of ~1,500 Japanese patients and an equal number of matched controls. [PMID 16740596] ...
Health, ...MONDAY March 7 (HealthDay News) -- Genetics may predispose some peopl...The culprit is a specific abnormality of the apolipoprotein E gene. Th...Now a team of researchers led by Brian K. Lee of Drexel University in...The observation is reported in the March issue of the Archives of ...,Mix,of,Genetics,and,Stress,Can,Impair,Mental,Abilities,medicine,medical news today,latest medical news,medical newsletters,current medical news,latest medicine news
Research opens the door to development of a drug that could be administered before age 40, and taken for life, to potentially prevent the disease in 50 to 80 percent of at-risk adults.
I know that [itex] \varepsilon \eta = r^2 - r^2 \cos^2(\phi) = r^2 \sin^2(\phi) = \rho^2[/itex] ([itex]\rho[/itex] the diagonal in the x-y plane) implies [itex] x = \rho \cos(\phi) = \sqrt{ \varepsilon \eta } \cos (\phi) [/itex] mathematically, but looking at the picture I have no physical or geometrical intuition as to why [itex] \rho = \sqrt{ \varepsilon \eta } [/itex ...
ApoE belongs to a group of proteins that bind reversibly with lipoprotein and play an important role in lipid metabolism.  In addition
I understand, to some extent, Tates thesis. Could somebody explain perhaps what are the epsilon factors in Beilinsons works, such as $\epsilon$-factors for Gauss-Manin determinants, or Topological $\epsilon$-factors? How do they mimic the usual ones? Are they some categorification (since the usual one is a number, and those ones seem to be lines)? Is there some intuition for the construction in Topological $\epsilon$-factors or, perhaps more importantly, for the need for construction?. Edit: I also know vaguely that epsilon-factors should be also associated to Galois-side-data, and the ones in Beilinsons works mimic those, and not the automorphic ones from Tates thesis.. Thank you, Sasha. ...
where ,math,\varepsilon_\infty,/math, (which [[Meep FAQ,must be positive]]) is the instantaneous dielectric function (the infinite-frequency response) and P is the remaining frequency-dependent polarization density in the material. P, in turn, has its own time-evolution equation, and the exact form of this equation determines the frequency-dependence ε(ω). [Note that Meeps definition of ω uses a sign convention ,math,\exp(-i\omega t),/math, for the time dependence-ε formulas in engineering papers that use the opposite sign convention for ω will have a sign flip in all the imaginary terms below. If you are using parameters from the literature, you should use *positive* values of γ and σ as-is for loss; dont be confused by the difference in ω sign convention and flip the sign of the parameters.] In particular, Meep supports any material dispersion of the form of a sum of harmonic resonances, plus a term from the ...
where ,math,\varepsilon_\infty,/math, (which [[Meep FAQ,must be positive]]) is the instantaneous dielectric function (the infinite-frequency response) and P is the remaining frequency-dependent polarization density in the material. P, in turn, has its own time-evolution equation, and the exact form of this equation determines the frequency-dependence ε(ω). [Note that Meeps definition of ω uses a sign convention ,math,\exp(-i\omega t),/math, for the time dependence-ε formulas in engineering papers that use the opposite sign convention for ω will have a sign flip in all the imaginary terms below. If you are using parameters from the literature, you should use *positive* values of γ and σ as-is for loss; dont be confused by the difference in ω sign convention and flip the sign of the parameters.] In particular, Meep supports any material dispersion of the form of a sum of harmonic resonances, plus a term from the ...
Epsilon dry disconnect coulings are designed to prevent chemical spills & reduce VOC emissions, particularly in the process facility & during transfer. RFQ!
Epsilon dry disconnect coulings are designed to prevent chemical spills & reduce VOC emissions, particularly in the process facility & during transfer. RFQ!
ACIDO EPSILON AMINOCAPROICO PDF - J. 47, () Gibelli, A.: Richerche sullazione antifibrinolitica dellacido epsilon-amino-caproico. III. Lazione dellacido epsilon-aminocaproico quale.
The two studies presented at ASH highlight new data on genomic and immune biomarkers, as well as biological pathways of the aggressive cancer diffuse large
The differential effects of apolipoproteins E3 and E4 were also examined on neuronal growth in vitro. Randomization Causality ... "Differential effects of apolipoproteins E3 and E4 on neuronal growth in vitro". Science. 264 (5160): 850-852. Science portal. ...
Specifically too, the apolipoprotein *e4 allele is linked to Alzheimer's disease as well. Also, there is increased coronary ... research has been put on concerning apolipoprotein E genotypes; this polymorphism has three alleles (*e2, *e3, and *e4)and was ...
Apolipoprotein E4 allele in a population based study of early onset Alzheimer's disease. Nat Genet. 1994;7:74-9. Hendriks L, et ... Atherosclerosis, apolipoprotein and prevalence of dementia and Alzheimer's disease. The Rotterdam Study. Lancet. 1997;349:151-4 ...
All members of this family are receptors for Apolipoprotein E (ApoE). Therefore, they are often synonymously referred to as ' ... ApoE receptors'. ApoE occurs in 3 common isoforms (E2, E3, E4) in the human population. ApoE4 is the primary genetic risk ... Andersen OM, Benhayon D, Curran T, Willnow TE (August 2003). "Differential binding of ligands to the apolipoprotein E receptor ... Herz J, Beffert U (October 2000). "Apolipoprotein E receptors: linking brain development and Alzheimer's disease". Nature ...
Mahley RW, Weisgraber KH, Huang Y (April 2006). "Apolipoprotein E4: a causative factor and therapeutic target in neuropathology ... Also, a specific isoform of apolipoprotein, APOE4, is a major genetic risk factor for AD. While apolipoproteins enhance the ... APOEε4 is one of four alleles of apolipoprotein E (APOE). APOE plays a major role in lipid-binding proteins in lipoprotein ... Xu H, Finkelstein DI, Adlard PA (12 June 2014). "Interactions of metals and Apolipoprotein E in Alzheimer's disease". Frontiers ...
... apolipoprotein E4 genotype, and biomarkers of brain injury". Anesthesiology. 112 (4): 852-9. doi:10.1097/ALN.0b013e3181d31fd7. ...
"Human Leukocyte Antigen as a Key Factor in Preventing Dementia and Associated Apolipoprotein E4 Risk". Frontiers in Aging ...
She demonstrated this by monitoring for the well-known Alzheimer's disease risk factors Apolipoprotein E (APOE) e4. Dubal ... whilst patients with APOE e4 and Klotho do not have these biomarkers. Dubal has identified a biological mechanism - an ... revealed that patients with the genetic variant APOE e4 have biomarkers of Alzheimer's disease, even before experiencing ...
2002). "Codon 311 (Cys --> Ser) polymorphism of paraoxonase-2 gene is associated with apolipoprotein E4 allele in both ...
More recent research suggests that ACE inhibitors can reduce risk of Alzheimer's disease in the absence of apolipoprotein E4 ... "Angiotensin converting enzyme inhibitors and the reduced risk of Alzheimer's disease in the absence of apolipoprotein E4 allele ...
Gain of toxic Apolipoprotein E4 effects in Human iPSC-Derived Neurons Is Ameliorated by a Small-Molecule Structure Corrector. ... Alzheimer's disease and apolipoprotein E (apoE). Uncovered the molecular pathways that link apoE and Alzheimer's disease, and ... In 2018 published an article in Nature Medicine about apolipoprotein E(apoE) gene expression-pluripotent stem cell cultures ...
In a secondary analysis, a subgroup of individuals with the apolipoprotein E4 genotype showed sustained benefits with donepezil ...
"Apolipoprotein E4: a causative factor and therapeutic target in neuropathology, including Alzheimer's disease". Proceedings of ... a specific isoform of apolipoprotein, APOE4, is a major genetic risk factor for AD. While apolipoproteins enhance the breakdown ... The best known genetic risk factor is the inheritance of the ε4 allele of the apolipoprotein E (APOE).[44][45] Between 40 and ... Leung K (8 April 2010). "(E)-4-(2-(6-(2-(2-(2-(18F-fluoroethoxy)ethoxy)ethoxy)pyridin-3-yl)vinyl)-N-methyl benzenamine [[18F]AV ...
"The Apolipoprotein E e4 Polymorphism Is Strongly Associated With Poor Mobility Performance Test Results But Not Self-Reported ...
a b Mahley RW, Weisgraber KH, Huang Y. Apolipoprotein E4: A causative factor and therapeutic target in neuropathology, ... Leung K: (E)-4-(2-(6-(2-(2-(2-(18F-fluoroethoxy)ethoxy)ethoxy)pyridin-3-yl)vinyl)-N-methyl benzenamine [[18F]AV-45]]]. W: ... Apolipoprotein E, dementia, and cortical deposition of beta-amyloid protein. „N Engl J Med". 333 (19), s. 1242-47, 11 1995. DOI ... Apolipoprotein E: high-avidity binding to beta-amyloid and increased frequency of type 4 allele in late-onset familial ...
Mahley RW, Weisgraber KH, Huang Y. Apolipoprotein E4: A causative factor and therapeutic target in neuropathology, including ... Apolipoprotein E)會導致類澱粉蛋白質斑塊在大腦中累積[83],因此推測Aβ是導致阿茲海默症的原因,進一步的證據則是來自於轉殖基因老鼠實驗,研究人員在實驗老鼠身上表現突變型人類APP基因,結果發現實驗老鼠的大腦會產生纖維狀的類澱粉蛋白質斑
"Apolipoprotein E4: a causative factor and therapeutic target in neuropathology, including Alzheimer's disease". Proceedings of ... isoform spesifik apolipoprotein, APOE4, adalah faktor risiko genetik utama untuk Alzheimer. Walaupun apolipoprotein ... Faktor risiko genetik yang paling terkenal adalah pewarisan alel ε4 apolipoprotein E (APOE).[44][45] Antara 40 dan 80% orang ... "Apolipoprotein E, dementia, and cortical deposition of beta-amyloid protein". The New England Journal of Medicine. 333 (19): ...
"Apolipoprotein (apo) E4 enhances HIV-1 cell entry in vitro, and the APOE epsilon4/epsilon4 genotype accelerates HIV disease ... E4 ten unha frecuencia alélica de aproximadamente o 14 %.[14] E4 foi implicada na aterosclerose,[21] enfermidade de Alzheimer,[ ... "Entrez Gene: APOE apolipoprotein E".. *↑ Liu CC, Liu CC, Kanekiyo T, Xu H, Bu G (Feb 2013). "Apolipoprotein E and Alzheimer ... A variante E4 é o factor de risco xenético coñecido maior para a enfermidade de Alzheimer esporádica de comezo tardío en varios ...
Research has also discovered the association of a fourth allele, apolipoprotein E4 (ApoE4), in the development of late-onset ...
However, in patients with increased apolipoprotein (APOE) e4 carriers, Bapineuzumab treatment is also accompanied by vasogenic ... and no significant reduction of Aβ concentration in APOE e4 patients and non-APOE e4 patients. Therefore, Aβ plaque ... Bapineuzumab treatment is associated with reduced rate of accumulation of Aβ in the brain in APOE e4 patients, ...
Apolipoprotein E are proteins that metabolize fats in the body. In studies of patients undergoing coronary artery bypass ... grafting, carriers of APO-E e4 allele was found to have a decreased risk of acute kidney injury compared to non-carriers of the ... Genes such as Apolipoprotein E (APO E), which controls cholesterol metabolism, NADPH Oxidase which regulates oxidative stress, ...
This included the investigation of the influence of the E4 allele on the Apolipoprotein E (APOE) gene on cognitive ageing as ... In an early LBC1921 study, E4 allele status was unrelated to Moray House Test scores at age 11, but at age 80 those with an E4 ... Schiepers O. J. G.; Harris S. E.; Gow A. J.; Pattie A.; Brett C. E.; Starr J. M.; Deary I. J. (2012). "APOE E4 status predicts ... The most consistent genetic finding from the LBC studies has been that the E4 allele on the APOE gene, which had previously ...
June 2008). "Apolipoprotein (apo) E4 enhances HIV-1 cell entry in vitro, and the APOE epsilon4/epsilon4 genotype accelerates ... Becher JC, Keeling JW, Bell J, Wyatt B, McIntosh N (August 2008). "Apolipoprotein E e4 and its prevalence in early childhood ... "Entrez Gene: APOE apolipoprotein E". Liu CC, Liu CC, Kanekiyo T, Xu H, Bu G (February 2013). "Apolipoprotein E and Alzheimer ... The gene, APOE, is mapped to chromosome 19 in a cluster with apolipoprotein C1 (APOC1) and the apolipoprotein C2 (APOC2). The ...
74.0 74.1 Mahley RW, Weisgraber KH, Huang Y (Aprili 2006). "Apolipoprotein E4: a causative factor and therapeutic target in ... Leung K (8 Aprili 2010). (E)-4-(2-(6-(2-(2-(2-(18F-fluoroethoxy)ethoxy)ethoxy)pyridin-3-yl)vinyl)-N-methyl benzenamine [[18F]AV ... Polvikoski T, Sulkava R, Haltia M, et al. (Novemba 1995). "Apolipoprotein E, dementia, and cortical deposition of beta-amyloid ... Strittmatter WJ, Saunders AM, Schmechel D, et al. (Machi 1993). "Apolipoprotein E: high-avidity binding to beta-amyloid and ...
By the time Alzheimer's has been diagnosed, DCGM occurs in genotypes APOE3/E4, APOE3/E3, and APOE4/E4. Thus, DCGM is a ... 1997). "No difference in cerebral glucose metabolism in patients with Alzheimer disease and differing apolipoprotein E ... such as patients homozygous for the epsilon 4 variant of the apolipoprotein E gene (APOE4, a genetic risk factor for ...
Mahley RW, Weisgraber KH, Huang Y (2006). «Apolipoprotein E4: a causative factor and therapeutic target in neuropathology, ... Xu H, Finkelstein DI, Adlard PA (12 de junho de 2014). «Interactions of metals and Apolipoprotein E in Alzheimer's disease». ... Strittmatter WJ, Saunders AM, Schmechel D, Pericak-Vance M, Enghild J, Salvesen GS, Roses AD (1993). «Apolipoprotein E: high- ... Bapineuzumab in Patients with Mild to Moderate Alzheimer's Disease/ Apo_e4 Non-carriers». US National Institutes of Health. 29 ...
Mahley RW, Weisgraber KH, Huang Y. Apolipoprotein E4: a causative factor and therapeutic target in neuropathology, including ... E)-4-(2-(6-(2-(2-(2-([18F]-fluoroethoxy)ethoxy)ethoxy)pyridin-3-yl)vinyl)-N-methylbenzenamine. Molecular Imaging and Contrast ... Interactions of metals and Apolipoprotein E in Alzheimer's disease. Frontiers in Aging Neuroscience. 2014-06-12, 6: 121. PMC ... Strittmatter WJ, Saunders AM, Schmechel D. Apolipoprotein E: high-avidity binding to beta-amyloid and increased frequency of ...
"Hyperlipidemia in patients with apolipoprotein E 2/2 phenotype: apolipoprotein A5 S19W mutation as a cofactor". Clinical ... 107741) three allelic (E2, E3, and E4) polymorphism, in the modulation of plasma lipids. In these cases, the interaction ... Apolipoprotein A-V is a protein that in humans is encoded by the APOA5 gene on chromosome 11. It is significantly expressed in ... Yin YW, Sun QQ, Wang PJ, Qiao L, Hu AM, Liu HL, Wang Q, Hou ZZ (2014-01-01). "Genetic polymorphism of apolipoprotein A5 gene ...
"Very early changes in olfactory functioning due to Alzheimer's disease and the role of apolipoprotein E in olfaction". Annals ...
3 (1): e4. doi:10.1371/journal.ppat.0030004. PMC 1779297. PMID 17238285. Yang, Zhi-Yong; et al. (2004). "pH-Dependent Entry of ... Monocytes can be induced to differentiate into dendritic cells by a self-peptide Ep1.B derived from apolipoprotein E. These are ... "Dendritic cell differentiation induced by a self-peptide derived from apolipoprotein E." (PDF). J Immunol. 181 (10): 6859-71. ... "Anti-atherogenic peptide Ep1.B derived from Apolipoprotein E induces tolerogenic plasmacytoid dendritic cells". Clin Exp ...
MeSH D12.776.070.400.200.100 - apolipoprotein A1 MeSH D12.776.070.400.200.150 - apolipoprotein A2 See List of MeSH codes ( ... adenovirus e4 proteins MeSH D12.776.964.700.750.320 - fusion proteins, gag-onc MeSH D12.776.964.700.750.320.700 - oncogene ... adenovirus e4 proteins MeSH D12.776.624.664.520.090 - antigens, polyomavirus transforming MeSH D12.776.624.664.520.420 - ...
Crystal Structure of the 22K Domain of Human Apolipoprotein E4. Verderame, J.R., Kantardjieff, K., Segelke, B., Weisgraber, K. ... APOLIPOPROTEIN E. A. 165. Homo sapiens. Mutation(s): 1 Gene Names: APOE. ...
Rabbit polyclonal Apolipoprotein E4 antibody conjugated to Biotin. Validated in WB, ELISA, RIA and tested in Human. Immunogen ...
The apolipoprotein E E4 allele and sex-specific risk of Alzheimers disease. J Am Med Assoc 1995:273:373-374. [ Links ]. ... Association of apolipoprotein E allele e4 with late onset familial and sporadic Alzheimers disease. Neurology 1993;43:1467- ... Payami H, Montee KR, Kaye JA et al Alzheimers disease, apolipoprotein E4, and gender. J Am Med Assoc 1994;271: 1316-1317. [ ... A role for apolipoprotein E, apolipoprotein A-l, and low density lipoprotein receptors in cholesterol transport during ...
Apolipoprotein E4 allele as a predictor of cholinergic deficits and treatment outcome in Alzheimer disease. J Poirier, M C ... Apolipoprotein E4 allele as a predictor of cholinergic deficits and treatment outcome in Alzheimer disease ... Apolipoprotein E4 allele as a predictor of cholinergic deficits and treatment outcome in Alzheimer disease ... Apolipoprotein E4 allele as a predictor of cholinergic deficits and treatment outcome in Alzheimer disease ...
Apolipoprotein E4 enhances brain inflammation by modulation of the NF-kappaB signaling cascade.. Ophir G1, Amariglio N, Jacob- ... Apolipoprotein E4 (apoE4), the major genetic risk factor of Alzheimers disease (AD), is associated with enhanced brain ...
... Bergdahl, Maud ... apolipoprotein, APOE e4, edentulous, genetic. Nationell ämneskategori Psykologi Forskningsämne. psykologi Identifikatorer. URN ... Objectives: To evaluate the frequency of apolipoprotein (APOE) alleles and determine whether APOE type 4 allele (e4) was ... and e4 = 15.8%. Age, living condition, years of education and APOE e4 were significant covariates in edentulous subjects (p £ ...
The apolipoprotein ApoE4 is a high-risk Alzheimer s gene that increases brain damage caused by another protein called Tau in ... Apolipoprotein E4 (ApoE4). ApoE proteins are a class of apolipoproteins essential for the normal break down of triglyceride- ... Apolipoprotein E4 (ApoE4). ApoE proteins are a class of apolipoproteins essential for the normal break down of triglyceride- ... New Role of Apolipoprotein E4 Variant in Alzheimer s Disease Suggests Possible Therapeutic Target. ...
The apolipoprotein e4 allele on chromosome 19 is an important risk factor for cognitive decline.4 We examined the association ... Alternatively, apolipoprotein e4 may play a role in inhibiting neuronal growth5 and may thus block the putative stimulating ... Apolipoprotein e4 allele and cognitive decline in elderly men. BMJ 1994;309:1202-6. ... The e4 allele may be such a strong risk factor for cognitive decline that cognitive performance in carriers of an e4 allele ...
Brain vascular and metabolic deficits can occur in cognitively normal apolipoprotein E ɛ4 carriers decades before the onset of ... Apolipoprotein E ɛ4 allele is a common susceptibility gene for late-onset Alzheimers disease. ... Rapamycin rescues vascular, metabolic and learning deficits in apolipoprotein E4 transgenic mice with pre-symptomatic ... Apolipoprotein E ɛ4 allele is a common susceptibility gene for late-onset Alzheimers disease. Brain vascular and metabolic ...
The additional risk for aggression/agitation conferred by e4 was also noted when e4 genotypes were compared against non-e4 ... Kanai M, Shizuka M, Urakami K, et al. Apolipoprotein E4 accelerates dementia and increases cerebrospinal fluid tau levels in ... risk for aggression/agitation conferred by e4 was also noted when e4 containing genotypes were compared against non-e4 ... ApoE e4 confers considerable risk for AD and is associated with more rapid progression and greater cortical amyloid burden,33- ...
... and blood pressure measurements and investigated the presence of the ε4 allele of apolipoprotein E (APOE4) to determine the ... In the Heart of the Amazon: Noncommunicable Diseases and Apolipoprotein E4 Genotype in the Riverine Population. Gabriela P. F. ... "In the Heart of the Amazon: Noncommunicable Diseases and Apolipoprotein E4 Genotype in the Riverine Population." Int. J. ... In the Heart of the Amazon: Noncommunicable Diseases and Apolipoprotein E4 Genotype in the Riverine Population. International ...
Apolipoprotein E4 Causes Age- and Tau-Dependent Impairment of GABAergic Interneurons, Leading to Learning and Memory Deficits ... Apolipoprotein E4 (apoE4) is the major genetic risk factor for Alzheimers disease. However, the underlying mechanisms are ... Apolipoprotein E4 Causes Age- and Tau-Dependent Impairment of GABAergic Interneurons, Leading to Learning and Memory Deficits ... Apolipoprotein E4 Causes Age- and Tau-Dependent Impairment of GABAergic Interneurons, Leading to Learning and Memory Deficits ...
Expression of Human Apolipoprotein E3 or E4 in the Brains ofApoe−/− Mice: Isoform-Specific Effects on Neurodegeneration. Manuel ... Expression of Human Apolipoprotein E3 or E4 in the Brains ofApoe−/− Mice: Isoform-Specific Effects on Neurodegeneration ... Expression of Human Apolipoprotein E3 or E4 in the Brains ofApoe−/− Mice: Isoform-Specific Effects on Neurodegeneration ... 1996) Human apolipoprotein E2, E3, and E4 isoform-specific transgenic mice: human-like pattern of glial and neuronal ...
The e4 allele of the apolipoprotein E (APOE) gene is a known risk factor for Alzheimers disease and may also affect cognitive ... Apolipoprotein E4 and a change in episodic memory functioning among normal aging Norwegian adults. Ananga, Mark Kwame ...
Apolipoprotein E4 disrupts the neuroprotective action of sortilin in neuronal lipid metabolism and endocannabinoid signaling ... INTRODUCTION: Apolipoprotein E (apoE) is a carrier for brain lipids and the most important genetic risk factor for Alzheimers ...
Apolipoprotein E4 genotype in combination with poor metabolic profile is associated with reduced cognitive performance in ...
Apolipoprotein E4 (apoE4) is the most prevalent genetic risk factor for Alzheimers disease. We utilized apoE4-targeted ... are similar in 4-month-old apoE4 and apolipoprotein E3 (apoE3) mice. Both parameters decrease with age. This decrease is, ...
Roles of apolipoprotein E4 (ApoE4) in the pathogenesis of Alzheimers disease: lessons from ApoE mouse models Yadong Huang ... ApoE4 (apolipoprotein E4) is the major known genetic risk factor for AD (Alzheimers disease). In most clinical studies, apoE4 ... Yadong Huang; Roles of apolipoprotein E4 (ApoE4) in the pathogenesis of Alzheimers disease: lessons from ApoE mouse models. ...
The APOE genotype exhibits opposite effects at the extremes of age with protective effects of e4 on perinatal mortality but ... Apolipoprotein E4 / genetics*. Child, Preschool. Female. Gene Frequency. Genetic Predisposition to Disease. Humans. Infant. ... The prevalence of e4 in SIDS is not of an order to contribute significantly to the age-related decline in e4.. ... The percentage of children with at least one e4 allele was significantly lower in non-SIDS compared to SIDS (p = 0.016). Non- ...
Apolipoprotein,E4,genotype,or,gender,medicine,medical news today,latest medical news,medical newsletters,current medical news, ... Treatment response to Aricept® (donepezil hydrochloride) not predicted by Apolipoprotein E4 genotype or gender ... treatment response was not predicted by Apolipoprotein E4 (ApoE4) genotype and/or gender, according to data presented today at ...
Decreased cerebrospinal fluid levels of L-carnitine in non-apolipoprotein E4 carriers at early stages of Alzheimers disease. - ...
Memory and self-appraisal in middle-aged and older adults with the apolipoprotein E-4 allele. Am J Psychiatry1999;156:1035-8. ... Apolipoprotein E4 is only a weak predictor of dementia and cognitive decline in the general population ... Apolipoprotein E4 is only a weak predictor of dementia and cognitive decline in the general population ... Apolipoprotein E genetic variation and Alzheimers disease. a meta-analysis. Dement Geriatr Cogn Disord1999;10:199-209. ...
Interestingly, the E4 allele of the Apolipoprotein E gene (ApoE4) is the strongest known genetic risk factor for late-onset, ... Gene-environment interactions between adult lead exposure and Apolipoprotein E4 on adult hippocampal neurogenesis and cognitive ...
Apolipoprotein E (Apo E) gene is mapped to chromosome 19 in a cluster with Apolipoprotein C1 and Apolipoprotein C2. Apo E is ... The aim of this study was to identify the association between Apolipoprotein E4 (Apo E4) genotype and VD in cerebrally ... Progressive Loss of Synaptic Integrity in Human Apolipoprotein E4 Targeted Replacement Mice and Attenuation by Apolipoprotein ... Apo E4 Genotyping. Two cm of venous blood sample was drawn from each participant on EDTA tube. Genotyping at the ApoE Locus ...
Apolipoprotein E4 (ApoE4) is the major genetic risk factor of Alzheimers disease (AD). ApoE4 carriers have cerebral ...
The E4 allele of APOE (E4) is the strongest genetic risk factor for the development of late onset Alzheimers disease (AD). ... We then probed fatty acid (FA) metabolism and found E4 astrocytes to exhibit decreased uptake of palmitate, and decreased ... We then measured oxygen consumption rate, and found E4 astrocytes to consume more oxygen for endogenous FA oxidation and ... We found that astrocytes expressing E4 accumulate significantly more and smaller LDs compared to E3 astrocytes. Accordingly, ...
Apolipoprotein E4 association with metabolic syndrome depends on body fatness Elena Torres-Perez 1 , Marta Ledesma 2 , Maria ... Apolipoprotein E4 association with metabolic syndrome depends on body fatness Elena Torres-Perez et al. Atherosclerosis. 2016 ... Diversity of apolipoprotein E genetic polymorphism significance on cardiovascular risk is determined by the presence of ... Background and aims: The human Apolipoprotein E (APOE) gene is polymorphic. The APOE*4 allele is a risk factor for ...
Apolipoprotein E e4 Allele Increases the Risk of Early Postoperative Delirium in Older Patients Undergoing Noncardiac Surgery ... Association between the Apolipoprotein E4 and Postoperative Cognitive Dysfunction in Elderly Patients Undergoing Intravenous ... Association between the Apolipoprotein E4 and Postoperative Cognitive Dysfunction in Elderly Patients Undergoing Intravenous ... Association between the Apolipoprotein E4 and Postoperative Cognitive Dysfunction in Elderly Patients Undergoing Intravenous ...
Anti-Apolipoprotein E4 antibody (Biotin). Apolipoprotein E4 一次抗体 製品一覧. ...
  • Apolipoprotein E (apoE) is critical in the modulation of cholesterol and phospholipid transport between cells of different types. (pnas.org)
  • Objectives: To evaluate the frequency of apolipoprotein (APOE) alleles and determine whether APOE type 4 allele (e4) was associated with edentulousness even when certain factors were controlled.Background: The APOE are important in lipid homeostasis, and APOE e4 has been found in many diseases and to have a negative impact on longevity. (diva-portal.org)
  • Logistic regression was performed with dentate/edentulous as dependent variables and years of education, socio-economic status, social network, stress level, handicap from birth, 23 various diseases and APOE e4 as covariates. (diva-portal.org)
  • Thereafter, APOE e4 frequencies were studied in 342 dentateand 336 edentulous subjects 50-85 years of age. (diva-portal.org)
  • Corresponding frequencies of APOE in the edentulous group were: e2 = 6.6%, e3 = 75.4% and e4 = 18.0%.Conclusion: Despite matching both groups with regard to different background factors, the edentulous group had a higher frequency of APOE e4 than the dentate group. (diva-portal.org)
  • Thus, genetic factors might contribute to greater risk in developing complex oral diseases leading to tooth loss or just be an indication that the subjects in our study carrying APOE e4 are more fragile. (diva-portal.org)
  • Aggressive change may result from known genetic risk factors for Alzheimer's disease (AD) and therefore accompany conventional markers such as apolipoprotein E (ApoE). (bmj.com)
  • The e4 allele of the apolipoprotein E (APOE) gene is a known risk factor for Alzheimer's disease and may also affect cognitive performance in normal aging. (uio.no)
  • INTRODUCTION: Apolipoprotein E (apoE) is a carrier for brain lipids and the most important genetic risk factor for Alzheimer's disease (AD). (mdc-berlin.de)
  • The APOE genotype exhibits opposite effects at the extremes of age with protective effects of e4 on perinatal mortality but detrimental effects as age progresses. (biomedsearch.com)
  • OBJECTIVE: To determine whether the APOE e4 allele is associated with early childhood (1 week-2 years) unexplained death ('sudden infant death syndrome', SIDS) or with recognised causes (non-SIDS) and to compare these cohorts with published perinatal and adult data. (biomedsearch.com)
  • APOE alleles (e2, e3, e4) were determined using PCR. (biomedsearch.com)
  • Apolipoprotein E ( APOE ) polymorphisms are unequivocally associated with risk for Alzheimer's disease (AD). (bmj.com)
  • Alzheimer's disease risk is unequivocally associated with polymorphisms in the apolipoprotein E ( APOE ) gene (chromosome 19q13.2). (bmj.com)
  • Lipid droplets (LDs) serve as energy rich reservoirs and have been associated with apolipoprotein E ( APOE ) and neurodegeneration. (uky.edu)
  • The E4 allele of APOE (E4) is the strongest genetic risk factor for the development of late onset Alzheimer's disease (AD). (uky.edu)
  • Since both E4 carriers and individuals with AD exhibit a state of cerebral lipid dyshomeostasis, we hypothesized that APOE may play a role in regulating LD metabolism. (uky.edu)
  • The following are available online at https://www.mdpi.com/2073-4409/8/2/182/s1 , Figure S1: E4 astrocytes express more perilipin-2, Figure S2: E4 astrocytes secrete less ApoE into the media and have less intracellular ApoE, Figure S3: E4 astrocytes form more lipid droplets. (uky.edu)
  • The human Apolipoprotein E (APOE) gene is polymorphic. (cdc.gov)
  • Gene polymorphism of apolipoprotein E (ApoE) has been associated with development of dementia. (asahq.org)
  • 5 Gene polymorphism of apolipoprotein E (ApoE) residing on chromosome 19 is associated with senile dementia. (asahq.org)
  • What is the Apolipoprotein E (APOE) Gene? (healthhelpzone.com)
  • The apolipoprotein E (APOE) gene is responsible for the production of a protein, called apolipoprotein E, that carries cholesterols and fats through the bloodstream. (healthhelpzone.com)
  • One variant or form of the APOE gene, called e4, has been linked to an increased risk of developing Alzheimer's disease. (healthhelpzone.com)
  • The exact mechanism of how the e4 variant of the APOE gene leads to the onset of Alzheimer's is unknown. (healthhelpzone.com)
  • However, researchers have seen that individuals with the e4 variant of the APOE gene possess clusters of proteins, called amyloid plaques, in their brain tissue. (healthhelpzone.com)
  • The apolipoprotein-E (apoE) protein has been implicated in controlling BBB integrity in an isoform dependent manner, via suppression of Cyclophilin A (CypA)-Matrix metallopeptidase-9 (MMP-9) signaling cascades, however the contribution of this pathway in TBI-induced BBB permeability is not fully investigated. (biomedcentral.com)
  • The human apolipoprotein-E protein (apoE) is a protein produced primarily by astrocytes and serves as a major lipid transport molecule in the central nervous system [ 3 ]. (biomedcentral.com)
  • The human apolipoprotein-E gene (APOE) and its 3 associated polymorphisms (APOE2, APOE3, and APOE4) are hypothesized to contribute to several secondary injury processes [ 8 ], including influencing BBB breakdown [ 10 , 11 ]. (biomedcentral.com)
  • Several studies have reported an association of the apolipoprotein E allele epsilon 4 (APOE*4) to familial and sporadic late-onset Alzheimer's disease (LOAD). (ox.ac.uk)
  • It has been suggested that apolipoprotein E4 expression leads to increased vascular amyloid deposition, which may explain the increased incidence of ICH in APOE *4 carriers. (duke.edu)
  • Hiroshi Mori on Sialylated human apolipoprotein E (apoEs) is preferentially associated with neuron-enriched cultures from APOE transgenic mice. (alzforum.org)
  • Interestingly, APOE -E4 seems to have no effect on the behavioral performance during a VFT in healthy elderly. (frontiersin.org)
  • Thus, the purpose of the present study was to reveal possible compensation mechanisms by investigating the effect of APOE -E4 on the hemodynamic response in non-demented elderly during a VFT by using functional near-infrared spectroscopy (fNIRS). (frontiersin.org)
  • APOE -E4/E4, -E3/E4 carriers had a decreased hemodynamic response in the right inferior frontal junction (IFJ) with a corresponding higher response in the left middle frontal gyrus (MFG) during category fluency. (frontiersin.org)
  • The presence of apolipoprotein E4 ( APOE * E4 ) is the strongest currently known genetic risk factor for Alzheimer disease and is associated with brain gray matter loss, notably in areas involved in Alzheimer disease pathology. (ajnr.org)
  • Our objective was to assess the effect of APOE * E4 on brain structures in healthy elderly controls who subsequently developed subtle cognitive decline. (ajnr.org)
  • APOE * E4 -related GM loss at baseline was found only in the cognitively deteriorating controls in the posterior cingulate cortex. (ajnr.org)
  • There was no APOE * E4- related effect in the hippocampus, mesial temporal lobe, or brain areas not involved in Alzheimer disease pathology. (ajnr.org)
  • APOE * E4 -related GM loss in the posterior cingulate cortex (an area involved in Alzheimer disease pathology) was found only in those elderly controls who subsequently developed subtle cognitive decline but not in cognitively stable controls. (ajnr.org)
  • Most important, APOE * E4 status had no impact on GM density in areas affected early by neurofibrillary tangle formation such as the hippocampus and mesial temporal lobe. (ajnr.org)
  • The APOE gene's e4 and e2 alleles are risk factors for CAA. (medscape.com)
  • The APOE e4 allele is associated with earlier onset of first hemorrhage and carries a significant risk of concomitant Alzheimer disease (AD). (medscape.com)
  • Apolipoprotein E (ApoE) and its isoforms (e2, e3, and e4) are involved in the regulation of lipid metabolism. (hindawi.com)
  • Specifically, ApoE e4 has been associated with atherosclerotic diseases, while e2 has a favorable effect. (hindawi.com)
  • We therefore hypothesized that ApoE e4 haplotype is frequently observed in IUGR neonates and contributes to impaired fetal growth and the association of IUGR with cardiovascular and metabolic diseases later in life. (hindawi.com)
  • Apolipoprotein E (ApoE) is an important circulating serum protein involved in transporting lipids and cholesterol and regulating lipid levels. (hindawi.com)
  • Objective: Investigate associations between indicators of sleep-disordered breathing (SDB) and cognitive function in the Multi-Ethnic Study of Atherosclerosis and assess effect modification by the apolipoprotein epsilon-4 (APOE-epsilon4) allele. (cdc.gov)
  • Apolipoprotein E ( ApoE ) is a class of proteins involved in the metabolism of fats in the body. (wikidoc.org)
  • APOE is primarily located in HDL and VLDL Apolipoproteins act as lipid transfer carrier enzymes, cofactors and receptor ligands which control lipoprotein metabolism. (prospecbio.com)
  • Apolipoprotein E (ApoE) ε4 genotype is a well-established risk factor for Alzheimer's disease (AD). (cmaj.ca)
  • In recent years, rapid progress in molecular genetics has fostered the discovery of at least 4 genes associated with AD: the amyloid precursor protein (APP), the presenilin-1 gene (PS-1), the presenilin-2 gene (PS-2) and the apolipoprotein E gene (ApoE). (cmaj.ca)
  • Apolipoprotein E (apoE) is an important transporter of fats in the blood. (clinicaltrials.gov)
  • ApoE comes in E2, E3 and E4 forms, depending on your genetic make up. (clinicaltrials.gov)
  • The 4 allele of the apolipoprotein E (APOE) gene is known as a risk factor for cognitive impairment. (dovepress.com)
  • The benefits of being cognitively engaged even were seen among apolipoprotein E (APOE) e4 carriers. (hindustantimes.com)
  • APOE e4 is a genetic risk factor for mild cognitive impairment and Alzheimer's dementia. (hindustantimes.com)
  • However, for APOE e4 carriers, only computer use and social activities were associated with a decreased risk of mild cognitive impairment. (hindustantimes.com)
  • APOE at the molecular level helps in the synthesis of apolipoprotein E, which is a cholesterol carrier in the brain, helping in amyloid aggregation and the clearing of deposits from the parenchyma of the brain. (medscape.com)
  • Apolipoprotein E (ApoE) regulates the metabolism of lipids by coordinating their transport and redistribution from one cell type to another via ApoE receptors and proteins associated with lipid transfer and lipolysis [1] . (plos.org)
  • There are three allelic variants of the ApoE gene in humans (E2, E3, E4) [3] . (plos.org)
  • One of the biggest risk factors for Alzheimer's disease is the apolipoprotein E (APOE) e4 gene. (medicalnewstoday.com)
  • According to the Alzheimer's Association, adults who possess one copy of the APOE e4 gene are three times more likely to develop the disease than those without the gene, while those with two copies are 8-12 times more likely to develop Alzheimer's. (medicalnewstoday.com)
  • For their study, Heisz and colleagues set out to investigate the association between physical activity and dementia risk among older adults with and without the APOE e4 gene. (medicalnewstoday.com)
  • Among adults who did not carry the APOE e4 gene, the researchers found that those who did not exercise were more likely to develop dementia than those who exercised. (medicalnewstoday.com)
  • For APOE e4 gene carriers, however, there was no significant difference in dementia risk between those who exercised and those who did not. (medicalnewstoday.com)
  • According to the researchers, these findings indicate that a lack of exercise may be just as risky for dementia development than carrying the APOE e4 gene. (medicalnewstoday.com)
  • the study results also suggest that increasing physical activity may protect against the development of dementia in people without the APOE e4 gene. (medicalnewstoday.com)
  • Apolipoprotein E4 (apoE4), the major genetic risk factor of Alzheimer's disease (AD), is associated with enhanced brain inflammation. (nih.gov)
  • This study performed fasting blood sugar (FBS) and blood pressure measurements and investigated the presence of the ε4 allele of apolipoprotein E (APOE4) to determine the prevalence of diabetes, hypertension and the genetic risk of NCDs. (mdpi.com)
  • Apolipoprotein E4 (apoE4) is the major genetic risk factor for Alzheimer's disease. (jneurosci.org)
  • This revealed that levels of the pre-synaptic cholinergic marker, vesicular acetylcholine transporter in the hippocampus and the corresponding electrically evoked release of acetylcholine, are similar in 4-month-old apoE4 and apolipoprotein E3 (apoE3) mice. (ovid.com)
  • In this study, treatment response was not predicted by Apolipoprotein E4 (ApoE4) genotype and/or gender, according to data presented today at the World Alzheimer Congress in Washington D.C. (bio-medicine.org)
  • Interestingly, the E4 allele of the Apolipoprotein E gene (ApoE4) is the strongest known genetic risk factor for late-onset, sporadic AD, and it is also associated with accelerated cognitive decline compared to ApoE4 non-carriers. (washington.edu)
  • The apolipoprotein E4 (ApoE4) is an established risk factor for Alzheimer's disease (AD). (plos.org)
  • 가족과 유전 링크는 Apolipoprotein E4 (ApoE4) 유전자 돌연변이를 관련시키는 가장 큰 위험 요소로 고려됩니다. (news-medical.net)
  • Several recently published studies showed the existence of an association between the allele ε4 of the apolipoprotein E and Alzheimer's disease (AD) in developed countries. (scielo.br)
  • Apolipoprotein E ɛ4 allele is a common susceptibility gene for late-onset Alzheimer's disease. (nih.gov)
  • Brain vascular and metabolic deficits can occur in cognitively normal apolipoprotein E ɛ4 carriers decades before the onset of Alzheimer's disease. (nih.gov)
  • The goal of this study was to determine whether early intervention using rapamycin could restore neurovascular and neurometabolic functions, and thus impede pathological progression of Alzheimer's disease-like symptoms in pre-symptomatic Apolipoprotein E ɛ4 transgenic mice. (nih.gov)
  • These results indicate that advanced Alzheimer's disease patients are at greater risk of aggressive symptoms because of a genetic weakness in apolipoprotein E. (bmj.com)
  • Apolipoprotein (apo) E isoforms are key determinants of susceptibility to Alzheimer's disease. (jneurosci.org)
  • Apolipoprotein E4 allele in a population-based study of early-onset Alzheimer's disease. (ox.ac.uk)
  • For example, issues are currently debated regarding population-based genetic testing for breast cancer in relation to BRCA1 (5), Alzheimer's disease in relation to the Apolipoprotein E-E4 allele (6), and iron overload in relation to the hemochromatosis gene (7). (cdc.gov)
  • Influence of apolipoprotein E genotype on blood redox status of Alzheimer's disease patients. (semanticscholar.org)
  • To determine the association between the e4 allele of apolipoprotein E and Alzheimer's disease in a randomly selected population sample. (bmj.com)
  • Presence of e4 allele and diagnosis of Alzheimer's disease by detailed neurological and neurophysiological evaluation. (bmj.com)
  • The prevalence of Alzheimer's disease was 2.9% in subjects with no e4 alleles, 7.6% in subjects with one e4 allele, and 21.4% in subjects with two e4 alleles of apolipoprotein E. (bmj.com)
  • Allele e4 of apolipoprotein is associated with Alzheimer's disease in a dose-response fashion in a randomly selected elderly population. (bmj.com)
  • The e4 allele seems to be a risk factor for Alzheimer's disease. (bmj.com)
  • RF 1-2* Evidence is accumulating that apolipoprotein E is important in late onset Alzheimer's disease. (bmj.com)
  • The first evidence that e4 allele of apolipoprotein E could be associated with Alzheimer's disease was published by Pericak-Vance et al. (bmj.com)
  • Recently, several studies based on clinical series have shown an association between the e4 allele and Alzheimer's disease in elderly subjects. (bmj.com)
  • All the studies that have investigated the relation between apolipoprotein E polymorphism and Alzheimer's disease have included highly selected patients and corresponding controls. (bmj.com)
  • Therefore we investigated whether the association of the e4 allele with Alzheimer's disease could be found also in a randomly selected elderly population living in eastern Finland. (bmj.com)
  • Treatment response to Aricept® (donepezil hydrochloride) not predicted by Apolipoprotein E4 genotype. (bio-medicine.org)
  • The aim of this study was to identify the association between Apolipoprotein E4 (Apo E4) genotype and VD in cerebrally infarcted patients. (scirp.org)
  • The study concluded that cerebrally infarcted patients with Apo E4 genotype are at high risk of developing VD. (scirp.org)
  • MCNS with risky HLA profile and E4/4 genotype could indicate the need for a longer steroid administration. (chikd.org)
  • Apolipoprotein E genotype and outcome after aneurysmal subarachnoid hemorrhage. (biomedsearch.com)
  • Influence of apolipoprotein E genotype and dietary alpha-tocopherol on redox status and C-reactive protein levels in apolipoprotein E3 and E4 targeted replacement mice. (semanticscholar.org)
  • Implications of apolipoprotein E genotype on inflammation and vitamin E status. (semanticscholar.org)
  • There is some evidence to suggest that an E4 genotype may put you at modestly higher risk of CVD. (clinicaltrials.gov)
  • Therefore, the aims of the Satgene study is to examine the impact of modifications in dietary total fat and saturated fat intakes, alone and in combination with fish oil supplement on LDL-cholesterol and other blood lipids, in individuals with an E3 and E4 genotype. (clinicaltrials.gov)
  • When only patients with the diagnosis of "probable AD" were included in the analysis (n=43), we observed that 22.1% of the alleles were e4, a rate that was significantly higher than the 8.9% of controls (p=0.024). (scielo.br)
  • When they adjusted for the number of alleles of apolipoprotein E4 , the top genetic risk factor for sporadic AD, the effect remained strong but lost statistical significance, possibly because only 769 of 1,102 participants were genotyped. (alzforum.org)
  • Apolipoprotein E epsilon4 magnifies lifestyle risks for dementia: a population-based study. (nih.gov)
  • 4 We examined the association between education and cognitive decline in elderly men with and without the e4 allele to see whether this genetic risk factor modified the association. (bmj.com)
  • Routine cerebrospinal fluid testing and genetic testing for the apolipoprotein E4 allele are not recommended. (aafp.org)
  • [8] found an association between Apo E4 polymorphism and VD. (scirp.org)
  • There was no linkage disequilibrium between the apolipoprotein E locus and a TaqI polymorphism at the Apo CII locus, and no allelic association between Apo CII and AD. (cf.ac.uk)
  • Apo E is polymorphic with three major isoforms: Apo E2, Apo E3 and Apo E4. (scirp.org)
  • The association between education and cognitive decline was examined by logistic regression in the total group and the carriers and non-carriers of e4, adjusting for age and baseline score for cognitive function. (bmj.com)
  • This was strong in non-carriers of e4, but in carriers of e4 it was absent (test for interaction not significant, P=0.11). (bmj.com)
  • For carriers and non-carriers of e4, the subjects who did not participate in 1993 showed a similar association between education and cognitive function in 1990 as did those who participated in 1993 (results not shown). (bmj.com)
  • In contrast, there was no association between education and cognitive decline in carriers of the e4 allele. (bmj.com)
  • The e4 allele may be such a strong risk factor for cognitive decline that cognitive performance in carriers of an e4 allele deteriorates regardless of educational level. (bmj.com)
  • Our results show that rapamycin improves functional outcomes in this mouse model and may have potential as an effective intervention to block progression of vascular, metabolic and early cognitive deficits in human Apolipoprotein E ɛ4 carriers. (nih.gov)
  • Approximately 60% of the UK population are E3/E3, 25% E4 carriers and 15% E2 carriers. (clinicaltrials.gov)
  • The E4 allele has been shown to confer a higher risk of developing both early onset and late onset AD [4] , [5] . (plos.org)
  • Using in vivo, multimodal neuroimaging, we found that apolipoprotein E ɛ4 mice treated with rapamycin had restored cerebral blood flow, blood-brain barrier integrity and glucose metabolism, compared to age- and gender-matched wild-type controls. (nih.gov)
  • Apolipoprotein E4 Alters Astrocyte Fatty Acid Metabolism and Lipid Dro" by Brandon C. Farmer, Jude Kluemper et al. (uky.edu)
  • We then probed fatty acid (FA) metabolism and found E4 astrocytes to exhibit decreased uptake of palmitate, and decreased oxidation of exogenously supplied oleate and palmitate. (uky.edu)
  • and Johnson, Lance A., "Apolipoprotein E4 Alters Astrocyte Fatty Acid Metabolism and Lipid Droplet Formation" (2019). (uky.edu)
  • Hiroshi Mori on Altered cholesterol metabolism in human apolipoprotein E4 knock-in mice. (alzforum.org)
  • Lipoprotein (a) and Low-density lipoprotein apolipoprotein B metabolism following apheresis in patients with elevated lipoprotein(a) and coronary artery disease. (harvard.edu)
  • Apo E (Apolipoprotein E) plays an important role in the metabolism of lipids in the plasma, and is also is a constituent of various plasma lipoprotein-lipid particles. (thermofisher.com)
  • Apolipoprotein (apo) E is a 34 kDa protein that participates in the transport of plasma lipids and in the redistribution of lipids among cells ( Mahley, 1988 ). (jneurosci.org)
  • Accordingly, expression of perilipin-2, an essential LD protein component, was higher in E4 astrocytes. (uky.edu)
  • Recombinant protein encompassing a sequence within the N-terminus region of human Apolipoprotein E. (thermofisher.com)
  • Apolipoprotein E is a fat-binding protein ( apolipoprotein ) that is part of the chylomicron and intermediate-density lipoprotein (IDLs) . (wikidoc.org)
  • The apolipoprotein e4 allele on chromosome 19 is an important risk factor for cognitive decline. (bmj.com)
  • Apolipoprotein E (Apo E) gene is mapped to chromosome 19 in a cluster with Apolipoprotein C1 and Apolipoprotein C2 . (scirp.org)
  • Human apolipoprotein E4 targeted replacement mice show increased prevalence of intracerebral hemorrhage associated with vascular amyloid deposition. (duke.edu)
  • Trends in Levels of Lipids and Apolipoprotein B in US Youths Aged 6 to 19 Years, 1999-2016. (harvard.edu)
  • Nevertheless, due to of their amphipathic/detergent like characteristics, Apolipoproteins fence in the lipids, forming a lipoprotein particle which is soluble in water, hence travel in blood. (prospecbio.com)
  • Apolipoproteins are composed from various lipoproteins such as exchangeable Apolipoprtoeins and non-exchangeable. (prospecbio.com)
  • Apolipoprotein (apo) E stimulates the secretion of very low density lipoproteins (VLDLs) by an as yet unknown mechanism. (tudelft.nl)
  • A significantly higher frequency of the e4 allele was found in individuals recording aggression/agitation in the month prior to interview (χ 2 = 6.69, df = 2, p = 0.03). (bmj.com)
  • The frequency of the e4 allele was significantly increased in the patient group (0.33) as compared with controls (0.12). (cf.ac.uk)
  • The Finnish population is of particular interest because the frequency of the e4 allele is high in this population. (bmj.com)
  • Apolipoprotein E e4 and its prevalence in early childhood death due to sudden infant death syndrome or to recognised causes. (biomedsearch.com)
  • The prevalence of e4 in SIDS is not of an order to contribute significantly to the age-related decline in e4. (biomedsearch.com)
  • [35] A notable advantage of the E4 allele (relative to E2 and E3) is a positive association with higher levels of vitamin D , which may help explain its prevalence despite its seeming complicity in various diseases or disorders. (wikidoc.org)
  • Apolipoproteins B" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (harvard.edu)
  • The additional risk for aggression/agitation conferred by e4 was also noted when e4 genotypes were compared against non-e4 genotypes (χ 2 = 5.45, df = 1, p = 0.02, OR = 1.60, confidence interval (CI) 1.06 to 2.43). (bmj.com)
  • RESULTS: Apolipoprotein E epsilon2 or epsilon4-containing genotypes were not associated with outcome, occurrence of cerebral infarction, or with any of their predictors, either in univariate or multivariate analysis. (biomedsearch.com)
  • Human Apolipoprotein E4 expressed in E. coli. (abcam.com)
  • Apolipoprotein E4 Human Recombinant produced in E.coli is a single, non-glycosylated polypeptide chain containing a total of 306 amino acids including a His Tag at N-terminus and having a molecular mass of 35.2kDa. (mylab.com.tw)
  • Alternatively, apolipoprotein e4 may play a role in inhibiting neuronal growth 5 and may thus block the putative stimulating effect of education on neuronal growth. (bmj.com)
  • The differential effects of apolipoproteins E3 and E4 were also examined on neuronal growth in vitro. (wikipedia.org)
  • The apolipoprotein (Apo)E4 allele is a risk factor for CAA ( 1 ). (aerzteblatt.de)
  • We observed a significantly increased risk of cognitive decline associated with a lower level of education in subjects without an apolipoprotein e4 allele. (bmj.com)
  • What is the role of apolipoprotein studies in the workup of cerebral amyloid angiopathy (CAA)? (medscape.com)
  • 3, 4 Furthermore, phenotypes E4/4 and E4/3 have been associated with the risk of myocardial infarction and coronary heart disease,*RF 5-7* particularly in young people, although there is some controversy about this. (bmj.com)
  • Plasma apolipoprotein E phenotypes modulate lipoprotein concentrations, particularly that of low density lipoprotein cholesterol. (bmj.com)
  • Furthermore although very inconclusive previous studies have suggested that E4 individuals are slightly more sensitive to the LDL-cholesterol modifying effects of dietary fats (saturated fat, total fat, fish oil) showing slightly, greater reductions when low levels of these fat are consumed, and greater increases when high levels of these fat are consumed. (clinicaltrials.gov)
  • The odds ratio in homozygotes for the e4 allele was 11.24 (95% confidence interval 2.45-51.50). (cf.ac.uk)
  • Serum samples were obtained in 1990 and frozen at -20°C until 1993, when the apolipoprotein E phenotype was determined by isoelectric focusing of delipidated plasma samples followed by immunoblotting. (bmj.com)
  • However, our data do not suggest that less educated men with e4 who did not participate in 1993 had a different risk of cognitive impairment than those who participated. (bmj.com)
  • The study showed that hypertension (p = 0.027, OR = 4.71), diabetes mellitus (p = 0.003, OR = 6.05) and Apo E4 allele (p = 0.017, OR = 13.39) were the independent risk factors of VD among studied participants. (scirp.org)