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Chylomicron remnants and very low density lipoprotein (VLDL) remnants are rapidly removed from the circulation by receptor-mediated endocytosis in the liver. Apolipoprotein E, a main apoprotein of the chylomicron, binds to a specific receptor on liver cells and peripheral cells. ApoE is essential for the normal catabolism of triglyceride-rich lipoprotein constituents. The APOE gene is mapped to chromosome 19 in a cluster with APOC1 and APOC2. Defects in apolipoprotein E result in familial dysbetalipoproteinemia, or type III hyperlipoproteinemia (HLP III), in which increased plasma cholesterol and triglycerides are the consequence of impaired clearance of chylomicron and VLDL remnants. 6 hour postprandial triglyceride values were correlated with fasting triglyceride levels, which showed association with the apolipoprotein E4 allele. A monomeric APOE carboxyl-terminal domain was engineered and studied. A peptide derived from the low density lipoprotein receptor-binding domain of apoE mediates an efficient, energy-dependent translocation of liposomes across the membrane of primary rat brain capillary endothelial cells. ABCA1 is essential for the biogenesis of high density-sized lipoprotein containing only apoE particles in vivo. APOE allele is not associated with cognitive impairment in normal aging. APOE does not play an important role in susceptibility to Parkinson's disease, but may play a role in dementia associated with Parkinson's disease. APOE domain structural requirements for the formation of SDS-stable complexes with beta-Amyloid(1-40). APOE epsilon 2 may be a risk factor for early malaria infection. APOE epsilon 4 carrier status by itself does not predict cognitive decline or conversion to Alzheimer's disease, indicating that APOE genotyping in patients with mild cognitive impairment may have limited clinical applicability for prediction of outcome. APOE epsilon4 may act by a lower neuronal metabolism as a risk factor for cognitive impairment in normal aging and early prodromal AD. APOE gene polymorphism as a risk factor for the severity of macular edema in Type 2 diabetes mexican patients. APOE genotype distribution strongly influences serum APOE concentration, not suggesting, at present, a possible role as a biochemical marker for AD, but only as a putative longevity factor. APOE genotype was evaluated for an association between infant genetic variation and the risk for spina bifida cystica. APOE genotypes strongly influenced cognitive function and decline in worman with cardiovascular disease. APOE has a role in regulating cholesteryl ester uptake by binding to SR-BI in human cells. APOE is not associated with the risk of Alzheimer disease. APOE isoproteins are inefficient at complexing with synthetic Alzheimer disease amyloid-beta protein in vitro. APOE may have a role along with HSV1 in dementia [review]. APOE may play a role in invasiveness of human prostate cancer. APOE polymorphisms in cerebral amyloid angiopathy. APOE worked as LPL-inhibitor of the lipolysis activated by APOC2. The binding density of APOE was less for small emulsion surfaces than for large ones. APOE*4, allele was associated with increased relative risk for elevated total cholesterol to high-density lipoprotein (HDL) ratios and low-density lipoprotein (LDL. APOE*2 was associated with a lower relative risk for total cholesterol to HDL ratios. APOE4,4 is associated with thinning of the microvascular basement membrane in Alzheimer's disease. Accelerated brain tissue loss and a higher proportion of lesions evolving into ""black holes"" therefore provide magnetic resonance imaging evidence for more pronounced tissue destruction in multiple sclerosis patients with APOE-epsilon 4. Accelerated memory decline in Alzheimer's disease with apolipoprotein epsilon4 allele. Accounted for 15-60% of variability of plasma LDL cholesterol or apoB levels in familial hypobetalipoproteinemia(FHBL). The physiologic bases for the greater effects of apoE in FHBL remain to be determined. Accumulation of potentially pathogenic C-terminal-truncated fragments of apoE depends on the isoform and cellular source. Neuron-specific cleavage of apoE4 is associated with increased tau phosphorylation and may play a role in Alzheimer disease. After mild head injury, participants with at least one APOE epsilon4 allele had a significantly decreased performance on neuropsychological tests. APOE genotype may influence the outcome following an MHI. Allele transmission in families with autism (apolipoprotein-E2). An interaction between apoE3 and CNTF occurs with both delipidated apeE3 and apoE3 found within a lipoprotein particle in cerebrospinal fluid. This interaction potentiates the survival-promoting activity of CNTF for hippocampal neurons. Analysis of transgenic mice overexpressing human apoE in the liver revealed that apoE was recruited from the circulation to the injured site of the carptod aartery wall. Apo E genotype affected the increase in aerobic capacity produced by exercise training possibly via undefined effects on nerve and skeletal muscle function. Apo E polymorphism was not found to be associated with maximal oxygen uptake (Vo(2max)) levels either in the sedentary state nor the Vo(2max) response to exercise training. Apo e iaoproteins might contribute to the pathology of alzheimer disease through several different mechanisms. (review). Apo e4 allele is associated with impairment of endothelium-dependent arterial dilation in the early stage of Type 2 diabetes. Apo epsilon4 allele ise predictor for stroke development. ApoE 4 genotype was more frequent in AD (41.4%) than in controls and In AD patients, CYP46*C along with ApoE epsilon4 genotype were associated with a higher cognitive decline at 1-year follow-up. ApoE affects the age of onset of Abeta deposition in amyloid precursor protein transgenic mice as well as the level, structure and anatomic distribution of brain Abeta deposits. ApoE concentration in combination with the ApoE polymorphism significantly influences serum lipid parameters in hemodialysis patients. ApoE e4 allele was associated with a marked reduction in LDL peak particle size and an increased plasma concentration of small dense LDL. ApoE inhibits the depolymerization of beta 2-microglobulin-related amyloid fibrils at pH 7.5, possibly by binding directly to the surface of the fibrils and stabilizing the conformation of beta 2-microglobulin in the fibrils. ApoE is dysregulated in nephrotic syndrome with marked increment in serum. Glomerular apoE is down regulated in focal segmental glomerulosclerosis and may contribute to pathogenesis. ApoE stimulates protein kinase CK2 autophosphorylation, and this can promote phosphorylation of additional substrates such as tau. ApoE varepsilon 4 allele occurs frequently in late-onset Alzheimer disease and we have found similar association in cognitively impaired individuals without clinical cerebrovascular disease. ApoE-epsilon 4 and butyrylcholinesterase-K variant alleles act synergistically to increase the risk of late-onset Alzheimer's disease, particularly in age group <75 years in Tehran, Iran. ApoE2, apoE3, and apoE4 are equally effective in inhibiting aortic smooth muscle cell migration toward platelet-derived growth factor, while apoE3 and apoE2 isoforms are preferred to apoE4 for inhibiting PDGF-stimulated smooth muscle cell proliferation. ApoE4 allele is not a contributory factor to cholesterol gallstone formation, at least in the Japanese population. Apoe4 affects the outcome of acute brain damage in an isoform-specific fashion (apoE4 > apoE3 = apoE2) and is detected in neurons and astrocytes in the peri-infarct area of genetically engineered mice. Apolipoprotein C-III and E polymorphisms and cardiovascular syndrome, hyperlipidemia, and insulin resistance in renal transplantation. Apolipoprotein E (apoE) polymorphisms were determined in 165 Saudis. Apolipoprotein E expression increases in fibroblasts during apoptosis, growth arrest and mitosis. Apolipoprotein E gene polymorphism has a role in hypercholesterolemia and type 2 diabetes, and affects glomerular filtration rate. Apolipoprotein E gene polymorphisms are associated with carotid plaque formation but not with intima-media wall thickening. Apolipoprotein E genotype and heterogeneity at the CETP gene locus have an interactive influence on plasma lipid and lipoprotein levels in children. Apolipoprotein E genotype influences lipid and lipoprotein levels in pregnant women. Apolipoprotein E polymorphism in Northern Indian patients with coronary heart disease: phenotype distribution and relation to serum lipids and lipoproteins. Apolipoprotein E polymorphism in childhood nephrotic syndrome. Apolipoprotein E polymorphism is associated with age of onset in schizophrenia. Apolipoprotein E promoter polymorphisms are unlikely to have a major impact on the pathophysiology of primary open angle glaucoma. Apolipoprotein E-epsilon 4 protects against severe liver disease caused by hepatitis C virus. Apolipoprotein E-promoter single-nucleotide polymorphisms affect the phenotype of primary open-angle glaucoma and demonstrate interaction with the myocilin gene. Apolipoprotein E4 potentiates amyloid beta peptide-induced lysosomal leakage and apoptosis in neuronal cells. Association of plasma lipid levels with apolipoprotein E polymorphism in Type 2 diabetes; carriers have increased risk of NIDDM. Both epsilon 4 allele and mutation -219G/T in the promoter are associated with early onset coronary heart disease in Finland. Cellular and secreted levels of apoE are reduced (15 and 30%, respectively, over a 24-h period) by addition of exogenous lactosyl ceramide (LacSer) to cultured macrophages, indicating a proatherogenic role for LacCer. Changes in cerebrospinal fluid apoE concentration occur after traumatic brain injury and may be important in the response of the human brain to injury. Chronic anxiety is associated with significantly greater decline in problem solving skills in cognitively normal APOE e4 homozygotes. Comparison of apoE epsilon genotypes in MS patients revealed no significant differences in frequencies between benign & severe septiles. The risk conferred by epsilon4 rose upon comparison of carriage rates in more narrowly defined anti-podal quantiles. Contributions of 18 additional DNA sequence variations in the gene encoding apolipoprotein E to explaining variation in quantitative measures of lipid metabolism. Data show that the apolipoprotein E receptor 2 binding domain of apolipoprotein E is in the 1-165 amino terminal region, whereas the carboxy terminal 230-299 region of apoE is required for efficient initial association with phospholipids. Data show that the apolipoprotein E4 (apoE4) isoform acts to aggravate delayed infarct expansion and peri-infarct reactive astrocytosis in genetically engineered apoE-knock-in mice. Discontinuation and poor adherence to therapy with statins is dependent on APO E genotype. E2 allele seems to be a risk factor of frontotemporal dementia but is associated with the lowest risk in Alzheimer's disease. Early recognition of severe hypertriglyceridemia in pregnancy may be caused by heterozygosity of this protein. Effect of long-term hormone replacement therapy on atherosclerosis progression in postmenopausal women relates to functional genotype. Effects of APOE genotype on component processes of cognition in healthy, middle-aged adults is consistent with the emergence in adulthood of an APOE-epsilon4 cognitive phenotype. Epsilon3-haplotypes containing the promoter allele -219T were associated with reduced amyloid deposition and reduced risk of neuropathologically verified Alzheimer disease as compared to epsilon3-haplotypes containing -219G. Ethnic differences and alterations of serum apoE levels significantly modify the relationship between apoE gene polymorphism and serum lipid variability. Family history of dementia is associated with an increased risk of dementia and Alzheimer's disease in a very old population, but only among APOE epsilon 4 carriers. Findings suggest that the epsilon2/2, epsilon3/4, and epsilon4/4 genotypes have greater early mortality risks. HFE and APOE genotypes are different between Alzheimer's disease patients, high cognitive impairment and low cognitive impairment controls. Healthy adult males carrying this genotype were used in the oral fat load experiments. Hepatic lipase promoter SNPs are associated with increased HDL cholesterol and, paradoxically, an increased risk of IHD after adjustment for HDL cholesterol, and particularly in individuals with apolipoprotein E epsilon43 genotype. Hyperlipidemia in APOE*3 Leiden transgenic mice resulted in a significant increase in accelerated atherosclerosis in vein grafts. In APOE epsilon 4 carriers in a Finnish population with Alzheimer's disease, HSPG2 A allele may possess an additive risk effect. In a Caucasian population, APOE may have effects on BMD variation in males but not females. In a family based study, the authors consistently found a significantly reduced transmission of allele 2 to newborns affected with intrauterine growth restriction (IUGR); in other words, allele 2 seems protective against IUGR. In a magnetic resonance spectroscopy study of the non-demented elderly occipital cortex, levels of creatine correlate significantly with age and performance on the Mini-Mental State Examination test in APOE epsilon 4 carriers, but not in the non-carriers. In a sample of mostly white, well-educated research participants with Alzheimer's disease, the APOE epsilon 4 allele was associated with shorter survival in men but not in women. In a study comparing brains from Alzheimer's patients and controls, it was found that hippocampal apolipoprotein D level depends on Braak stage and APOE genotype. In addition to the APOE epsilon2/epsilon3/epsilon4 polymorphism, the promoter polymorphisms -219G/T and +113G/C as well as their haplotype modulate lipid and lipoprotein concentrations in middle-aged Finnish men. In conclusion, our finding suggests that the MMP3 gene, especially together with APOE 4, may contribute to the development of AD. In elderly subjects who carry an APOE epsilon 4 allele, plasma amyloid beta protein levels are positively associated with lacunar infarcts and white matter lesions, whereas in APOE epsilon 4 noncarriers no associations are observed. In human brain, apoE4 dose correlates inversely with dendritic spine density of dentate gyrus neurons in the hippocampus of both Alzheimer's disease patients and aged normal controls. In our cohort, the APOE genotype does not constitute a risk factor for developing POAG (primary open-angle glaucoma). In schizophrenia, there was increased apoE in BA9 and BA46. In bipolar I disorder, increased levels of the apolipoprotein were detected in the caudate putamen and BA9 with a decrease in apoE being measured in BA10. In the ApoE4 genotype group, low LDL cholesterol was associated with good performance in the mental arithmetic test, whereas for those without ApoE4 genotype. In this study, variations in the frequencies of the apo epsilon4 allele and the apo E3/E4 and E4/E4 genotypes were found in patients with NIDDM, GN and ADPKD. In young adults, the APOE epsilon4 allele and cigarette smoking act synergistically, increasing an individual's propensity to have a cerebral ischemic event. Increased expression of neuronal apolipoprotein E in cerebral infarction. Interactions with APOE genotype, cigarette smoking, and alcohol intake. Isoforms of apolipoprotein E modulate tissue plasminogen activator-induced clot lysis in an in vitro clot assay system. Lack of an association of apolipoprotein E gene polymorphisms with familial age-related macular degeneration. Longitudinal analysis of several components of memory over a 2-year interval showed a significant Age-by-APOE interaction reflecting a decline in new learning for the > or =60 epsilon4+ group only. Mild cognitive impairment subjects with APOE epsilon4 had distinct cognitive & imaging profiles, resembling early Alzheimer patients. APOE4 was associated with greater impairments in memory & functional activities & hippocampal atrophy. NMR structure of apolipoprotein E carboxyl-terminal domain. New role of apoE in cancer as apoE expression is important for the proliferation and survival in apoE-expressing ovarian cancer cells. Niemann-Pick type C disease: accelerated neurofibrillary tangle formation and amyloid beta deposition associated with apolipoprotein E epsilon 4 homozygosity. No association is observed between the APOE epsilon 4 allele and clinical characteristics of the multiple sclerosis study population. No differences in ApoE allele or genotype frequencies were observed between schizophrenic patients and controls, except for a possible association between male schizophrenic patients and the ApoE epsilon 2 epsilon 3 genotype. No significant association was detected between the APOE epsilon 4 allele and the rate of decline on measures of specific cognitive functions. No significant associations between apoE genotype and rectal cancer, survival after diagnosis with colorectal cancer, stage of disease at diagnosis or type of tumor mutation. No significant differences in allele or genotype frequency for APOE gene were detected between patients with myocardial infarction and healthy controls. Our data do not support the hypothesis that the ApoE*4 risk allele is associated with BMD, increased bone loss, or an increased risk of osteoporotic fractures. PON2*S and apoE4 alleles have interactive effect on the development of the two most common forms of dementias AD and VD, and further support the hypothesis that cardiovascular factors contribute to the development of AD. Patients with multiple sclerosis and allelic polymorphism of APOE epsilon 4 have a significantly higher progression index of disability and a worse ranked multiple sclerosis severity score than their non-epsilon 4 counterparts. Polymorphism is associated with neurodegenerative diseases, notably Alzheimer disease. Polymorphisms do not contribute substantially to the risk of holoprosencephaly. Polymorphisms in the APOE promoter are found not to be risk factors for Alzheimer's disease nor are they associated with parenchymal or vascular accumulation of amyloid-beta protein. Polymorphisms of ApoE, independent of gender or other known factors, may affect serum creatinine levels and predict glomerular filtration rate in healthy persons. Presence of TNFB*A329G polymorphism in addition to APOE*E4 variant is associated with significantly higher releases of interleukin 8 and tumor necrosis factor alpha, prolonged intubation, and increased transfusion. Regulated expression of gene cluster in mascrophages. Relative bioavailability of natural to synthetic vitamin E in apoE4 males was close to the currently accepted biopotency ratio of 1.36:1. Results confirm that the apolipoprotein E epsilon 4 genotype is associated with Alzheimer's disease and its cognitive impairment pattern. Results demonstrate that apoE4-202 functions even in the presence of clearance-defective apoE2. Results describe the relative roles of apolipoprotein E isoforms in low density lipoprotein receptor (LDLR)- and non-LDLR-mediated very low density lipoprotein (VLDL) clearance. Results examine the impact of apolipoprotein E genetic variation on fertility in two Ecuadorian populations. Results indicate that adipose tissue expression of apolipoprotein E is modulated by physiologic regulators of insulin sensitivity. Shows normal apoE expression. Neurobiology of human apoE isoforms can now be studied in both normal and post-injury state. All apoE regulatory sequences intact. May explain regional vulnerability of neuronal degeneration in Alzheimer's disease. Single nucleotide polymorphisms in the promoter of APOE modify the phenotype of open-angle glaucoma and result in increased optic-nerve damage. Specific interaction of heterogeneous nuclear ribonucleoprotein A1 with the -219T allelic form modulates APOE promoter activity. The -219G/T polymorphism may influence triacylglycerol-rich lipoprotein metabolism during the postprandial period. The APOE epsilon-4 allele seems to influence the risk of Alzheimer disease by a relatively selective effect on episodic memory. The APOE epsilon4 allele has a negative effect on the course of MS, and increasing axonal damage may be an important mechanism. The APOE epsilon4 allele is associated with increased risk of obstructive sleep apnea/hypoxia, particularly in individuals under age 65, possibly by affecting brainstem degeneration or adipokine-related ventilatory drive. The APOE*E4 genotype status appears to have a greater deleterious effect on gross hippocampal pathology and memory performance in women than in men. The APOE-4 allele increases risk and decreases age at onset of PD, an association that may not be dependent upon cognitive impairment. The APOE/epsilon 4 was associated with an increase of plasma lipid levels and with a decrease of systolic blood pressure. The ApoE epsilon4 allele was not related to the disease course of multiple sclerosis or the ApoE epsilon2 to the intensity of demyelination on MRI. The ApoE4 is strongly associated with reduced Abeta42 CSF levels in Alzheimer's disease pts & controls. As no associations of APOE variants with other indexes of AD severity were seen, this may reflect fundamental ApoE involvement in Abeta metabolism. The ability of APOE4/4 VLDL to inhibit the antiapoptotic effects of HDL presents a potential mechanism by which the expression of several diseases, including atherosclerosis, is enhanced by the APOE4 genotype. The alleles of apoE appear to have a role in the etiology of AMD, with the epsilon4 allele being protective, whereas the epsilon2 allele appears to have a modifier effect by bringing forward the mean age of disease diagnosis. The antioxidant domain of apoE has been localized to its receptor-binding N-terminal domain; the basic amino acids in this domain are important for protecting low-density lipoproteins against lipid oxidation. The apoE epsilon4 allele is associated with chronic cerebral infarction detected at autopsy in older persons. The association between the APOE-epsilon4 allele and a reduced risk of AMD (age-related macular degeneration) was established in a large cohort with sufficient statistical power. The association of APOE epsilon 4 allele with less favorable outcome in multiple sclerosis is reviewed. The distributions of ApoE epsilon 2, epsilon 3 and epsilon 4 were similar in both clinical patient groups and in the non-diabetic group and unrelated to progression of disease. The effect of APOE genes on brain MRI measures were studied in subjects with age-associated memory impairment. No APOE effects were observed when analyses accounted for other potential confounding variables. The microenvironments of all 12 lysine residues in intact apoE3 were determined and their relative contributions to heparin binding were examined. The presence of 2 epsilon4 alleles is an important determinant of both plaques & tangles. A putative protective role for the epsilon2 allele in AD may be mediated by reduced plaque burden. The presence of one or more epsilon4 alleles of ApoE is a significant predictor for the incidence of delusions in the course of Alzheimer disease. The presence of the ApoE epsilon4 allele carried a 19.0-fold risk for developing hallucinations and a 3.4-fold risk for delusions in Alzheimer disease. The relationship between APOE genotype and its influence on memory performance following traumatic brain injury have been demonstrated. The results of the present study offer new insight into how recognition memory is affected by Alzheimer disease , the epsilon4 allele, and the modality of the stimulus to be remembered. The unfavorable effect of ApoE 4 genotype on lipoproteins is not altered by HRT, but ApoE 2 genotype modulates the HDL-ERT association in older women. There is a higher prevalence of the apo E2 allele in patients with severe aortic valve stenosis. There is a minor association between BChE-K and early-onset coronary artery disease, especially in the presence of the APOE-epsilon 4 allele. There is no linkage between Apo E polymorphism and autism. There was no association between the APOE genotype and the cognitive change caused by electroconvulsive therapy in major depressive disorder population as a whole. There was no evidence for an APOE allele effect on thyroid status in males. There was no evidence for an APOE allele effect on hepatitis B virus status (HBV), or for an HBV status effect on thyroid status. These data may support the importance of Apo E 4 allele in determining postmenopausal spine bone mass. These data provide a novel explanation for the apparent AD-protective effect of inheriting an epsilon2 APOE allele, and suggest that optimizing AT enrichment of CNS lipoproteins or devising APOAI mimetics may augment AT efficacy in treating AD. These data support the hypothesis that increased levels of apoE may be associated with the pathology of schizophrenia and that antipsychotic drugs decrease apoE levels as part of their therapeutic actions. These experiments demonstrate the roles of Chol and ApoE in the modulation of membrane insertion of APP. These findings suggest that ApoE epsilon4 plays no significant role in the development of ICVD and VaD, but that ApoE epsilon2 has a protective effect with regard to the development of ICVD and VaD for Taiwan Chinese below the age of 65. These results indicate that oleic acid increases apolipoprotein E secretion from macrophages at a locus involving post-translational glycosylation. These results indicate that, in fetus, the character and metabolism of HDL, especially of apo E-rich HDL cholesterol, are distinct from those in adults. This data confirm a specific effect caused by the presence and amount of ApoE epsilon4 allele and suggest that a susceptibility factor to AD. This protein protects PC12 rat cells against the cytotoxicity of APP. This review examines key scientific advances which focus on possible therapeutic strategies encompassing the use of apoE in the amelioration of atherosclerosis, based on its direct effects on the vascular wall. This study confirmed the risk association between APOE epsilon 4 and AD. The observation that APOE epsilon 4 is associated with mixed dementia reflected the role of AD in the aetiopathogenesis of this condition. This study found that APOE promoter polymorphisms and APOC1 insertion alleles were significantly associated with AD. Thus, the present study provides evidence that the efficiency of intestinal absorption and synthesis of cholesterol in humans are not related to the apoE phenotype. To determine whether late cognitive decline after head injury is more prevalent among carriers of APOE epsilon 4. Using human monocyte-derived macrophages (MDM), we show a significantly greater increase in NO production during immune activation in MDM from APOE4 AD patients compared to normal, age-matched individuals or to AD patients with an APOE 3/3 genotype. Variability in apoE-related risk was found in both Alzheimers disease(AD) and non-AD cases, depending on the subgroup /Review/meta-analysis/. Variant alleles of APOE and APOC3 contribute to an unfavorable lipid profile in patients with HIV, who are therefore at high risk for severe ritonavir-associated hypertriglyceridemia. We conclude that APOE allelic patterns in healthy Kuwaiti blood donors and a smaller group of patients with CH do not satisfactorily predict circulating blood levels of lipids and lipoproteins. We have retested non-demented 80-year-olds who were participants in the Scottish Mental Survey of 1932, and find that the variation in their non-pathological cognitive change from age 11 to 80 is related to their apolipoprotein E (APOE) genotype. A less organized structure in the C-terminal domain of apoE4 leads to the higher affinity for lipid as compared to apoE3, contributing to its preferential association with VLDL. A looped-back model of apoE4 is proposed in lipid-bound state, including spherical lipoprotein particles, wherein residues Arg-61 and Glu-255 are proximal to one another. A significant deficit in prospective memory for epsilon4 allele carriers. Alpha-helices in receptor-binding region and CT domain of apoE align perpendicular to the fatty acyl chains of the phospholipid bilayer and residues of helix 4 are arrayed in a positively charged, curved helical segment for receptor interaction. Amyloidogenic effects of apoE4 are exacerbated by polymorphisms in the APOE promoter that enhance apoE production. Analysis of a novel, ABCA-1-independent, positive feedback pathway for stimulation of potentially anti-atherogenic apoE secretion by alpha-helix-containing molecules including apoA-I and apoE. ApoE binds to the LDL receptor by interacting with more than one of the receptor ligand-binding repeats. ApoE deficiency results in: impaired catabolism of VLDL/chylomicron and their remnants; 2) an increased rate of catabolism of LDL apoB-100; 3) reduced VLDL apoB production; and 4) a delayed catabolism of Lp(a). ApoE increases the rate of HL-mediated phospholipid and triacylglycerol hydrolysis in rHDL. ApoE inhibits cell migration via cAMP-dependent protein kinase A activation as a consequence of its binding to LRP-1. ApoE4 inhibits synaptic plasticity following environmental stimulation and that this effect is both isoform- and brain area-specific. Apoe4 allele frequency is increased in patients with the temporal variant of frontotemporal dementia compared to non-demented controls. Apolipoprotein E epsilon4 haplotype is a predictor for recurrence in ischemic cerebrovascular disease. Apolipoprotein e4 allele works through amyloid deposition and subsequent tangle formation to cause cognitive impairment. Association between ApoE polymorphism and specific components of visuospatial attention. Carotid ultrasound results (intimal-medial thickness and stenosis) were related to three APOE genotypes. Cell-surface heparan sulfate proteoglycan localizes apoE-enriched remnant lipoproteins to the vicinity of receptors by fast association and dissociation. Combined frequency of the apoE alleles in the Malays, Chinese and Indians in Malaysia was 0.058, 0.829 and 0.114 for epsilon2, epsilon3 and epsilon4, respectively. Compared with all the other APOE genotypes, those carrying the Leu28-->Pro mutation were at a substantially higher risk of developing AD (OR=4.25; 95% CI=1.21-14.97). Data indicated that upstream-stimulatory-factor (USF) might be involved in the basal transcriptional machinery of apolipoprotein E by binding to a non-canonical E-box motif within the proximal promoter. Data suggested that the ApoE epsilon2/epsilon4 genotype might be a susceptibility variant of moderate effect for sporadic idiopathic Parkinson disease in our samples, whereas the ACT gene signal peptide polymorphism might not. Differences in binding capacity of apolipoprotein E3 and E4 isoforms to lipid emulsions. Differential effects of apoE3 and apoE4 on HDL metabolism. E*2 allele seems to be associated with the lowest reproductive efficiency and the e*3 allele, with the highest. Effects of apoE genotype and plasma concentration on cholesterol and triglycerides (TG) levels in subjects from five countries: Finland, France, Northern Ireland, Portugal, and Spain. Effects of the apolipoprotein E (ApoE) genotype and gender on the response to donepezil treatment in Alzheimer's disease. Epsilon4 gene dose is correlated with lower cerebral metabolic rate for glucose in regions of the precuneus and the posterior cingulate, parietotemporal, and frontal cortex. Findings indicate that residues Leu-261, Trp-264, Phe-265, Leu-268, and Val-269 of apoE are responsible for hypertriglyceridemia and also interfere with the formation of HDL. Findings suggest that the APOE4 carriers are particularly susceptible to the atherogenic effects of smoking; this interaction is particularly clear in hypertensive subjects. Gene polymorphism as a risk factor for cerebral amyloid angiopathy-related hemorrhage. Generation and characterization of two transgenic mouse lines expressing human ApoE2 in neurons and glial cells. Impaired recycling of apoE4 could interfere with intracellular cholesterol transport and contribute to the pathophysiological lipoprotein profile observed in apoE4 homozygotes. In individuals with age-associated memory impairment APOE E4 allele carriers performed worse on memory; this effect was only observed in females. Inheritance of the APOE epsilon4 allele is associated with increased risk of late posttraumatic seizures. Investigated the effect of APO E gene polymorphism over lipid profile, macular toxicity and clinical manifestations in rheumatoid arthritis and systemic lupus erythematosus patients treated with chloroquine. Involvement of ApoE in the hematogenous route of HSV-1 to the CNS. Neuronal expression of apoE is regulated by a diffusible factor or factors released from astrocytes. No association of the ApoE genotype with multiple sclerosis disease susceptibility nor clinical and MRI measures could be identified. No association seen between APOE genotype and time to psychosis in Alzheimer's disease. No relation between APOE gene polymorphisms and Japanese patients with multiple sclerosis. No significant difference when APOE and SCA2 allele frequencies of cases and controls were compared for multiple sclerosis. No significant differences were observed between the frequency of apolipoprotein E epsilon3/epsilon3 genotype and epsilon3/epsilon4 genotype in the control group compared to Alzheimer patients' group. Onset, diagnosis, and epidemiology of AD, specifically with regard to the APOE genotype and the interaction of the genotype with (review). Phenotype is associated with glucose metabolism and cognitive function. Polymorphism of apolipoprotein E gene is associated with longevity. Polymorphisms in the apolipoprotein E region with susceptibility to and progression of multiple sclerosis. Possession of an epsilon4 allele does increase risk of Alzheimer's disease in persons with mild cognitive impairment. Possession of epsilon4 does not by itself confer an increased risk of cerebral amyloid angiopathy but may be associated with reduced longevity even in the absence of alzheimer's disease or cerebral haemorrhage. Results confirm the hypothesis that serum ApoE concentration is dependent on ApoE genotype, but do not support the view that it has to be considered a relevant biochemical marker for Alzheimer disease and vascular dementia. Role in amyloid foundation but not amyloid growth in vitro; is a risk factor for AD not due to a pathological gain of function of apoE4 but to a loss of protective function of apoE3. Role of ApoE3 and ApoE4 isoforms in lipid release from astrocytes. Role of alleles in dyslipemia and kidney transplantation. Sequence variation in the BACE1 or BACE 2 gene is not a significant risk factor for AD; but, a combination of a specific BACE1 allele and APOE epsilon 4 may increase the risk for Alzheimer disease over and above that attributed to APOE epsilon 4 alone. Single nucleotide polymorphism +5361, or a SNP in strong linkage disequilibrium, may confer some additional risk for developing AD beyond the risk due to APOE-4; however, the effect independent of APOE-4 is likely to be small. That the epsilon4 allele of apolipoprotein E and the -491A allele are over-represented among individuals who complain of memory difficulties. The -491AA APOE promoter genotype is associated with elevated brain apolipoprotein E levels, suggesting that the risk for AD may be modulated by the apoE protein level as well as by the apoE protein isoform. The APOE varepsilon 4 allele is a predisposing factor for Alzheimer disease, but not for cerebrovascular disease or vascular dementia. The APOE4 allele may have a protective role in children with a history of heavy burdens of diarrhea in their first 2 y of life. The ApoE E2 allele is a risk factor for the occurrence of type 2 diabetes mellitus in Chinese general population. The ApoE polymorphism was associated with higher risk of MI in Russians and Tatars under 45. The epsilon2 allele of the APOE polymorphism is a prognostic risk factor for both the onset and the progression of diabetic nephropathy in Japanese type 2 diabetes. The increased risk of developing Alzheimer's disease and vascular dementia is similar among Asian Indians with ApoE epsilon4 compared with the Caucasian population. The presence of apoE2/3 genotype, high HDL-cholesterol levels and the absence of apoE3/3 genotype can be regarded as risk factors for superficial fungal disease, especially dermatophytosis. The response to plant stanol ester ingestion was not influenced by apolipoprotein E phenotype. We did not find APOE associated with ALS risk. We have now investigated whether the different apolipoprotein E (APO E) genotypes, in pairwise combinations with the MTHFR 677TT or ACE D/D mutation, could lead to an increased risk of leukoaraiosis. Young adult epsilon4 carriers, at genetic risk for late-onset Alzheimer's dementia, had abnormally low rates of brain glucose metabolism.
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