Apolipoproteins E: 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.Apolipoprotein E4: 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.Apolipoprotein E3: 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.Apolipoprotein E2: 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.Apolipoprotein A-I: 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.Apolipoprotein B-100: 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.Apolipoproteins B: 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.Apolipoproteins: 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.Apolipoprotein C-III: 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).Apolipoprotein C-I: 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.Apolipoprotein A-II: 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.Apolipoprotein C-II: 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.Apolipoproteins A: 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.Apolipoprotein B-48: 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.Cholesterol: The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils.Apolipoproteins C: 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.Lipoproteins, VLDL: 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.Lipoproteins: 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.Lipoproteins, HDL: 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, LDL: 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.Alzheimer Disease: 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)Hyperlipoproteinemia Type III: 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.TriglyceridesGenotype: The genetic constitution of the individual, comprising the ALLELES present at each GENETIC LOCUS.Lipids: 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)Atherosclerosis: A thickening and loss of elasticity of the walls of ARTERIES that occurs with formation of ATHEROSCLEROTIC PLAQUES within the ARTERIAL INTIMA.Alleles: Variant forms of the same gene, occupying the same locus on homologous CHROMOSOMES, and governing the variants in production of the same gene product.Arteriosclerosis: 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.Mice, Knockout: 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.Apoprotein(a): 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.Lipoproteins, LDL: 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.Hyperlipoproteinemias: 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.Receptors, Lipoprotein: 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.Polymorphism, Genetic: 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.Mice, Inbred C57BLLipoprotein(a): 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.LDL-Receptor Related Proteins: A family of proteins that share sequence similarity with the low density lipoprotein receptor (RECEPTORS, LDL).Apolipoproteins D: 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, HDL: Cholesterol which is contained in or bound to high-density lipoproteins (HDL), including CHOLESTEROL ESTERS and free cholesterol.Low Density Lipoprotein Receptor-Related Protein-1: A LDL-receptor related protein involved in clearance of chylomicron remnants and of activated ALPHA-MACROGLOBULINS from plasma.Liver: A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.Hyperlipidemias: Conditions with excess LIPIDS in the blood.Amyloid beta-Peptides: 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, LDL: Cholesterol which is contained in or bound to low density lipoproteins (LDL), including CHOLESTEROL ESTERS and free cholesterol.Lipid Metabolism: Physiological processes in biosynthesis (anabolism) and degradation (catabolism) of LIPIDS.ATP Binding Cassette Transporter 1: 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.Gene Frequency: The proportion of one particular in the total of all ALLELES for one genetic locus in a breeding POPULATION.Aorta: The main trunk of the systemic arteries.Chylomicrons: 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.Diet, Atherogenic: A diet that contributes to the development and acceleration of ATHEROGENESIS.Hypercholesterolemia: 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.Mice, Transgenic: Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.Lipoprotein Lipase: 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.Cholesterol Esters: 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, VLDL: 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.Heterozygote: An individual having different alleles at one or more loci regarding a specific character.Phosphatidylcholine-Sterol O-Acyltransferase: 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.Phenotype: The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.Isoelectric Focusing: 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, Messenger: 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.Hyperlipoproteinemia Type II: 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).Macrophages: 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.)Hypertriglyceridemia: A condition of elevated levels of TRIGLYCERIDES in the blood.Lipoproteins, IDL: 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.Molecular Sequence Data: 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.Hypolipoproteinemias: 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).Genetic Predisposition to Disease: A latent susceptibility to disease at the genetic level, which may be activated under certain conditions.Homozygote: An individual in which both alleles at a given locus are identical.Disease Models, Animal: 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.Aortic Diseases: Pathological processes involving any part of the AORTA.Brain: 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.Dietary Fats: 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.Base Sequence: The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.Cells, Cultured: 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, Dietary: Cholesterol present in food, especially in animal products.Foam Cells: Lipid-laden macrophages originating from monocytes or from smooth muscle cells.Clusterin: 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.Dimyristoylphosphatidylcholine: A synthetic phospholipid used in liposomes and lipid bilayers for the study of biological membranes.Hyperlipoproteinemia Type V: 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 .Protein Isoforms: Different forms of a protein that may be produced from different GENES, or from the same gene by ALTERNATIVE SPLICING.Risk Factors: 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.Cerebral Amyloid Angiopathy: 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)Peptide Fragments: Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.Hyperlipoproteinemia Type IV: 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.ATP-Binding Cassette Transporters: 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.Phospholipids: 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.Amino Acid Sequence: 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, Polyacrylamide Gel: Electrophoresis in which a polyacrylamide gel is used as the diffusion medium.Protein Binding: 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.Hypobetalipoproteinemias: 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.Gene Expression Regulation: 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.Brachiocephalic Trunk: 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.Kinetics: The rate dynamics in chemical or physical systems.Cognition Disorders: Disturbances in mental processes related to learning, thinking, reasoning, and judgment.Plaque, Atherosclerotic: Lesions formed within the walls of ARTERIES.Cholesterol Ester Transfer Proteins: Proteins that bind to and transfer CHOLESTEROL ESTERS between LIPOPROTEINS such as LOW-DENSITY LIPOPROTEINS and HIGH-DENSITY LIPOPROTEINS.Lipase: 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.Dementia: 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.Plaque, Amyloid: Accumulations of extracellularly deposited AMYLOID FIBRILS within tissues.Age of Onset: 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.Lipoproteins, HDL3: 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.Reference Values: 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.Neurofibrillary Tangles: 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.Scavenger Receptors, Class B: A family of scavenger receptors that are predominately localized to CAVEOLAE of the PLASMA MEMBRANE and bind HIGH DENSITY LIPOPROTEINS.Amyloid beta-Protein Precursor: 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.Cell Line: Established cell cultures that have the potential to propagate indefinitely.Kringles: 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.Neuropsychological Tests: 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.Aging: The gradual irreversible changes in structure and function of an organism that occur as a result of the passage of time.Time Factors: Elements of limited time intervals, contributing to particular results or situations.DNA: 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).Particle Size: Relating to the size of solids.Ultracentrifugation: 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)Case-Control Studies: 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.Polymerase Chain Reaction: 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.Sinus of Valsalva: The dilatation of the aortic wall behind each of the cusps of the aortic valve.Tangier Disease: 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.Genetic Variation: Genotypic differences observed among individuals in a population.Hyperlipidemia, Familial Combined: 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.Dementia, Vascular: 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)Recombinant Proteins: Proteins prepared by recombinant DNA technology.Serum Amyloid A Protein: 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.Mutation: 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.Polymorphism, Restriction Fragment Length: 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.Receptors, Scavenger: 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.Immunohistochemistry: Histochemical localization of immunoreactive substances using labeled antibodies as reagents.Macrophages, Peritoneal: Mononuclear phagocytes derived from bone marrow precursors but resident in the peritoneum.Gene Expression: The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.Carrier Proteins: Transport proteins that carry specific substances in the blood or across cell membranes.Biological Markers: 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.Anticholesteremic Agents: Substances used to lower plasma CHOLESTEROL levels.Triolein: (Z)-9-Octadecenoic acid 1,2,3-propanetriyl ester.Blotting, Western: 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.Cysteamine: 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.Lipolysis: 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.High-Density Lipoproteins, Pre-beta: 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.Heparin Lyase: 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.Aryldialkylphosphatase: 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, Agar Gel: Electrophoresis in which agar or agarose gel is used as the diffusion medium.Disease Progression: 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.Phosphatidylcholines: 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.Biological Transport: 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.Hypolipidemic Agents: Substances that lower the levels of certain LIPIDS in the BLOOD. They are used to treat HYPERLIPIDEMIAS.tau Proteins: 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).Chylomicron Remnants: 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.Rabbits: 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.Cytidine Deaminase: An enzyme that catalyzes the deamination of cytidine, forming uridine. EC 3.5.4.5.Glycoproteins: Conjugated protein-carbohydrate compounds including mucins, mucoid, and amyloid glycoproteins.Dyslipidemias: 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.Heparin: 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.Coronary Disease: 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.Abetalipoproteinemia: 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.Protein Structure, Secondary: 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.Amyloid: 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.Antigens, CD36: 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.Circular Dichroism: 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, Mutant Strains: Mice bearing mutant genes which are phenotypically expressed in the animals.Emulsions: 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.RNA Editing: 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).Immunoblotting: 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.Heterozygote Detection: Identification of genetic carriers for a given trait.Protein Conformation: 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).Transfection: 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.Mild Cognitive Impairment: 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 Factors: 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.Receptors, Immunologic: 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.Binding, Competitive: 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.Carotid Arteries: 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.Vascular Cell Adhesion Molecule-1: 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)Postprandial Period: The time frame after a meal or FOOD INTAKE.Pedigree: 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.Sterol O-Acyltransferase: 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.Nephelometry and Turbidimetry: 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.Genetic Testing: 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.Cognition: Intellectual or mental process whereby an organism obtains knowledge.Diet: Regular course of eating and drinking adopted by a person or animal.Analysis of Variance: A statistical technique that isolates and assesses the contributions of categorical independent variables to variation in the mean of a continuous dependent variable.Xanthomatosis: 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, Electron: 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.Enzyme-Linked Immunosorbent Assay: 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.Lecithin Acyltransferase Deficiency: 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.Cohort Studies: 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.Sex Factors: 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.Astrocytes: 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.Polymorphism, Single Nucleotide: A single nucleotide variation in a genetic sequence that occurs at appreciable frequency in the population.Fasting: Abstaining from all food.Inflammation: 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, Gel: Chromatography on non-ionic gels without regard to the mechanism of solute discrimination.Probucol: 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).Tunica Intima: The innermost layer of an artery or vein, made up of one layer of endothelial cells and supported by an internal elastic lamina.Cell Adhesion Molecules, Neuronal: 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.Aorta, Thoracic: The portion of the descending aorta proceeding from the arch of the aorta and extending to the DIAPHRAGM, eventually connecting to the ABDOMINAL AORTA.Amyloidosis, Familial: Diseases in which there is a familial pattern of AMYLOIDOSIS.Monocytes: 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.Hepatocytes: The main structural component of the LIVER. They are specialized EPITHELIAL CELLS that are organized into interconnected plates called lobules.DNA Primers: 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.Gene Knock-In 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.Sex Characteristics: 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.Binding Sites: The parts of a macromolecule that directly participate in its specific combination with another molecule.Peptides: 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.Promoter Regions, Genetic: 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.

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)

*Albert Hofman

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 ...

*Postoperative cognitive dysfunction

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

*Alzheimer's disease research

"Rosiglitazone increases dendritic spine density and rescues spine loss caused by apolipoprotein E4 in primary cortical neurons ... apolipoprotein E, and β-synuclein in skeletal muscle. ... active immunization markedly reduces intracellular Aβ deposits and ...

*PON2

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

*Angiotensin-converting enzyme

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 ...

*Donepezil

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

*Japanese Americans

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) ...

*Genetic heterogeneity

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

*Age-related mobility disability

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

*Apolipoprotein E

"Apolipoprotein (apo) E4 enhances HIV-1 cell entry in vitro, and the APOE epsilon4/epsilon4 genotype accelerates HIV disease ... Apolipoprotein E is a fat-binding protein (apolipoprotein) that is part of the chylomicron and Intermediate-density lipoprotein ... The gene, APOE, is mapped to chromosome 19 in a cluster with apolipoprotein C1 (APOC-I) and the apolipoprotein C2. The APOE ... "Genetic studies of human apolipoproteins. X. The effect of the apolipoprotein E polymorphism on quantitative levels of ...

*Monoclonal antibody therapy

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, ...

*Nutritional genomics

Individuals with the E4 allele in the apolipoprotein E gene show higher low-density lipoprotein-cholesterol (bad cholesterol) ... One single nucleotide polymorphism (-75 G/A) in the apolipoprotein A1 gene in women is associated with an increase in High ... Genetic variations in genes encoding for apolipoproteins, some enzymes and hormones can alter individual sensitivity to ...

*Lothian birth-cohort studies

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 ...

*Reelin

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 (Aug 2003). "Differential binding of ligands to the apolipoprotein E receptor 2 ... Herz J, Beffert U (Oct 2000). "Apolipoprotein E receptors: linking brain development and Alzheimer's disease". Nature Reviews. ...

*Biochemistry of Alzheimer's disease

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 ...

*APOA5

"Hyperlipidemia in patients with apolipoprotein E 2/2 phenotype: apolipoprotein A5 S19W mutation as a cofactor". Clinical ... 107741) three allelic (E2, E3, and E4) polymorphism, in the modulation of plasma lipids. In these cases, the interaction ... Apolipoprotein A-V is a protein that in humans is encoded by the APOA5 gene on chromosome 11. It is significantly expressed in ... Yin YW, Sun QQ, Wang PJ, Qiao L, Hu AM, Liu HL, Wang Q, Hou ZZ (2014-01-01). "Genetic polymorphism of apolipoprotein A5 gene ...

*Alpha-synuclein

498 (7453): E4-6; discussion E6-7. doi:10.1038/nature12125. PMID 23765500. Theillet FX, Binolfi A, Bekei B, Martorana A, Rose ... Alpha-synuclein has also been shown to form lipid disc-like particles similar to apolipoproteins. Studies have also suggested a ... This sequence has a structural alpha helix propensity similar to apolipoproteins-binding domains Residues 61-95: A central ... "Membrane curvature induction and tubulation are common features of synucleins and apolipoproteins". The Journal of Biological ...

*List of MeSH codes (D12.776)

File "2006 MeSH Trees".) MeSH D12.776 - proteins MeSH D12.776.070.400.200.100 - apolipoprotein A1 MeSH D12.776.070.400.200.150 ... adenovirus e4 proteins MeSH D12.776.964.700.750.320 - fusion proteins, gag-onc MeSH D12.776.964.700.750.320.700 - oncogene ... apolipoprotein A2 MeSH D12.776.167.200.067.249 - cdc2 protein kinase MeSH D12.776.167.200.067.500 - cdc28 protein kinase, s ... adenovirus e4 proteins MeSH D12.776.624.664.520.090 - antigens, polyomavirus transforming MeSH D12.776.624.664.520.420 - ...
By 2050, individuals over the age of 60 years are likely to make up about 30% of the population in developed countries.1 The number of people with cognitive impairment is rising in the same way and the next 30 years will see an anticipated threefold increase in Alzheimers disease (AD) sufferers in the US alone.2 These changes are likely to put healthcare budgets under significant strain, especially with regard to the provision of nursing care.3 Half of all patients diagnosed will need help with personal care, and one third will eventually be institutionalised.4,5. Intensive research into the pathophysiology of dementia has failed to identify disease modifying therapeutic agents; however, greater understanding of the components of dementia that finally necessitate admission to residential or nursing home care is also very necessary. Older dementia sufferers living alone, or those with greater functional disability seem more at risk.6,7 Carer provision and coping skills are also important.8-10 ...
Results from two small studies, involving a total of only 174 cases, have suggested that the increased risk of coronary heart disease conferred by cigarette smoking is substantially affected by genotype at the apolipoprotein E (APOE) epsilon2/epsilon3/epsilon4 polymorphism. We have established APOE genotypes in 4484 patients with acute myocardial infarction diagnosed before the age of 55 years for male and 65 years for female patients, and in 5757 controls with no history of cardiovascular disease. On average, the hazard ratio for myocardial infarction was 1.17 (95% CI 1.09-1.25; p|0.00001) per stepwise change from epsilon3/2 to epsilon3/3 to epsilon3/4 genotype. Among individuals in this study with known cigarette smoking status, the hazard ratio for myocardial infarction in smokers versus non-smokers was 4.6 (4.2-5.1). There was, however, no significant difference between the smoker/non-smoker hazard ratios for those with different APOE genotypes (chi2(2)=0.69; p=0.7). When differences in risk between
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An excel sheet containing data for the 2 APOE SNPs (rs429358 and rs7412), translation rules for the SNPs, failures by individual, failures by rs number, and genotyping errors (the last 3 only if applicable). It is very important to note that these results are only to be used for research purposes. This test is not approved for clinical use and therefore the data cannot be returned to subjects. ...
A well-known result, due to Ostrowski, states that if $\Vert P-Q \Vert_2< \varepsilon$, then the roots $(x_j)$ of $P$ and $(y_j)$ of $Q$ satisfy $,x_j -y_j,\le C n \varepsilon^{1/n}$, where $n$ is the degree of $P$ and $Q$. Though there are cases where this estimate is sharp, it can still be made more precise in general, in two ways: first by using Bombieris norm instead of the classical $l_1$ or $l_2$ norms, and second by taking into account the multiplicity of each root. For instance, if $x$ is a simple root of $P$, we show that $,x-y,< C \varepsilon$ instead of $\varepsilon^{1/n}$. The proof uses the properties of Bombieris scalar product and Walsh Contraction Principle ...
Despite apolipoprotein Es important role in cholesterol transport and metabolism in the brain as well as its influence on Alzheimers disease, the impact of the human APOE genotype on cholesterol metabolism in brain has not been fully examined. This study was carried out to investigate APOE genotype effects on oxysterols measured. In this study the measurement of cholesterol and several oxysterols in the brains of human APOE ε2, ε3 and ε4 knock-in mice at 8 weeks and 1 year of age using gas chromatography mass spectrometry (GC-MS) demonstrated no APOE genotype or age effect on total brain cholesterol and the oxysterol 24-hydroxycholesterol. The level of 27-hydroxycholesterol was elevated in 1 year old animals for all APOE genotypes. Interestingly, lathosterol an indicator of cholesterol synthesis was significantly reduced in the 1 year old animals for all APOE genotypes. APOE ε4 expressing mice exhibited statistically lower levels of lathosterol compared to APOE ε2 in both the young and ...
OBJECTIVE:To investigate the association between the apolipoprotein E (APOE) genotypes and dementia in patients with stroke, defined as either vascular dementia (VaD) or Alzheimer disease with cerebrovascular disease (AD with CVD). DESIGN AND SETTING:Population-based, case-control study from Rotterdam, the Netherlands, and New York City. PARTICIPANTS:A total of 187 patients with dementia and stroke were compared with 507 controls similar in age and ethnic group. MAIN OUTCOME MEASURES:The APOE allele frequencies in patients and controls; the odds ratio of dementia with stroke, VaD, and AD with CVD, adjusted for age, sex, residency, and education; and the percent attributable risk related to the APOE epsilon4 allele. RESULTS:Overall, patients with dementia and stroke had a higher APOE epsilon4 allele frequency than controls. Compared with APOE epsilon3 homozygote individuals, APOE epsilon4 homozygotes had a 7-fold increased risk of dementia with stroke (OR=6.9; 95% CI, 1.6-29.4), while APOE epsilon4
Human apolipoprotein E4 targeted replacement mice show increased prevalence of intracerebral hemorrhage associated with vascular amyloid deposition.
Strong evidence of linkage to late-onset Alzheimer disease (LOAD) has been observed on chromosome 10, which implicates a wide region and at least one disease-susceptibility locus. Although significant associations with several biological candidate genes on chromosome 10 have been reported, these findings have not been consistently replicated, and they remain controversial. We performed a chromosome 10-specific association study with 1,412 gene-based single-nucleotide polymorphisms (SNPs), to identify susceptibility genes for developing LOAD. The scan included SNPs in 677 of 1,270 known or predicted genes; each gene contained one or more markers, about half (48%) of which represented putative functional mutations. In general, the initial testing was performed in a white case-control sample from the St. Louis area, with 419 LOAD cases and 377 age-matched controls. Markers that showed significant association in the exploratory analysis were followed up in several other white case-control sample sets to
Background: Apolipoprotein E4 (ApoE4) is the major genetic risk factor of Alzheimer’s disease (AD). ApoE4 carriers have cerebral hypometabolism which is thought as a harbinger of AD. Our previous studies indicated ketones improved mitochondria energy metabolism via sirtuin 3 (Sirt3). However, it is unclear whether ketones upregulate Sirt3 and improve ApoE4-related learning and memory deficits.Results: Ketones improved learning and memory abilities of ApoE4 mice but not ApoE3 mice. Sirt3, synaptic proteins, the NAD+/ NADH ratio, and ATP production were significantly increased in the hippocampus and the cortex from ketone treatment.Methods: Human ApoE3 and ApoE4 transgenic mice (9-month-old) were treated with either ketones or normal saline by daily subcutaneous injections for 3 months (ketones, beta-hydroxybutyrate (BHB): 600 mg/kg/day; acetoacetate (ACA): 150 mg/kg/day). Learning and memory ability of these mice were assessed. Sirt3 protein, synaptic proteins (PSD95, Synaptophysin),
Sporadic, late-onset Alzheimers disease has no known cause and shows no obvious inheritance pattern. However, in some families, clusters of cases are seen. Although a specific gene has not been identified as the cause of late-onset Alzheimers, genetic factors do appear to play a role in the development of this form.. Two risk factor genes have been linked to Alzheimers diseases so far. Researchers have identified an increased risk of developing late-onset Alzheimers related to the apolipoprotein E (APOE) gene found on chromosome 19. The APOE gene comes in several different forms, but three occur most frequently: APOE e2, APOE e3, and APOE e4. People inherit one APOE from each parent. Having the e4 form is a risk factor for Alzheimers disease, but it does not mean that Alzheimers disease will necessarily develop. The e3 form is the most common form found in the general population and may play a neutral role in AD. The rarer e2 form appears to be associated with a lower risk of AD.. The ...
...The apolipoprotein E gene ε4 allele is considered a negative fact......,A,non-invasive,,rapid,screening,method,for,Alzheimers,disease,biological,biology news articles,biology news today,latest biology news,current biology news,biology newsletters
January 15, 2006. In a scientific paper published today a team of scientists from deCODE genetics (Nasdaq:DCGN) and colleagues report the discovery of a variant in a gene on chromosome 10 that represents the most significant genetic risk factor for type 2 diabetes (T2D) found to date. More than one third of individuals in the populations studied carry one copy of the at-risk variant and are at an approximately 45% increased risk of the disease compared to controls; 7% carry two copies and are at a 141% greater risk. The original finding was made in Iceland and was subsequently confirmed in studies in Denmark and the United States. The paper is published today in the online edition of Nature Genetics at www.nature.com/ng, and will appear in the journals February print edition.. "This is a milestone in human genetics. A common gene variant conferring elevated risk of T2D has been earnestly sought by the genetics community for many years. We have found such a variant, which we estimate accounts ...
Authors: Blautzik, Janusch , Kotz, Sebastian , Brendel, Matthias , Sauerbeck, Julia , Vettermann, Franziska , Winter, Yaroslav , Bartenstein, Peter , Ishii, Kazunari , Rominger, Axel Article Type: Research Article Abstract: Body weight loss in late-life is known to occur at a very early stage of Alzheimers disease (AD). Apolipoprotein E4 (ApoE4) represents a major genetic risk factor for AD and is linked to an increased cortical amyloid-β (Aβ) accumulation. Since the relationship between body weight, ApoE4, and AD pathology is poorly investigated, we aimed to evaluate whether ApoE4 allelic status modifies the association of body mass index (BMI) with markers of AD pathology. A total of 368 Aβ-positive cognitively healthy or mild cognitive impaired subjects had undergone [18 F]-AV45-PET, [18 F]-FDG-PET, and T1w-MRI examinations. Composite cortical [18 F]-AV45 uptake and …[18 F]-FDG uptake in posterior cingulate cortex were calculated as surrogates of cortical Aβ load and glucose ...
Lipnicki DM; Crawford JD; Dutta R; Thalamuthu A; Kochan NA; Andrews G; Fernanda Lima-Costa M; Castro-Costa E; Brayne C; Matthews FE, 2017, Age-related cognitive decline and associations with sex, education and apolipoprotein E genotype across ethnocultural groups and geographic regions: a collaborative cohort study, PLOS ONE, vol. 12, http://dx.doi.org/10.1371/journal.pmed.1002261. Opel N; Redlich R; Kaehler C; Grotegerd D; Dohm K; Heindel W; Kugel H; Thalamuthu A; Koutsouleris N; Arolt V, 2017, Prefrontal gray matter volume mediates genetic risks for obesity, Molecular Psychiatry, vol. 22, pp. 703 - 710, http://dx.doi.org/10.1038/mp.2017.51. Lipnicki DM; Crawford JD; Dutta R; Thalamuthu A; Kochan NA; Andrews G; Lima-Costa MF; Castro-Costa E; Brayne C; Matthews FE, 2017, Age-related cognitive decline and associations with sex, education and apolipoprotein E genotype across ethnocultural groups and geographic regions: a collaborative cohort study, PLoS Medicine, vol. 14, ...
Background Epilepsy is associated with precocious development of Alzheimer-type neuropathological changes, including appearance of senile plaques, neuronal loss and glial activation. As inheritance of ...
This SNP, located in the fourth exon of the ApoE gene, affects the amino acid at position 130 of the resulting protein. The more common rs429358 allele is (T). If the allele is (C) and the same chromosome also harbors the rs7412(C) allele, the combination is known as an APOE-ε4 allele. The APOE-ε4 allele has a strong influence on the risk of Alzheimers disease. Many studies have estimated the level of risk, and it varies depending on age, sex, ethnicity, and other factors. One meta-analysis estimated the odds ratios for homozygous rs429358(C;C) individuals compared to the more common ApoE3/ApoE3 homozygotes to be 12x for late-onset Alzheimers and 61x for early-onset disease. [PMID 10325447] Meta-analyses have also supported the association between the APOE-ε4 allele and somewhat increased risk for heart disease, with an odds ratio of 1.42 (CI: 1.26 - 1.61).[15488874?dopt=Abstract PMID 15488874] Note: Although ApoE status is technically defined by these two SNPs, rs429358 and rs7412, a SNP ...
A recent article in this month s Archives of General Psychiatry underscores all this hoopla about the Apo E4 alleles. Apolipoprotein E Genotype and Age-Related Mylein Breakdown in Healthy Individuals by George Bartzokis M.D. et al. These authors discuss that In addition to genotype-phenotype associations with vascular disease, the alleles and isoforms of Apo E4 have been related to dementias, most commonly Alzheimer s disease. Apolipoprotein E (APOE) genotype is the most influential Alzheimer disease (AD) risk factor after advanced age. The APOE4 alleles decrease and the APOE2 alleles increase age at onset of AD. Human and nonhuman primate data suggest that in midlife, the structural integrity of myelin sheaths begins breaking down, with an accelerating age-related trajectory most evident in the brains later-myelinating association regions. This may result in a progressive "disconnection" of widely distributed neural networks that may underlie the age risk factor for AD. The authors of this ...
Sept. 25, 2013 - Researchers have identified and validated two rare gene mutations that appear to cause the common form of Alzheimers disease (AD) that strikes after the age of 60. The two mutations occur in a gene called ADAM10 coding for an enzyme involved in processing the amyloid precursor protein which now becomes the second pathologically-confirmed gene for late-onset AD and the fifth AD gene overall.
Alleles of the apolipoprotein E (ApoE) gene are known to modulate the genetic risk for developing late-onset Alzheimers disease (AD) and have been associated with hippocampal volume differences in AD. However, the effect of these alleles on hippocam
Buy anti-APOE antibody, anti-Mouse Apolipoprotein E (Apo E) Polyclonal Antibody-P02649.1 (MBS315478) product datasheet at MyBioSource, Primary Antibodies. Application: DD, IEP, RID, Western Blot
Effective immediately, SpectraCell Laboratories now offers apolipoprotein E genotyping. This test determines a persons genetic risk for heart disease associated with the commonly
Daw EW, Payami H, Nemens EJ, Nochlin D, Bird TD, Schellenberg GD, Wijsman EM. The number of trait loci in late-onset Alzheimer disease ...
Blood donors of the Madrid area show a 6% frequency of apolipoprotein E genotype carrying allele epsilon 4. This frequency is smaller than other populations of Caucasian origin. This proportion decreases to 4% in a selected sample of healthy individuals of ages | 60 years. The frequency (34%) of the allele epsilon 4 was significantly increased in patients of late onset Alzheimers disease, similarly to other populations. An earlier age of onset of the dementia is observed in the patients of late-onset Alzheimers disease carrying the allele epsilon 4. No increased frequency in allele epsilon 4 frequency was found in patients of early-onset Alzheimers disease. Patients of Parkinsons disease do not show any differences in the frequency of the alleles of apolipoprotein E when compared with healthy individuals.
Effect of Dietary Fat on LDL Size Influenced by Apolipoprotein E Genotype in Healthy Subjects - posted in Lifestyle: Any thoughts? I read this laymans article here which explains how smaller LDL particle size is a better predictor for increased risk of heart disease, and how high carbohydrate diets decrease the size of LDL particles.The paper below claims the opposite if you are ApoE3/4. Im ApoE3/4, and Ive discussed this topic on longecity before, so I guess Ill contin...
Meckes, C., Moyna, N., Tsongalis, G., Miles, M. (2001). Apolipoprotein E Genotype Does Not Affect the Changes in Serum Lipids with Exercise Training. Circulation, 104(17), 343-343 ...
The human APOE gene, which codes for apolipoprotein E (apoE), has three major polymorphic alleles: ε2, ε3, and ε4 that give rise to amino acid substitutions. APOE-ε4 is a strong risk factor of sporadic Alzheimers disease (AD) but the reason why is still unknown despite intense research for more than 20 years. The aim of the study was to investigate if the concentrations of total apoE and the specific apoE isoforms in cerebrospinal fluid (CSF) differ between various neurodegenerative diseases and control individuals, as well as among the APOE genotypes. Quantification of total apoE and specific apoE isoforms (E2, E3, and E4) in CSF was performed using high-resolution parallel reaction monitoring mass spectrometry. In total, 1820 individuals were involved in the study including clinically diagnosed AD patients (n = 228), cognitively unimpaired (CU) patients (n = 896), and patients with other neurodegenerative disorders (n = 696). Follow-up data was available for 100 individuals, assessed at two time
The APOE e4 allele polymorphism is associated with the increased risk of behavioral and psychological signs and symptoms of dementia. Treatment strategies based on APOE genotypes are being developed. In this study, we aimed to assess the frequencies of APOE4 alleles in patients with Alzheimers disease (AD) and vascular dementia (VaD) in different ethnic and geographic groups, and compare them with our results. Method: We determined APOE polymorphisms in patients with VaD, AD, and in controls. For comparison, the literature was searched systematically. Out of 80 papers, 42 papers were assessed for APOE genotype and allele frequencies from several regions of America, Asia and Europe. Results: There were marked variations in the APOE allele and genotype frequencies in all groups. The strength of association between AD and APOE e4 allele carrying was found significant [OR:2.905 (95%CI: 1.237-6.823)]. APOE e4 allele frequencies (%) showed gradual increase from controls to the AD patients (Control: ...
In this study, we examined Abca1 gene dose effect on the phenotype of APP transgenic mice expressing human ApoE3 or ApoE4 isoforms. Surprisingly, our results demonstrate that the lack of one copy of Abca1 significantly aggravates memory deficits and amyloid pathology in APP/E4 but not in APP/E3 mice. An important finding of the study was that Aβ clearance from the brain was decreased by Abca1 deficiency in APP/E4/Abca1−/+ but not in APP/E3/Abca1−/+ mice. In contrast, Abca1 deficiency did not affect cognition, amyloid phenotype, and Aβ clearance in APP mice expressing ApoE3. Interestingly, the correlation between plasma HDL and brain amyloid load (Fig. 7) suggests that there may be a causative connection between peripheral lipoproteins and Aβ load in the CNS.. Previous studies demonstrated that ABCA1 affects amyloid deposition and memory deficits in experimental animals (Hirsch-Reinshagen et al., 2005; Koldamova et al., 2005b; Wahrle et al., 2005; Lefterov et al., 2009). Furthermore, ...
BACKGROUND: Compared to the epsilon 2 or epsilon 3 alleles, the epsilon 4 allele of apolipoprotein E (ApoE4) is associated with twice the prevalence of late-onset Alzheimers disease (AD). Epidemiological studies show that risk of AD varies inversely with consumption of omega-3 fatty acids from fish and seafood. Despite apparently lower fish intake in AD, pooled analysis of the literature shows that plasma and brain docosahexaenoic acid (DHA) is actually the same in AD as in healthy age-matched controls. Fish oil trials in AD are also not convincing. We recently shown that ApoE4 carriers have 41% higher fasting plasma EPA and DHA compared to non-carriers, but the plasma EPA and DHA response to fish oil in ApoE4 carriers was half that seen in non-carriers.. HYPOTHESES: (i) Carriers of ApoE4 have altered metabolism of carbon-13 (13C)-DHA as well as EPA and DHA provided in a dietary supplement. (ii) A dietary supplement of EPA+DHA will improve cognitive performance but only in non-carriers of ...
Several studies have reported evidence for linkage of late-onset Alzheimers disease (LOAD) to chromosome 9. Recently, an intronic polymorphism affecting alternative splicing of exon 8 of ubiquilin 1 (UBQLN1) was reported to be associated with LOAD. We attempted to replicate this observation by genotyping this polymorphism, rs12344615 (also known as UBQ-8i), in a large sample of 1,544 LOAD cases and 1,642 nondemented controls. We did not find any evidence that this single nucleotide polymorphism, or any of six others tested in UBQLN1, increases risk for LOAD.
FITC偶联Apolipoprotein E 抗体(ab27613)可与人样本反应并经ICC/IF实验严格验证,实验条件参看说明书。Abcam对所有产品均提供质保服务和专属技术支持,中国75%以上现货。
The PREVENT Research Programme has established a cohort of individuals to explore differences in the brain and cognitive function in healthy people in mid-life (aged 40-59). People are grouped into high, mid and low risk based on their family history and APOE status (a well-known risk gene for Alzheimers disease). Participants are assessed on biological indicators including markers in blood, saliva, urine and spinal fluid as well as direct imaging of the brains structure and function. Changes in all of these markers will be monitored at 2 years to work out if risks that predict these changes. One of the main aims of the study is to identify the earliest signs of changes in the brain whilst people are still in good health ...
Published on 10/1/2017. Neu SC, Pa J, Kukull W, Beekly D, Kuzma A, Gangadharan P, Wang LS, Romero K, Arneric SP, Redolfi A, Orlandi D, Frisoni GB, Au R, Devine S, Auerbach S, Espinosa A, Boada M, Ruiz A, Johnson SC, Koscik R, Wang JJ, Hsu WC, Chen YL, Toga AW. Apolipoprotein E Genotype and Sex Risk Factors for Alzheimer Disease: A Meta-analysis. JAMA Neurol. 2017 Oct 01; 74(10):1178-1189. PMID: 28846757.. Read at: PubMed ...
Common variants of the ApoE gene are strongly associated with the risk of developing late-onset Alzheimers disease, but the genes role in the disease has been unclear. Now, researchers funded by the National Institutes ...
Amino Acid SequenceMHHHHHHKVE QAVETEPEPE LRQQTEWQSG QRWELALGRF WDYLRWVQTL SEQVQEELLS SQVTQELRAL MDETMKELKA YKSELEEQLT PVAEETRARL SKELQAAQAR LGADMEDVRG RLVQYRGEVQ AMLGQSTEEL RVRLASHLRK LRKRLLRDAD DLQKRLAVYQ AGAREGAERG LSAIRERLGP LVEQGRVRAA TVGSLAGQPL QERAQAWGER LRARMEEMGS RTRDRLDEVK EQVAEVRAKL EEQAQQIRLQ AEAFQARLKS WFEPLVEDMQ RQWAGLVEKV QAAVGTSAAP VPSDNH.DescriptionApolipoprotein E4 Human Recombinant produced in E.coli is a single, non-glycosylated polypeptide chain containing a total of 306 amino acids including a His Tag at N-terminus and having a molecular mass of 35.2kDa. The Accession # is P02649 VAR_000652.FormulationLyophilized from a sterile (0.2µm) filtered aqueous solution containing 10mM sodium phosphate, pH 7.5.Physical AppearanceSterile Filtered White lyophilized (freeze-dried) powder.PurityGreater than 90% as determined by SDS-PAGE.SolubilityIt is recommended to reconstitute the lyophilized APOE4 in sterile 18M-cm H2O not less than 100µg/ml, which can then be further diluted to other
Mouse Monoclonal Anti-Apolipoprotein E/ApoE Antibody (WUE-4) [DyLight 650]. Validated: WB, ELISA, Flow, ICC/IF, IHC. Tested Reactivity: Human, Mouse. 100% Guaranteed.
Researchers have identified a protein called apolipoprotein E (ApoE) which affects your chances of developing Alzheimers disease. There are three forms of ApoE: ApoE2, ApoE3 and ApoE4.. Having one or two copies of ApoE4 increases someones chance of developing the disease, but does not make it certain. Some researchers think that ApoE4 does not affect whether a person will get the disease but, rather, when they get it, causing people with ApoE4 to develop the disease before people with ApoE2.. ...
Rebeck GW, Reiter JS, Strickland DK, Hyman BT. Apolipoprotein E in sporadic Alzheimers disease: allelic variation and receptor interactions ...
rs911541 increases susceptibility to late-onset Alzheimers disease 1.58 times for heterozygotes (A;G) and 1.48 times for homozygotes (G;G,) based on a case-control study of ~1,500 Japanese patients and an equal number of matched controls. [PMID 16740596] ...
Health, ...MONDAY March 7 (HealthDay News) -- Genetics may predispose some peopl...The culprit is a specific abnormality of the apolipoprotein E gene. Th...Now a team of researchers led by Brian K. Lee of Drexel University in...The observation is reported in the March issue of the Archives of ...,Mix,of,Genetics,and,Stress,Can,Impair,Mental,Abilities,medicine,medical news today,latest medical news,medical newsletters,current medical news,latest medicine news
I know that [itex] \varepsilon \eta = r^2 - r^2 \cos^2(\phi) = r^2 \sin^2(\phi) = \rho^2[/itex] ([itex]\rho[/itex] the diagonal in the x-y plane) implies [itex] x = \rho \cos(\phi) = \sqrt{ \varepsilon \eta } \cos (\phi) [/itex] mathematically, but looking at the picture I have no physical or geometrical intuition as to why [itex] \rho = \sqrt{ \varepsilon \eta } [/itex ...
ApoE belongs to a group of proteins that bind reversibly with lipoprotein and play an important role in lipid metabolism.  In addition
I understand, to some extent, Tates thesis. Could somebody explain perhaps what are the epsilon factors in Beilinsons works, such as "$\epsilon$-factors for Gauss-Manin determinants", or "Topological $\epsilon$-factors"? How do they mimic the usual ones? Are they some categorification (since the usual one is a number, and those ones seem to be lines)? Is there some intuition for the construction in "Topological $\epsilon$-factors" or, perhaps more importantly, for the need for construction?. Edit: I also know vaguely that epsilon-factors should be also associated to Galois-side-data, and the ones in Beilinsons works mimic those, and not the "automorphic" ones from Tates thesis.. Thank you, Sasha. ...
where ,math,\varepsilon_\infty,/math, (which [[Meep FAQ,must be positive]]) is the instantaneous dielectric function (the infinite-frequency response) and P is the remaining frequency-dependent polarization density in the material. P, in turn, has its own time-evolution equation, and the exact form of this equation determines the frequency-dependence ε(ω). [Note that Meeps definition of ω uses a sign convention ,math,\exp(-i\omega t),/math, for the time dependence-ε formulas in engineering papers that use the opposite sign convention for ω will have a sign flip in all the imaginary terms below. If you are using parameters from the literature, you should use *positive* values of γ and σ as-is for loss; dont be confused by the difference in ω sign convention and flip the sign of the parameters.] In particular, Meep supports any material dispersion of the form of a sum of harmonic resonances, plus a term from the ...
where ,math,\varepsilon_\infty,/math, (which [[Meep FAQ,must be positive]]) is the instantaneous dielectric function (the infinite-frequency response) and P is the remaining frequency-dependent polarization density in the material. P, in turn, has its own time-evolution equation, and the exact form of this equation determines the frequency-dependence ε(ω). [Note that Meeps definition of ω uses a sign convention ,math,\exp(-i\omega t),/math, for the time dependence-ε formulas in engineering papers that use the opposite sign convention for ω will have a sign flip in all the imaginary terms below. If you are using parameters from the literature, you should use *positive* values of γ and σ as-is for loss; dont be confused by the difference in ω sign convention and flip the sign of the parameters.] In particular, Meep supports any material dispersion of the form of a sum of harmonic resonances, plus a term from the ...
Epsilon dry disconnect coulings are designed to prevent chemical spills & reduce VOC emissions, particularly in the process facility & during transfer. RFQ!
Epsilon dry disconnect coulings are designed to prevent chemical spills & reduce VOC emissions, particularly in the process facility & during transfer. RFQ!
... - J. 47, () Gibelli, A.: Richerche sullazione antifibrinolitica dellacido epsilon-amino-caproico. III. Lazione dellacido epsilon-aminocaproico quale.
TY - JOUR. T1 - Influence of apolipoprotein e ε4 on rates of cognitive and functional decline in mild cognitive impairment. AU - Whitehair, Danielle C.. AU - Sherzai, Abdullah. AU - Emond, Jennifer. AU - Raman, Rema. AU - Aisen, Paul S.. AU - Petersen, Ronald Carl. AU - Fleisher, Adam S.. PY - 2010/9. Y1 - 2010/9. N2 - Background: Apolipoprotein E ε4 (APOE ε4) allele carrier status has been well established as a risk factor for developing Alzheimers disease. However, the specific influence of APOE ε4 allele status on cognitive and functional rates of decline in mild cognitive impairment (MCI) is poorly understood. We examine the prospective association of APOE ε4 allele status on measures of cognitive and functional decline in subjects with amnestic MCI (aMCI). Methods: A total of 516 aMCI participants aged 55-90 years who received placebo or vitamin E from the Alzheimers Disease Cooperative Studys MCI treatment trial were evaluated. During the 36-month study period, neurocognitive and ...
Alzheimers disease (AD) is characterized by progressive cognitive decline and memory loss. It has been hypothesized that environmental factors and gene-environment interactions (GXE) may increase AD risk and accelerate cognitive decline. However, there is currently little direct evidence supporting this hypothesis. 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. Furthermore, the heavy metal lead is a neurotoxicant of major public health importance and is associated with persistent cognitive and behavior deficits in humans. Using transgenic knock-in (KI) mice that express the human ApoE4 allele (ApoE4-KI), I found that adult-only lead exposure is sufficient to impair cognitive behavior and that lead-exposed ApoE4-KI mice develop more severe or exhibit earlier deficits in learning and memory compared to ApoE3-KI ...
Exposure to radiation can lead to deficits in cognitive function, including impairments in hippocampal-dependent learning and memory. However, not all individuals exposed to irradiation develop cognitive impairments, suggesting the involvement of genetic risk factors. Apolipoprotein E (apoE), a protein important for neuronal repair, might influence susceptibility to developing radiation-induced cognitive impairments. Humans express three major apoE isoforms, apoE2, apoE3 and apoE4. Compared to apoE3, apoE4 increases the risk to develop Alzheimers disease while apoE2 decreases this risk. ApoE4 is also associated with cognitive deficits following neurotrauma. Moreover, deficiency of apolipoprotein E (apoE) in mice worsens cognitive impairments following irradiation. There might also be sex differences in the risk for developing radiation-induced cognitive impairments. In both humans and rodents, females are more susceptible to the effects of irradiation on cognition than males. The neur
TY - JOUR. T1 - Gene-behavior interaction of depressive symptoms and the apolipoprotein e ε4 allele on cognitive decline. AU - Rajan, Kumar. AU - Wilson, Robert S.. AU - Skarupski, Kimberly A.. AU - Mendes De Leon, Carlos F.. AU - Evans, Denis A.. PY - 2014/1/1. Y1 - 2014/1/1. N2 - Objective: Depressive symptoms and the apolipoprotein E (APOE) [Latin Small Letter Open ε4 allele are independent risk factors for cognitive decline. However, it is not clear whether the presence of both depressive symptoms and the APOE [Latin Small Letter Open ε4 allele increases cognitive decline. METHODS: A prospective study of a population-based sample of 4150 (70% African American and 63% women) participants 65 years and older who were interviewed at 3-year intervals was conducted. Depressive symptoms were measured using the 10-item version of the Center for Epidemiologic Studies Depression scale, with each item coded as presence or absence of a symptom. The APOE genotype was ascertained by DNA samples ...
Role of apolipoprotein E in neurodegenerative diseases Vo Van Giau,1 Eva Bagyinszky,1 Seong Soo A An,1 SangYun Kim2 1Department of Bionano Technology, Gachon Medical Research Institute, Gachon University, Seongnam, South Korea; 2Department of Neurology, Seoul National University College of Medicine in Seoul National Bundang Hospital, Seoul, South Korea Abstract: Apolipoprotein E (APOE) is a lipid-transport protein abundantly expressed in most neurons in the central nervous system. APOE-dependent alterations of the endocytic pathway can affect different functions. APOE binds to cell-surface receptors to deliver lipids and to the hydrophobic amyloid-β peptide, regulating amyloid-β aggregations and clearances in the brain. Several APOE isoforms with major structural differences were discovered and shown to influence the brain lipid transport, glucose metabolism, neuronal signaling, neuroinflammation, and mitochondrial function. This review will summarize the updated research progress on APOE functions
Wragg, M., Hutton, M., Talbot, C., Busfield, F., Han, S., Lendon, C., ... Goate, A. (1996). Genetic association between intronic polymorphism in presenilin-1 gene and late-onset Alzheimers disease. Lancet, 347(9000), 509 - 512 ...
According to a recent study reported in the Neural Regeneration Research, APOE ε4 plays an important role in augmenting cognitive decline, and APOC1 H2 may act synergistically with APOE ε4 in increasing the risk of cognitive decline in Chinese patients with late-onset Alzheimers disease.
This section examines evidence for neurovascular changes during normal ageing and for neurovascular and/or BBB dysfunction in various neurodegenerative diseases, as well as the possibility that vascular defects can precede neuronal changes.. Age-associated neurovascular changes. Normal ageing diminishes brain circulatory functions, including a detectable decay of CBF in the limbic and association cortices that has been suggested to underlie age-related cognitive changes77. Alterations in the cerebral microvasculature, but not changes in neural activity, have been shown to lead to age-dependent reductions in functional hyperaemia in the visual system in cats78 and in the sensorimotor cortex in pericyte-deficient mice33. Importantly, a recent longitudinal CBF study in neurologically normal individuals revealed that people bearing the apolipoprotein E (APOE) ɛ4allele - the major genetic risk factor for late-onset Alzheimers disease79, 80, 81 - showed greater regional CBF decline in brain regions ...
A brain scanning study using Pittsburgh Compound B, involving 42 healthy individuals (aged 50-80), of whom 14 had mothers who developed Alzheimers, 14 had fathers with Alzheimers, and 14 had no family history of the disease, has found that those with a maternal history had 15% more amyloid-beta plaques than those with a paternal history, and 20% more than those with no family history. The findings add to evidence that having a mother with Alzheimers is a greater risk factor than having a father with Alzheimers. The groups did not differ in age, gender, education, or apolipoprotein E (ApoE) status.. ...
Abstract: This study examined the effects of apolipoprotein E4 (APOE4), the most prevalent genetic risk factor for Alzheimers disease (AD), on proteins involved in mitochondrial dynamics and autophagy, in the hippocampus of targeted replacement mice. Immunohistochemical measurements revealed that the levels of the mitochondrial fusion-mediating protein, MFN1, were higher, whereas those of corresponding fission-regulating protein, DRP-1, were lower in the hippocampus of ApoE4 mice than in the corresponding ApoE3 mice, indicating that APOE4 is associated with increased mitochondrial fusion and decreased fission. A similar ApoE4-driven decrease in DRP-1 was also observed in AD brains. The levels of the mitochondrial proteins COX1 and Tom40, were higher in the ApoE4 mice, which is consistent with the increased fusion. Measurements of the levels of cleaved PINK1 and parkin, which mark and target mitochondria for mitophagic degradation, revealed lower levels of cleaved PINK1, suggesting reduced ...
Mouse Apolipoprotein E SimpleStep ELISA® Kit is a highly sensitive (130 pg/ml), single-wash 90 min immunoassay suitable for Serum, Heparin Plasma, EDTA Plasma, Citrate Plasma samples.
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The National Institutes of Health-funded study was expanded in 1991 to all the SSND provinces in the United States. This longitudinal study accepted anyone 75 and older who was interested in participating and has been following them ever since. As of December 2017, there are three sisters still living who are enrolled in the Nun Study.. In 1991, 1,027 sisters were eligible, and 678 enrolled - an astounding 66 percent participation rate. Yearly evaluations included various memory tests and physical functioning assessments, a one-time blood test for genetic evaluation of apolipoprotein E (a variation of which increases the risk for developing late-onset Alzheimers disease), and brain donation at death.. The Nun Study was incredibly unique at its initiation and has altered research ever since. There are multiple evaluations, some have completed 14 rounds. SSND archives have provided extensive data from sisters early lives. There also was homogeneity in living conditions, health care, and ...
The genetic profile of two large Georgia families with high rates of late-onset Alzheimers disease points to a gene that may cause the disease, researchers say. Genetic variations called single n ...
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Epsilon polymorphism of apolipoprotein E gene and insertion-deletion polymorphism of ACE gene and brain ischemic stroke in children: association pilot-study ...
TY - JOUR. T1 - Avian and murine lr8b and human apolipoprotein E receptor 2. T2 - Differentially spliced products from corresponding genes. AU - Brandes, Christian. AU - Novak, Sabine. AU - Stockinger, Walter. AU - Herz, Joachim. AU - Schneider, Wolfgang J.. AU - Nimpf, Johannes. PY - 1997/6/1. Y1 - 1997/6/1. N2 - Apolipoprotein E-mediated lipid metabolism in the central nervous system plays an important role in cholesterol and phospholipid homeostasis of this organ, which is separated from the circulation by the blood-brain barrier. Moreover, in late-onset familial Alzheimer disease the frequency of the apolipoprotein E4 allele is significantly increased and the apoprotein is localized to extracellular plaques, one of the histological hallmarks of this disease. Recently, two distinct novel members of the low-density lipoprotein (LDL) receptor family, with the potential to bind apolipoprotein E and preferentially expressed in brain, have been characterized from human (D. Kim et al., 1996, J. ...
ANESTHESIA (Bassline) As recorded by Bad Religion (From the 1990 Album AGAINST THE GRAIN) Words and Music by Brett Gurewitz Transcribed by Matt Curry Gtr I (E A D G) - Untitled Intro Q=160 $ 4/4 Gtr I E E E Q E Q E E E Q E Q Q H. ,,-----------------,,---------------,----------, ,,o---------------o,,---------------,----------, ,,o---------------o,,---------------,----------, ,,--6-6-6-6--4-4---,,-6-6-6-6--4-4--,-6--------, E E E E E E E E E E E E E E E E E E E E E E E E E E E E E E E E ,,------------------,-----------------,-----------------,------------------,, ,,o-----------------,-----------------,-----------------,-----------------o,, ,,o-----------------,-6-6-6-6-6-6-6-6-,-8-8-8-8-8-8-8-8-,-6-6-6-6-8-8-6-6-o,, ,,--3-3-3-3-3-3-3-3-,-----------------,-----------------,------------------,, Verse E E E E E E E E E E E E E E E E E E E E E E E E ,,------------------,-----------------,-----------------, ,,o-----------------,-----------------,-----------------, ...
article{3f0ddea8-dd33-4fdd-a777-97a29bef9f47, abstract = {Stroke outcome is determined by a complex interplay, where age and stroke severity are predominant predictors. Studies on hemorrhagic stroke indicate that APOE genotype is a predictor of poststroke outcomes,1,2 but results from studies on ischemic stroke are more conflicting.1,3 There is 1 study suggesting an influence of APOE genotype on age at ischemic stroke onset,4 and sex-specific effects on outcome have been reported.5 Taken together, there is a need for larger studies on APOE and ischemic stroke outcomes with integrated information on age, severity, and sex.,br/,,br/,The 3 common APOE alleles ε2, ε3, and ε4 can be separated by a combination of 2 single nucleotide polymorphisms (SNPs), rs429358 and rs7412. Thus, associations with APOE alleles are not directly captured in a regular genome-wide association study (GWAS), where each SNP is investigated separately. We derived the 3 common APOE alleles and investigated the interplay ...
Previous studies have demonstrated that endogenous mouse apoE is protective against transient focal and global brain ischemia and traumatic brain injury.34-36⇓⇓ Although human apoE isoforms markedly delay the appearance of Aβ deposition in APPV717F transgenic mice,14 apoE ultimately facilitates the neuritic degeneration associated with amyloid deposits and with conversion of Aβ into mature fibrillar amyloid,15 which is thought to be neurotoxic.37 In the present study, we show that neuronal overexpression of human APP751 at the level detected in early AD and Downs syndrome28 dramatically increases the susceptibility to ischemic brain damage in the absence of apoE. Moreover, expression of human apoE3 or apoE4 in astrocytes significantly reduces the neuronal vulnerability to ischemia in APP751 transgenic mice. These results indicate that even though apoE may be a contributory factor in Aβ-induced toxicity in AD, it has a beneficial role against APP751-induced ischemic vulnerability. ...
Apolipoprotein E (apoE) is critical in the modulation of cholesterol and phospholipid transport between cells of different types. Human apoE is a polymorphic protein with three common alleles, APO epsilon 2, APO epsilon 3, and APO epsilon 4. ApoE4 is associated with sporadic and late-onset familial Alzheimer disease (AD). Gene dose was shown to have an effect on risk of developing AD, age of onset, accumulation of senile plaques in the brain, and reduction of choline acetyltransferase (ChAT) activity in the hippocampus of AD subjects. To characterize the possible impact of the apoE4 allele on cholinergic markers in AD, we examined the effect of apoE4 allele copy number on pre- and postsynaptic markers of cholinergic activity. ApoE4 allele copy number showed an inverse relationship with residual brain ChAT activity and nicotinic receptor binding sites in both the hippocampal formation and the temporal cortex of AD subjects. AD cases lacking the apoE4 allele showed ChAT activities close or within ...
The APOE gene has other symbols as "AD2", "LPG", "APO-E", and "LDLCQ5". It is located at 19q13.2. The APOE gene has important roles in cardiovascular diseases including myocardial infarction, ischemic stroke, and coronary heart disease (Kathiresan et al. 2008).. The APOE gene is involved in immune responses to lipid antigens (Van den Elzen et al. 2005). It has also been connected with Alzheimers disease (Lambert et al. 2002), cognitive impairment (Caselli et al. 2009), multiple sclerosis (MS) (Enzinger et al. 2003).. In addition, it is associated with neurologic disorders such as epilepsy (Busch et al. 2007) and age-related macular degeneration (ARMD) (Anderson et al. 2001).. References:. Anderson, D. H., Ozaki, S., Nealon, M., Neitz, J., Mullins, R. F., Hageman, G. S., Johnson, L. V. Local cellular sources of apolipoprotein E in the human retina and retinal pigmented epithelium: implications for the process of drusen formation. Am. J. Ophthal. 131: 767-781, 2001.. Busch, R. M., Lineweaver, T. ...
Reduced testosterone levels have been implicated as a potential causative factor in cognitive decline with older age. Men who possess the apolipoprotein E (APOE) 4 allele have an increased risk of developing Alzheimers disease; however, no studies have examined whether the influence of testosterone on cognition in healthy older men may be modulated by this geneticpredisposition. The objective of the study was to investigate the association between serum testosterone concentrations and cognitive performance in healthy older men, taking into account APOE 4 status. This was a cross-sectional study conducted from 2003 to 2004. The study population consisted of community-dwelling males residing in Perth, Western Australia. Healthy men over 55 yr, free of cognitive impairment and dementia (n = 45), were included in the study. Participants had fasting early morning blood samples for testosterone and SHBG and were assessed for mood as well as indices of general cognition, verbal and visual memory, ...
Attempts to find a lone biomarker for Alzheimers disease - whether its in blood, spinal fluid, or the brain - have largely failed. The Texas Alzheimers Research Consortium project conducted a longitudinal case-control study, using stored blood samples to develop an algorithm that separates patients with Alzheimers disease from controls. The biomarker assays looked at hundreds of proteins, including thrombopoietin, TNF-alpha, creatine kinase, and various interleukins. The his team focused on a large array of blood-based proteins, since assay technology has now made it possible to evaluate large amounts of data. Screening for these biomarkers and factoring in age, sex, education, and APOE status led to a sensitivity of 0.94 and a specificity of 0.84, as reported by Sid OBryant, PhD, of Texas Tech University, in Lubbock, Texas, and colleagues in the Archives of Neurology. They also saw that many of the proteins with the highest importance were inflammatory in nature, which suggests that the ...
For a conventional 2D elastic solid, the mean stress ,math,,\sigma,=\frac{\sigma _1+\sigma _2}{2},/math,, and strain ,math,,\varepsilon ,=\frac{\varepsilon _1+\varepsilon _2}{2},/math, ( Where the subscripts 1,2 denote the two principal directions), are related by ,math,\ \ \ \ \ \ \ \ \ \ \ ,\varepsilon,=\frac{1-\nu}{E},\sigma,,/math, If we replace the stress by a thickness-averaged isotropic tension ,math,\tau \equiv ,\sigma,d,/math,, then this relation reads ,math,\ \ \ \ \ \ \ \ \ \ \ ,\varepsilon ,=\frac{1-\nu}{Ed}\tau,/math, ,math,\ \ \ \ \ \ \ \ \ \ \Longrightarrow \frac{1-\nu}{Ed}=\frac{d,\varepsilon,}{d\tau}=\frac{1}{A}\frac{dA}{d\tau}=\frac{1}{A_1+A_s}\frac{d(A_1+A_s)}{d\tau},/math, ,math,A_1,/math,: the area of the system covered by liquid. ,math,A_s,/math,: the area covered by solid particles. ,math,A=A_1+A_s,/math,: the total area of the system. ,math,\Longrightarrow E\propto \frac{1-\nu}{1-\phi}\frac{\gamma}{d},/math, (Here ,math,A_s \ \ is\ \ constant,\ \ ...
For a conventional 2D elastic solid, the mean stress ,math,,\sigma,=\frac{\sigma _1+\sigma _2}{2},/math,, and strain ,math,,\varepsilon ,=\frac{\varepsilon _1+\varepsilon _2}{2},/math, ( Where the subscripts 1,2 denote the two principal directions), are related by ,math,\ \ \ \ \ \ \ \ \ \ \ ,\varepsilon,=\frac{1-\nu}{E},\sigma,,/math, If we replace the stress by a thickness-averaged isotropic tension ,math,\tau \equiv ,\sigma,d,/math,, then this relation reads ,math,\ \ \ \ \ \ \ \ \ \ \ ,\varepsilon ,=\frac{1-\nu}{Ed}\tau,/math, ,math,\ \ \ \ \ \ \ \ \ \ \Longrightarrow \frac{1-\nu}{Ed}=\frac{d,\varepsilon,}{d\tau}=\frac{1}{A}\frac{dA}{d\tau}=\frac{1}{A_1+A_s}\frac{d(A_1+A_s)}{d\tau},/math, ,math,A_1,/math,: the area of the system covered by liquid. ,math,A_s,/math,: the area covered by solid particles. ,math,A=A_1+A_s,/math,: the total area of the system. ,math,\Longrightarrow E\propto \frac{1-\nu}{1-\phi}\frac{\gamma}{d},/math, (Here ,math,A_s \ \ is\ \ constant,\ \ ...
Published on: January 6, 2015. by Daniel M. Keller, PhD for MedScape:. Hypertension interacts with genetic risk to increase the burden of amyloid beta (Aβ) in the brain, a new study suggests.. In Alzheimers disease (AD), individuals with the apolipoprotein E (APOE) ε4 gene, indicating higher AD risk, had higher levels of Aβ, researchers report. Even in healthy control patients, the presence of hypertension and APOE ε4-positivity was associated with a greater level of Aβ in the brains of adults older than 70 years.. Despite the strong risk conferred by APOE ε4, age remains the greatest risk factor for AD, suggesting that age-related comorbidities may be important. Among them, "poor vascular health is a significant medical issue in aging populations," Karen Rodrigue, PhD of the Center for Vital Longevity at the University of Texas at Dallas told delegates here at the 7th Clinical Trials on Alzheimers Disease (CTAD).. Previous studies have implicated hypertension in this process. The ...
In an animal model, a novel approach toward correct structural problems in apolipoprotein E 4 protein aims to prevent the misfolding, which triggers proteolysis, and the cascade leading to Alzheimers disease.. A new treatment for Alzheimers disease that focuses on correcting the structure of the apolipoprotein E4 (APOE4) protein has been shown to work in mice and could be ready for testing in humans within two years.. The treatment, tentatively named PY-101, would dissolve the bond that causes two domains of the APOE4 protein to fuse within neurons and cause misfolding, which triggers proteolysis. The breakdown of the protein then produces toxic fragments that disrupt mitochondrial function and promote cell death.. This process, rather than the accumulation of amyloid-beta (Abeta) accounts for the strong correlation between the APOE4 allele and numerous neurological disorders, including Alzheimers disease, according to Robert W. Mahley, MD, PhD, president emeritus of the J. David Gladstone ...
Methods We performed a systematic review and meta-analysis of 14 cross-sectional studies identified in Pubmed from 1996 to 2014 (n=1628). The pooled standard mean difference (SMD) was used to estimate the association between APOE and hippocampal volume and amyloid deposition. Meta-analysis was performed using effect size signed differential mapping using coordinates extracted from clusters with statistically significant difference in cerebral metabolic rate for glucose between APOE ɛ4+ and ɛ4− groups.. ...
We have demonstrated that there is a strong association between polymorphic poly-T variant of TOMM40 and the age of onset of late-onset Alzheimers disease (AD)...
Late-onset Alzheimers Disease most likely occurs from any amount of changes in the brain that occur over a lifetime or it can also be genetic.
Apolipoprotein (apolipoprotein) je bílkovinná složka lipoproteinů. Apolipoproteinů existuje více druhů a jednotlivé typy se vyskytují v konkrétních lipoproteinech. Apolipoproteiny mají více funkcí, jsou strukturálně důležité, pomáhají transportu lipoproteinových částic, a dokonce mohou fungovat jako koenzymy některých enzymů ...
For a two-state system (Figure 12.1)$$\frac{1}{T}=k\left(\frac{d\ln(W)}{dn}\right)_{V,N} \left(\frac{dn}{dU}\right)$$The multiplicity term can be rewritten as $$\ln(W)=\ln\left(\frac{N!}{n!(N-n)!}\right)\approx-n\ln\left(\frac{n}{N}\right)-(N-n)\ln\left(\frac{N-n}{N}\right)$$where the last term used Stirlings approximation $x!\approx (x/e)^x$. The internal energy is given by$$U=n\varepsilon_0\Rightarrow\frac{dn}{dU}=\frac{1}{\varepsilon_0}$$so $T$ can be defined in terms of the fraction of molecules in the ground $(f_{ground}=n/N)$ and excited state $(f_{excited}=1-n/N)$ $$\frac{1}{T}=\frac{k}{\varepsilon_0}\ln\left(\frac{f_{ground}}{f_{excited}}\right) $$At equilibrium these fractions are determined by the Boltzmann distribution$$\frac{f_{ground}}{f_{excited}}=e^{\varepsilon_0/kT},1$$This is the $T$ you measure with a thermometer and this $T$ can never be negative at equilibrium. However, if you create a excited macrostate for which $f_{ground}/f_{excited},1$ then the corresponding variable ...
Interferon-beta (IFN-beta) therapy for multiple sclerosis (MS) is associated with a potential for induction of neutralizing antibodies (NAbs). Because immune reactivity depends on changes in lipoprote
Bathing the mouse brain in the APOE2 form of apolipoprotein E reduced levels of abnormal beta-amyloid protein compared with controls, suggesting that the protein could prevent Alzheimers disease, res
The chemical potential of a species is defined as the change in free energy with respect to the number of molecules of that species, when temperature, volume, and the number of other species are all kept constant:$$\mu_I=\left(\frac{\partial A}{\partial N_I}\right)_{V,T,N_{J\ne I}}$$Lets explore this for the simple four-bead polymer shown in the figure above. In a previous post I derived the expression for the free energy:$$A=N\varepsilon_0 p_{uf}+TNk\left( p_f\ln(p_f)+p_{uf}\ln\left(\frac{p_{uf}}{4}\right) \right)\\A=\varepsilon_0 N_{uf}+Tk\left( N_f\ln\left(\frac{N_{f}}{N_{f}+N_{uf}}\right)+N_{uf}\ln\left(\frac{N_{uf}}{4(N_{f}+N_{uf})}\right)\right)$$Starting from the latter expression finding the chemical potentials for the folded and unfolded macrostates are: $$\mu_{f}=\left(\frac{\partial A}{\partial N_f}\right)_{V,T,N_{uf}}=kT\ln(p_f)$$ $$\mu_{uf}=\left(\frac{\partial A}{\partial N_{uf}}\right)_{V,T,N_{f}}=\varepsilon_0+kT\ln\left(\frac{p_{uf}}{4}\right)$$The free energy is the sum of the ...
APOE (Human) ELISA Kit is an enzyme-linked immunosorbent assay for the quantitative measurement of human APOE2/APOE3/APOE4. (KA4736) - Products - Abnova
The ApoE gene may have a more influential role than first thought; it may amplify the damage done by the tau protein, causing neurodegeneration.
APOE formation and its role in redistribution of lipids to the cells of CNS: the neuropathological effects of the neurotoxic APOE fragments.Notes: ① APOE main
Chlamydia pneumoniae is detectable in the blood vessels of patients suffering from arteriosclerosis. Risk for arteriosclerosis is modulated by the apolipoprotein E (apoE) allele. We assessed the significance of the apoE genotype as a risk factor for vascular C. pneumoniae infection by determining the genotype of 30 coronary heart disease patients with PCR-proven C. pneumoniae infection of coronary artery tissue. The apoE genotype is not distinctly associated with an increased risk for vascular C. pneumoniae infection.. ...
TY - JOUR. T1 - Binding of apolipoprotein E inhibits the oligomer growth of amyloid-β peptide in solution as determined by fluorescence cross-correlation spectroscopy. AU - Ly, Sonny. AU - Altman, Robin. AU - Petrlova, Jitka. AU - Lin, Yu. AU - Hilt, Silvia. AU - Huser, Thomas R. AU - Laurence, Ted A.. AU - Voss, John C. PY - 2013/4/26. Y1 - 2013/4/26. N2 - One of the primary neuropathological hallmarks of Alzheimer disease is the presence of extracellular amyloid plaques resulting from the aggregation of amyloid-β (Aβ) peptides. The intrinsic disorder of the Aβ peptide drives self-association and progressive reordering of the conformation in solution, and this dynamic distribution of Aβ complicates biophysical studies. This property poses a challenge for understanding the interaction of Aβ with apolipoprotein E (apoE). ApoE plays a pivotal role in the aggregation and clearance of Aβ peptides in the brain, and the ε4 allele of APOE is the most significant known genetic modulator of ...
Lower cognitive performance in normal older adult male twins carrying the apolipoprotein E epsilon 4 allele.: The apoE epsilon 4 allele may be associated with d
Despite pleiotropic immunomodulatory effects of apolipoprotein E (apoE) in vitro, its effects on the clinical course of experimental autoimmune encephalomyelitis (EAE) and multiple sclerosis (MS) are still controversial. As sex hormones modify immunomodulatory apoE functions, they may explain contentious findings. This study aimed to investigate sex-specific effects of apoE on disease course of EAE and MS. MOG35-55 induced EAE in female and male apoE-deficient mice was assessed clinically and histopathologically. apoE expression was investigated by qPCR. The association of the MS severity score (MSSS) and APOE rs429358 and rs7412 was assessed across 3237 MS patients using linear regression analyses. EAE disease course was slightly attenuated in male apoE-deficient (apoE −/− ) mice compared to wildtype mice (cumulative median score: apoE −/− = 2 [IQR 0.0-4.5];
A study carried out with a new human stem cell-derived model reveals that the most prevalent genetic risk factor of Alzheimers disease (AD), apolipoprotein E4 (APOE4), impairs the function of human brain immune cells, microglia.
Recent reports have shown that patients with Alzheimers disease have significantly higher frequency of the e4 allele of apolipoprotein E than corresponding controls.*RF 10-13* These studies, however, can be criticised because they have been based on clinical series of patients with Alzheimers disease rather than on population based cohorts. Our study of a random sample of 980 elderly Finnish subjects showed that the presence of the e4 allele is associated strongly with Alzheimers disease. Furthermore, there was a clear gene dose effect of the e4 allele. Our results therefore confirm those in selected patients and extend the findings to randomly selected populations.. We found that the e4 allele frequency was twice as high in patients with Alzheimers disease as in subjects without dementia (0.359 v 0.165). Other studies have reported a higher allele frequency ranging from 0.36 to 0.50.. The prevalence of Alzheimers disease in this study was 4.7%, and it was the commonest type of dementia. ...
1OR3: Conformational flexibility in the apolipoprotein E amino-terminal domain structure determined from three new crystal forms: implications for lipid binding.
10 late-onset Alzheimers disease genes were tested for association with human aging in the dataset (1385 samples with documented age at death, age range: 58-108 years; mean age at death: 80.2 years) using the most significant SNPs found in the previous studies. A set of 41 tentative SNPs span the genome were identified in this study ...
Consider the linear regression model, $$ y_i=f_i(\boldsymbol{x},\boldsymbol{\beta})+\varepsilon_i, $$ where $y_i$ is the response or the dependent variable at the $i$th case, $i=1,\cdots, N$ and the predictor or the independent variable is the $\boldsymbol{x}$ term defined in the mean function $f_i(\boldsymbol{x},\boldsymbol{\beta})$. For simplicity, consider the following simple linear regression (SLR) model, $$ y_i=\beta_0+\beta_1x_i+\varepsilon_i. $$ To obtain the (best) estimate of $\beta_0$ and $\beta_1$, we solve for the least residual sum of squares (RSS) given by, $$ S=\sum_{i=1}^{n}\varepsilon_i^2=\sum_{i=1}^{n}(y_i-\beta_0-\beta_1x_i)^2. $$ Now suppose we want to fit the model to the following data, Average Heights and Weights for American Women, where weight is the response and height is the predictor. The data is available in R by default. ...
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Late-onset Alzheimers disease (LOAD) is a common neurodegenerative disorder, with a complex etiology. APOE is the only confirmed susceptibility gene for LOAD. Others remain yet to be found. Evidence from linkage studies suggests that a gene (or genes) conferring susceptibility for LOAD resides on chromosome 10. We studied 23 positional/functional candidate genes from our linkage region on chromosome 10 (APBB1IP, ALOX5, AD037, SLC18A3, DKK1, ZWINT, ANK3, UBE2D1, CDC2, SIRT1, JDP1, NET7, SUPV3L1, NEN3, SAR1, SGPL1, SEC24C, CAMK2G, PP3CB, SNCG, CH25H, PLCE1, ANXV111) in the MRC genetic resource for LOAD. These candidates were screened for sequence polymorphisms in a sample of 14 LOAD subjects and detected polymorphisms tested for association with LOAD in a three-stage design involving two stages of genotyping pooled DNA samples followed by a third stage in which markers showing evidence for association in the first stages were subjected to individual genotyping. One hundred and twenty polymorphisms were
Most people with Alzheimers disease have the late-onset form of the disease, in which symptoms become apparent in their mid-60s.The apolipoprotein E (APOE) gene is involved in late-onset Alzheimers. This gene has several forms. One of them, APOE ε4, increases a persons risk of developing the disease and is also associated with an earlier age of disease onset. However, carrying the APOE ε4 form of the gene does not mean that a person will definitely develop Alzheimers disease, and people with no APOE ε4 may also develop the disease.. Also, scientists have identified a number of regions of interest in the genome (an organisms complete set of DNA) that may increase a persons risk for late-onset Alzheimers to varying degrees.. Early-onset Alzheimers disease occurs in people age 30 to 60 and represents less than 5 percent of all people with Alzheimers. Most cases are caused by an inherited change in one of three genes, resulting in a type known as early-onset familial Alzheimers disease, ...
TY - JOUR. T1 - APOE genotype and functional outcome following aneurysmal subarachnoid hemorrhage. AU - Gallek, Matthew J. AU - Conley, Yvette P.. AU - Sherwood, Paula R.. AU - Horowitz, Michael B.. AU - Kassam, Amin. AU - Alexander, Sheila A.. PY - 2009/1. Y1 - 2009/1. N2 - Apolipoprotein E (apoE), the major apolipoprotein in the central nervous system, has been shown to influence neurologic disease progression and response to neurologic injury in a gene-specific manner. Presence of the APOE4 allele is associated with poorer response to traumatic brain injury and ischemic stroke, but the association between APOE genotype and outcome following aneurysmal subarachnoid hemorrhage (SAH) remains unclear. The purpose of this project was to investigate the association between APOE genotype and outcome after SAH. We also explored the association of APOE4 genotype and cerebral vasospasm (CV) presence in a subsample of our population with available angiographic data. A sample of 206 aneurysmal SAH ...

Journal Club Review: Cerebral Amyloid Angiopathy with and without Haemorrhage | Neurology Online Journal ClubJournal Club Review: "Cerebral Amyloid Angiopathy with and without Haemorrhage | Neurology Online Journal Club

On the other hand one ε2 allele is protective versus the e4 allele in relation to various neurodegenerative conditions ... Potential markers include the apolipoprotein (APO) E ε2 genotype and imaging markers such as superficial siderosis and centrum ...
more infohttps://neurologyonlinejournalclub.com/2015/05/12/journal-club-review-cerebral-amyloid-angiopathy-with-and-without-haemorrhage/

Anti-Apolipoprotein E4/ApoE4 antibody (Biotin) | AbcamAnti-Apolipoprotein E4/ApoE4 antibody (Biotin) | Abcam

Anti-Apolipoprotein E4 antibody conjugated to Biotin validated for WB, ELISA, RIA and tested in Human. Immunogen corresponding ...
more infohttp://www.abcam.com/Apolipoprotein-E4-antibody-Biotin-ab85976.html

New Role of Apolipoprotein E4 Variant in Alzheimer s Disease Suggests Possible Therapeutic TargetNew Role of Apolipoprotein E4 Variant in Alzheimer s Disease Suggests Possible Therapeutic Target

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

Apolipoprotein E4 enhances brain inflammation by modulation of the NF-kappaB signaling cascade.  - PubMed - NCBIApolipoprotein E4 enhances brain inflammation by modulation of the NF-kappaB signaling cascade. - PubMed - NCBI

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 ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed/15979312

Apolipoprotein E4 allele as a predictor of cholinergic deficits and treatment outcome in Alzheimer disease | PNASApolipoprotein E4 allele as a predictor of cholinergic deficits and treatment outcome in Alzheimer disease | PNAS

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

Apolipoprotein E4 reduces evoked hippocampal acetylcholine release in adult miceApolipoprotein E4 reduces evoked hippocampal acetylcholine release in adult mice

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, ...
more infohttps://insights.ovid.com/jneur/201602000/00005064-201602000-00008

Apolipoprotein E4 and a change in episodic memory functioning among normal aging Norwegian adultsApolipoprotein E4 and a change in episodic memory functioning among normal aging Norwegian adults

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 ...
more infohttps://www.duo.uio.no/handle/10852/18543

Longitudinal study of the effect of apolipoprotein e4 allele on the association between education and cognitive decline in...Longitudinal study of the effect of apolipoprotein e4 allele on the association between education and cognitive decline in...

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 ...
more infohttp://www.bmj.com/content/314/7073/34

IJERPH | Free Full-Text | In the Heart of the Amazon: Noncommunicable Diseases and Apolipoprotein E4 Genotype in the Riverine...IJERPH | Free Full-Text | In the Heart of the Amazon: Noncommunicable Diseases and Apolipoprotein E4 Genotype in the Riverine...

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

Roles of apolipoprotein E4 (ApoE4) in the pathogenesis of Alzheimers disease: lessons from ApoE mouse models | Biochemical...Roles of apolipoprotein E4 (ApoE4) in the pathogenesis of Alzheimer's disease: lessons from ApoE mouse models | Biochemical...

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

Treatment response to Aricept® (donepezil hydrochloride) not predicted by Apolipoprotein E4 genotype...(  WASHINGTON D.C. 11...Treatment response to Aricept® (donepezil hydrochloride) not predicted by Apolipoprotein E4 genotype...( WASHINGTON D.C. 11...

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 ...
more infohttp://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/

Gene-environment interactions between adult lead exposure and Apolipoprotein E4 on adult hippocampal neurogenesis and cognitive...Gene-environment interactions between adult lead exposure and Apolipoprotein E4 on adult hippocampal neurogenesis and cognitive...

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 ...
more infohttps://digital.lib.washington.edu/researchworks/handle/1773/36645

Aging | Ketones improves Apolipoprotein E4-related memory deficiency via sirtuin 3 - FigureAging | Ketones improves Apolipoprotein E4-related memory deficiency via sirtuin 3 - Figure

Apolipoprotein E4 (ApoE4) is the major genetic risk factor of Alzheimers disease (AD). ApoE4 carriers have cerebral ...
more infohttps://www.aging-us.com/figure/102070/f1

Anti-Apolipoprotein E4 抗体 (Biotin) (ab85976)Anti-Apolipoprotein E4 抗体 (Biotin) (ab85976)

Anti-Apolipoprotein E4 antibody (Biotin). Apolipoprotein E4 一次抗体 製品一覧. ...
more infohttp://www.abcam.co.jp/apolipoprotein-e4-antibody-biotin-ab85976.html

Buy Recombinant Human Apolipoprotein E4 Protein (cyt-968)Buy Recombinant Human Apolipoprotein E4 Protein (cyt-968)

Buy online Recombinant Human Apolipoprotein E4 Protein from Prospec cat# cyt-968. ProteoGenix provides you the best Cytokines ...
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High apolipoprotein E4 allele frequency in FXTAS patients.  - PubMed - NCBIHigh apolipoprotein E4 allele frequency in FXTAS patients. - PubMed - NCBI

High apolipoprotein E4 allele frequency in FXTAS patients.. Silva F1, Rodriguez-Revenga L, Madrigal I, Alvarez-Mora MI, Oliva R ... All the apolipoprotein E ε4/4 genotype carriers detected (100%), and six of the seven apolipoprotein E ε4/3 genotype carriers ( ... On the basis of these results, we conclude that the presence of at least one apolipoprotein E ε4 allele might act as a genetic ... It is well known that the apolipoprotein E ε4 allele is a risk factor for neurodegenerative disease. The main goal of this work ...
more infohttps://phgkb.cdc.gov/PHGKB/phgHome.action?action=forward&dbsource=huge&id=81996

The Role of the Apolipoprotein E4 (APOE4) Gene in Triggering AlzheimersThe Role of the Apolipoprotein E4 (APOE4) Gene in Triggering Alzheimer's

The Role of the Apolipoprotein E4 (APOE4) Gene in Triggering Alzheimers. By Editor, September 4, 2018, 9:54 pm, (Category: ... What is the Apolipoprotein E (APOE) Gene?. The apolipoprotein E (APOE) gene is responsible for the production of a protein, ... One variant or form of the APOE gene, called e4, has been linked to an increased risk of developing Alzheimers disease. It is ... The exact mechanism of how the e4 variant of the APOE gene leads to the onset of Alzheimers is unknown. However, researchers ...
more infohttps://healthhelpzone.com/health_guide/the-role-of-the-apolipoprotein-e4-apoe4-gene-in-triggering-alzheimers-57089902.shtml

Apolipoprotein E e4 allele influences aggressive behaviour in Alzheimers disease | Journal of Neurology, Neurosurgery &...Apolipoprotein E e4 allele influences aggressive behaviour in Alzheimer's disease | Journal of Neurology, Neurosurgery &...

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- ...
more infohttp://jnnp.bmj.com/content/75/9/1327

mylab | 細胞因子 / APOE4 Human; Apolipoprotein E4 Human Recombinant 100µgmylab | 細胞因子 / APOE4 Human; Apolipoprotein E4 Human Recombinant 100µg

APOE*E4-Associated, Late Onset), Apolipoprotein E3, LDLCQ5, LPG, AD2, APOE.Linkhttp://www.prospecbio.com/APOE4_Human_3 ... LRARMEEMGS RTRDRLDEVK EQVAEVRAKL EEQAQQIRLQ AEAFQARLKS WFEPLVEDMQ RQWAGLVEKV QAAVGTSAAP VPSDNH.DescriptionApolipoprotein E4 ... Apolipoprotein E, APO-E, Alzheimer Disease 2 (APOE*E4-Associated, Late Onset), Apolipoprotein E3, LDLCQ5, LPG, AD2, APOE. ... 細胞因子 / APOE4 Human; Apolipoprotein E4 Human Recombinant. 型號: CYT-968 規格: 100µg 產地: 以色列 報價: 3,000 元 運費: 以PDF報價單為準 交期: 期貨,
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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...

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

Apolipoprotein E4 allele presence and functional outcome after severe traumatic brain injury.  - PubMed - NCBIApolipoprotein E4 allele presence and functional outcome after severe traumatic brain injury. - PubMed - NCBI

Apolipoprotein E4 allele presence and functional outcome after severe traumatic brain injury.. Alexander S1, Kerr ME, Kim Y, ... Presence of the apolipoprotein E (APOE) 4 allele has been associated with increased incidence and faster progression of ...
more infohttps://phgkb.cdc.gov/PHGKB/phgHome.action?action=forward&dbsource=huge&id=28078

Apolipoprotein E e4 and its prevalence in early childhood death due to sudden infant death syndrome or to recognised causes.Apolipoprotein E e4 and its prevalence in early childhood death due to sudden infant death syndrome or to recognised causes.

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

Human apolipoprotein E4 targeted replacement mice show increased prevalence of intracerebral hemorrhage associated with...Human apolipoprotein E4 targeted replacement mice show increased prevalence of intracerebral hemorrhage associated with...

Human apolipoprotein E4 targeted replacement mice show increased prevalence of intracerebral hemorrhage associated with ... Human apolipoprotein E4 targeted replacement mice show increased prevalence of intracerebral hemorrhage associated with ... It has been suggested that apolipoprotein E4 expression leads to increased vascular amyloid deposition, which may explain the ...
more infohttps://scholars.duke.edu/display/pub707166

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 |...

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

EvidenceEvidence

Randox offers The Apolipoprotein E4 (ApoE4) Array.. The Apolipoprotein E4 (ApoE4) Array is a research use-only product ... E4/E4 (homozygous) and E2/E3, E2/E4, E3/E4 (heterozygous). Medical professionals recognise the presence of the ApoE4 isoform as ... The Apolipoprotein E4 (ApoE4) Array is a research use only product developed for the Evidence Investigator. The ApoE4 Array ... ApoE exists in three common isoforms (ApoE2, ApoE3 and ApoE4) which are coded by three co-dominant alleles (e2, e3, e4). As ...
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  • The main goal of this work was to evaluate the apolipoprotein E genotypes and allelic distribution among patients with fragile X-associated tremor/ataxia syndrome. (cdc.gov)
  • 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)
  • 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)