Apolipoprotein e4. Medical search

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 3.1.1.34.

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 2.3.1.43.

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.

Proteins that bind to and transfer CHOLESTEROL ESTERS between LIPOPROTEINS such as LOW-DENSITY LIPOPROTEINS and HIGH-DENSITY LIPOPROTEINS.

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 3.1.1.3.

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 4.2.2.7.

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 3.1.1.2).

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 3.5.4.5.

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 2.3.1.26.

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)

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. ...

https://en.wikipedia.org/wiki/Differential_effects

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 ...

https://en.wikipedia.org/wiki/Albert_Hofman

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 ...

https://en.wikipedia.org/wiki/Reelin

Specifically too, the apolipoprotein *e4 allele is linked to Alzheimer's disease as well. Also, there is increased coronary ... Also, research has been put on concerning apolipoprotein E genotypes; this polymorphism has three alleles (*e2, *e3, and *e4) ...

https://en.wikipedia.org/wiki/Japanese_Americans

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 ...

https://en.wikipedia.org/wiki/Alzheimer's_disease

... apolipoprotein E4 genotype, and biomarkers of brain injury". Anesthesiology. 112 (4): 852-9. doi:10.1097/ALN.0b013e3181d31fd7. ...

https://en.wikipedia.org/wiki/Postoperative_cognitive_dysfunction

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 ...

https://en.wikipedia.org/wiki/Dena_Dubal

2002). "Codon 311 (Cys --> Ser) polymorphism of paraoxonase-2 gene is associated with apolipoprotein E4 allele in both ...

https://en.wikipedia.org/wiki/PON2

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 ...

https://en.wikipedia.org/wiki/Angiotensin-converting_enzyme

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 ...

https://en.wikipedia.org/wiki/Gladstone_Institutes

In a secondary analysis, a subgroup of individuals with the apolipoprotein E4 genotype showed sustained benefits with donepezil ...

https://en.wikipedia.org/wiki/Donepezil

"The Apolipoprotein E e4 Polymorphism Is Strongly Associated With Poor Mobility Performance Test Results But Not Self-Reported ...

https://en.wikipedia.org/wiki/Age-related_mobility_disability

"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 ...

https://en.m.wikipedia.org/wiki/Alzheimer's

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 ...

https://pl.wikipedia.org/wiki/Choroba_Alzheimera

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

https://zh.wikipedia.org/wiki/阿兹海默病

"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): ...

https://ms.wikipedia.org/wiki/Penyakit_Alzheimer

Research has also discovered the association of a fourth allele, apolipoprotein E4 (ApoE4), in the development of late-onset ...

https://en.wikipedia.org/wiki/Genetic_heterogeneity

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, ...

https://en.wikipedia.org/wiki/Monoclonal_antibody_therapy

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, ...

https://en.wikipedia.org/wiki/Kidney_ischemia

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 ...

https://en.wikipedia.org/wiki/Lothian_birth-cohort_studies

"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 ...

https://gl.wikipedia.org/wiki/Apolipoproteína_E

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 ...

https://en.wikipedia.org/wiki/Apolipoprotein_E

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 ...

https://sw.wikipedia.org/wiki/Ugonjwa_wa_Alzheimer

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 ...

https://en.wikipedia.org/wiki/Biochemistry_of_Alzheimer's_disease

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 ...

https://pt.m.wikipedia.org/wiki/Alzheimer

Mahley RW, Weisgraber KH, Huang Y (2006). «Apolipoprotein E4: a causative factor and therapeutic target in neuropathology, ... 1995). «Apolipoprotein E, dementia, and cortical deposition of beta-amyloid protein». N Engl J Med. 333 (19): 1242-47. PMID ... Den mest kjente genetiske risikofaktoren er arv av ε4-allelet av apolipoprotein E (APOE).[74][75] Mellom 40 og 80 % av ... 1993). «Apolipoprotein E: high-avidity binding to beta-amyloid and increased frequency of type 4 allele in late-onset familial ...

https://no.m.wikipedia.org/wiki/Alzheimers

儘管抗體是用於對抗外來異物的免疫手段，但在部分人群中卻存在著因為抗體異常導致的自體免疫

https://zh.wikipedia.org/zh-tw/抗体

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 ...

https://zh.m.wikipedia.org/wiki/阿兹海默病

a b Apolipoprotein E4: a causative factor and therapeutic target in neuropathology, including Alzheimer's disease. Proceedings ... Apolipoprotein E, Dementia, and Cortical Deposition of Beta-amyloid Protein. The New England Journal of Medicine. 1995;333(19): ... Apolipoprotein E: high-avidity binding to beta-amyloid and increased frequency of type 4 allele in late-onset familial ... allellen tilhørende apolipoprotein E (APOE).[42][43] Mellem 40 og 80% af patienterne med AD har mindst én APOEε4-allel.[43] ...

https://da.wikipedia.org/wiki/Alzheimers_sygdom

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 ...

https://en.wikipedia.org/wiki/Japanese-American

"Very early changes in olfactory functioning due to Alzheimer's disease and the role of apolipoprotein E in olfaction". Annals ...

https://en.wikipedia.org/wiki/Olfactory_tubercle

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 ...

https://en.wikipedia.org/wiki/Dendritic_cell

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 - ...

https://en.wikipedia.org/wiki/List_of_MeSH_codes_(D12.776)

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. ...

https://www.rcsb.org/structure/1gs9

Rabbit polyclonal Apolipoprotein E4 antibody conjugated to Biotin. Validated in WB, ELISA, RIA and tested in Human. Immunogen ...

https://www.abcam.com/Apolipoprotein-E4-antibody-Biotin-ab85976.html

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 ...

http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0004-282X1997000100001

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 ...

https://www.pnas.org/content/92/26/12260?ijkey=8db609a2ef1c585197232112a720d4975e521d2d&keytype2=tf_ipsecsha

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 ...

https://www.ncbi.nlm.nih.gov/pubmed/15979312

... 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 £ ...

http://www.diva-portal.org/smash/record.jsf?faces-redirect=true&language=sv&searchType=SIMPLE&query=&af=%5B%5D&aq=%5B%5B%5D%5D&aq2=%5B%5B%5D%5D&aqe=%5B%5D&pid=diva2%3A219137&noOfRows=50&sortOrder=author_sort_asc&sortOrder2=title_sort_asc&onlyFullText=false&sf=all

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. ...

https://www.medindia.net/news/healthinfocus/new-role-of-apolipoprotein-e4-variant-in-alzheimers-disease-suggests-possible-therapeutic-target-173194-1.htm

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 ...

http://www.bmj.com/content/314/7073/34

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 ...

https://pubmed.ncbi.nlm.nih.gov/26721390/

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- ...

http://jnnp.bmj.com/content/75/9/1327

... 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 ...

https://www.mdpi.com/1660-4601/15/9/1957

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 ...

https://www.jneurosci.org/content/30/41/13707.short

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 ...

http://www.jneurosci.org/content/19/12/4867?ijkey=b5941efb8950a529a966f846402ba0cfc52f80e0&keytype2=tf_ipsecsha

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 ...

https://www.duo.uio.no/handle/10852/18543

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 ...

https://www.mdc-berlin.de/research/publications/apolipoprotein-e4-disrupts-neuroprotective-action-sortilin-neuronal-lipid

Apolipoprotein E4 genotype in combination with poor metabolic profile is associated with reduced cognitive performance in ...

https://pubmed.ncbi.nlm.nih.gov/29975287/

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, ...

https://insights.ovid.com/jneur/201602000/00005064-201602000-00008

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. ...

https://portlandpress.com/biochemsoctrans/article-abstract/39/4/924/65285/Roles-of-apolipoprotein-E4-ApoE4-in-the

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- ...

http://www.biomedsearch.com/nih/Apolipoprotein-E-e4-its-prevalence/18280677.html

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 ...

http://news.bio-medicine.org/medicine-news-2/Treatment-response-to-Aricept-26-23174--28donepezil-hydrochloride-29-not-predicted-by-Apolipoprotein-E4-genotype-or-gender-9740-1/

Decreased cerebrospinal fluid levels of L-carnitine in non-apolipoprotein E4 carriers at early stages of Alzheimers disease. - ...

http://digital.csic.es/handle/10261/99915?mode=full

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. ...

https://jmg.bmj.com/content/39/9/639

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 ...

https://digital.lib.washington.edu/researchworks/handle/1773/36645

Physical Activity May Reduce Apolipoprotein E4-Associated Cognitive Decline in Parkinson Disease. Jacob Raber, Sirwan K.L. ... Physical Activity May Reduce Apolipoprotein E4-Associated Cognitive Decline in Parkinson Disease ...

https://n.neurology.org/content/96/19/877.full

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 ...

https://file.scirp.org/Html/2-2420106_48048.htm

Apolipoprotein E4 (ApoE4) is the major genetic risk factor of Alzheimers disease (AD). ApoE4 carriers have cerebral ...

https://www.aging-us.com/figure/102070/f1

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, ...

https://uknowledge.uky.edu/physiology_facpub/142/

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 ...

https://phgkb.cdc.gov/PHGKB/phgHome.action?action=forward&dbsource=huge&id=122727

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 ...

http://anesthesiology.pubs.asahq.org/article.aspx?articleid=1933714

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)
The gene is called apolipoprotein E-4 (ApoE-4). (nashunchealthcare.org)
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)
Apolipoprotein E ( apoE - e2, e3, e4 alleles ) plays a role in the regulation of lipid metabolism , with the e4 considered to be a risk factor for coronary artery disease (CAD). (bvsalud.org)
To elucidate apolipoprotein [ ApoE ] and neurodevelopment in children with Giardiasis and the role of ApoE isoforms in childhood cognition and infant development . (bvsalud.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)
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) 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)
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)
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)
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)

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 on blood redox status of Alzheimer's disease patients. (semanticscholar.org)
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)

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)
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)

Apolipoprotein E epsilon4 magnifies lifestyle risks for dementia: a population-based study. (nih.gov)

[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)
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)

Apolipoprotein (apo) E isoforms are key determinants of susceptibility to Alzheimer's disease. (jneurosci.org)
Apo E is polymorphic with three major isoforms: Apo E2, Apo E3 and Apo E4. (scirp.org)

To determine the association between the e4 allele of apolipoprotein E and Alzheimer's disease in a randomly selected population sample. (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)

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)
Brain vascular and metabolic deficits can occur in cognitively normal apolipoprotein E ɛ4 carriers decades before the onset of Alzheimer's disease. (nih.gov)
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)
The frequency of risk factors was higher in the CAD group (P association with the lipid profile was not demonstrable in e4 carriers. (bvsalud.org)

Apolipoprotein E ɛ4 allele is a common susceptibility gene for late-onset Alzheimer's disease. (nih.gov)
RF 1-2* Evidence is accumulating that apolipoprotein E is important in late onset Alzheimer's disease. (bmj.com)
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)
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)
Lipoprotein (a) and Low-density lipoprotein apolipoprotein B metabolism following apheresis in patients with elevated lipoprotein(a) and coronary artery disease. (harvard.edu)

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)
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 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)
Presence of e4 allele and diagnosis of Alzheimer's disease by detailed neurological and neurophysiological evaluation. (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)
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)
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)

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)

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)

Human apolipoprotein E4 targeted replacement mice show increased prevalence of intracerebral hemorrhage associated with vascular amyloid deposition. (duke.edu)

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)
However, its frequency in the non-CAD group is associated with increased levels of LDL- cholesterol , suggesting an independent effect of the e4 allele on lipid profile when the low frequency of other risk factors in this group is taken into account. (bvsalud.org)
The Finnish population is of particular interest because the frequency of the e4 allele is high in this population. (bmj.com)

Apolipoprotein (apo) E stimulates the secretion of very low density lipoproteins (VLDLs) by an as yet unknown mechanism. (tudelft.nl)
Apolipoproteins are composed from various lipoproteins such as exchangeable Apolipoprtoeins and non-exchangeable. (prospecbio.com)

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)
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)
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)

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)

Plasma apolipoprotein E phenotypes modulate lipoprotein concentrations, particularly that of low density lipoprotein cholesterol. (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)

What is the role of apolipoprotein studies in the workup of cerebral amyloid angiopathy (CAA)? (medscape.com)

Routine cerebrospinal fluid testing and genetic testing for the apolipoprotein E4 allele are not recommended. (aafp.org)

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)

Anatomy25

Organisms8

Diseases35

Chemicals and Drugs99

Analytical, Diagnostic and Therapeutic Techniques and Equipment36

Psychiatry and Psychology8

Phenomena and Processes48

Disciplines and Occupations1

Technology, Industry, Agriculture1

Information Science3

Health Care12

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

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

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

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

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

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

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

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)

Apolipoproteins E

Apolipoprotein E4

Apolipoprotein E3

Apolipoprotein E2

Apolipoprotein A-I

Apolipoprotein B-100

Apolipoproteins B

Apolipoproteins

Apolipoprotein C-III

Apolipoprotein C-I

Apolipoprotein A-II

Apolipoprotein C-II

Apolipoproteins A

Apolipoprotein B-48

Cholesterol

Apolipoproteins C

Lipoproteins, VLDL

Lipoproteins

Lipoproteins, HDL

Receptors, LDL

Alzheimer Disease

Hyperlipoproteinemia Type III

Triglycerides

Genotype

Lipids

Atherosclerosis

Alleles

Arteriosclerosis

Mice, Knockout

Apoprotein(a)

Lipoproteins, LDL

Hyperlipoproteinemias

Receptors, Lipoprotein

Polymorphism, Genetic

Mice, Inbred C57BL

Lipoprotein(a)

LDL-Receptor Related Proteins

Apolipoproteins D

Cholesterol, HDL

Low Density Lipoprotein Receptor-Related Protein-1

Liver

Hyperlipidemias

Amyloid beta-Peptides

Cholesterol, LDL

Lipid Metabolism

ATP Binding Cassette Transporter 1

Gene Frequency

Aorta

Chylomicrons

Diet, Atherogenic

Hypercholesterolemia

Mice, Transgenic

Lipoprotein Lipase

Cholesterol Esters

Cholesterol, VLDL

Heterozygote

Phosphatidylcholine-Sterol O-Acyltransferase

Phenotype

Isoelectric Focusing

RNA, Messenger

Hyperlipoproteinemia Type II

Macrophages

Hypertriglyceridemia

Lipoproteins, IDL

Molecular Sequence Data

Hypolipoproteinemias

Genetic Predisposition to Disease

Homozygote

Disease Models, Animal

Aortic Diseases

Brain

Dietary Fats

Base Sequence

Cells, Cultured

Cholesterol, Dietary

Foam Cells

Clusterin

Dimyristoylphosphatidylcholine

Hyperlipoproteinemia Type V

Protein Isoforms