Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0038454 (stroke)
147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A relationship between apolipoprotein E (Apo E) genotype and angiotensin-converting enzyme (ACE) insertion-deletion (Ins-Del) mutation and stroke was suggested. We investigated the association of Apo E4 and ACE Ins/Del genotypes with stroke risk and changes in serum lipids in 228 consecutive Tunisian stroke patients, and 323 age-and gender-matched controls. Comparable frequencies of ACE Ins/Del alleles were seen between patients and controls. The prevalence of Apo epsilon3 allele and Apo E3/E3 were lower (P < 0.001), while the frequency of Apo epsilon4 allele and epsilon4-containing genotypes (E3/E4 and E4/E4) were elevated (P < 0.001) among patients. Higher proportion of Apo E4-carrying + ACE Del/Del positive cases were seen in young (<50 years) patients (P = 0.012), and was associated with large vessel stroke (P = 0.035). Mean serum cholesterol, LDL, HDL, and triglycerides were comparable between E4-containing and no E4-containing and ACE Del/Del-positive patients. Apo E4 and ACE Del/Del genotype combination substantially increase stroke risk, supporting the notion that interactions of multiple gene variants influence stroke pathogenesis.
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PMID:Interaction of angiotensin-converting enzyme and apolipoprotein E gene polymorphisms in ischemic stroke involving large-vessel disease. 1802 70

The aim of this study was to clarify whether the apolipoprotein E gene (APOE) is related to ischemic stroke subtypes in Taiwan's Chinese population. Using the classification of Cerebrovascular Diseases III, 143 patients with lacunar infarction, 114 patients with atherothrombotic infarction, and 112 healthy controls were enrolled. APOE genotype was determined using polymerase chain reaction. Regarding the distribution of APOE genotypes, the frequency of epsilon3/epsilon4 genotypes in lacunar patients was significantly different from that in control subjects, by logistic regression, using epsilon3/epsilon3 as a reference group. There was no significant difference between atherothrombotic patients and the control group in the distribution of APOE genotypes or alleles. The present finding suggests that there is a probable association between epsilon3/epsilon4 genotype and lacunar infarcts, but not atherothrombotic infarcts. This indicates that genetic factors may play a role, at least partially, in lacunar infarction in Taiwan's Chinese population.
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PMID:Association of apolipoprotein E polymorphism with ischemic stroke subtypes in Taiwan. 1805 94

The apolipoprotein E (APOE) epsilon4 allele is associated with elevated cholesterol and risk of atherosclerosis. However, its role in ischemic stroke (IS) remains controversial. We investigated a possible link between IS or the severity of intracranial atherosclerosis and the APOE promoter polymorphisms -219G/T and +113G/C, involved in regulating APOE transcription. We genotyped subjects from a multicentric Belgian case-control study, including 237 middle-aged patients with IS due to small- or large-vessel atherosclerotic stroke and 326 ethnicity- and gender-matched controls and a Finnish autopsy series of 1004 non-stroke cases, who had received a quantitative score of atherosclerosis in the circle of Willis. The APOE epsilon4+ genotype did not associate with IS, but was related to more severe intracranial atherosclerosis score in men (5.4 vs 4.6, P=0.044). Within the most common APOE epsilon3/epsilon3 genotype group, the risk of IS associated with the G-allele of the tightly linked -219G/T (OR=6.2; 95% CI: 1.6-24.3, P=0.009) and +113G/C (OR=7.1; 95% CI: 1.7-29.9, P=0.007) promoter polymorphisms. There was no difference in the severity of intracranial atherosclerosis between -219G/G genotype carriers and non-carriers. This study suggests a multifaceted role of apoE on the risk of cerebrovascular diseases. The APOE epsilon4+ genotype did not predict the risk of IS but was associated with severity of subclinical intracranial atherosclerosis in men on the autopsy study. In contrast, the promoter variants were significant predictors of IS, suggesting that quantitative rather than qualitative variation of apoE is related to IS.
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PMID:Associations of apolipoprotein E gene with ischemic stroke and intracranial atherosclerosis. 1830 47

Although elevated levels of C-reactive protein (CRP) independently predict increased risk of development of metabolic syndrome, diabetes, myocardial infarction, and stroke, comprehensive analysis of the influence of genetic variation on CRP is not available. To address this issue, we performed a genome-wide association study among 6345 apparently healthy women in which we evaluated 336,108 SNPs as potential determinants of plasma CRP concentration. Overall, seven loci that associate with plasma CRP at levels achieving genome-wide statistical significance were found (range of p values for lead SNPs within the seven loci: 1.9 x 10(-)(8) to 6.2 x 10(-)(28)). Two of these loci (GCKR and HNF1A) are suspected or known to be associated with maturity-onset diabetes of the young, one is a gene-desert region on 12q23.2, and the remaining four loci are in or near the leptin receptor protein gene, the apolipoprotein E gene, the interleukin-6 receptor protein gene, or the CRP gene itself. The protein products of six of these seven loci are directly involved in metabolic syndrome, insulin resistance, beta cell function, weight homeostasis, and/or premature atherothrombosis. Thus, common variation in several genes involved in metabolic and inflammatory regulation have significant effects on CRP levels, consistent with CRP's identification as a useful biomarker of risk for incident vascular disease and diabetes.
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PMID:Loci related to metabolic-syndrome pathways including LEPR,HNF1A, IL6R, and GCKR associate with plasma C-reactive protein: the Women's Genome Health Study. 1843 48

The distribution of allele and genotype frequencies of the Alu-insertion polymorphism of the angiotensin-converting enzyme (ACE) gene and missence mutations leading to the substitution of arginine to cysteine in positions 112 and 158 of apolipoprotein E (APOE) has been studied in 166 patients with brain intracranial aneurysms and in 192 controls of Russian origin from Ural region. Brain vascular aneurysms with hypertension were associated with the D*D* ACE genotype in men and with the e2 allele and the e2/e3 APOE genotype in women. The association was also observed between the e2 allele and the e2/e3 APOE genotype and family history of stroke, hemorrhages and aneurysms in patients. Men with the I*D* ACE genotype and the e4 APOE allele were at lower risk.
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PMID:[The role of angiotensin-converting enzyme and apolipoprotein E in the development of intracranial aneurysms.]. 1847 80

In this review we examine the evidence for ovarian hormone neuroprotection in chronic neurological diseases, including stroke. We propose that neuroprotection may involve the ability of estrogens to modulate apolipoprotein E (apoE) and its receptor, the low density lipoprotein receptor related protein (LRP). Results from numerous studies have demonstrated that (1) nerve regeneration is severely delayed in apoE-gene knockout (KO) mice as compared to wild-type (WT) littermates; (2) 17beta estradiol replacement in ovariectomized mice resulted in a significant increase in levels of apoE and LRP, in the olfactory bulb (OB) and other brain areas; (3) estradiol treatment increased both apoE and neurite outgrowth in cortical and olfactory neuronal cultures; and (4) estradiol treatment had no effect on neurite outgrowth in cultures deprived of apoE or in the presence of apoE4. In essence these studies suggest that apoE is a critical intermediary for the beneficial effects of 17beta estradiol on nerve repair, which can lead to functional reorganization (plasticity). Future studies of HT should evaluate the effects of apoE genotype and production estradiol on neuroprotection.
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PMID:Apolipoprotein E may be a critical factor in hormone therapy neuroprotection. 1850 94

The purpose of the present study was to investigate the predictive role of apolipoprotein E genotypes for stroke-related risk factors in the Turkish population. Among 100 stroke patients and 30 healthy subjects included in the study, most frequent Apo E genotype was epsilon3/3, compatible with polymorphic distribution of Asian population. VLDL and triglyceride levels in epsilon2/4(+) subjects were higher than in epsilon2/4(-) patients. HDL and homocysteine levels were higher in epsilon4/4 (+) subjects than in epsilon4/4 (-) stroke patients. These results suggest that ApoE polymorphism in this population was not associated with any other demographic or clinical variables except for lipid profiles and homocysteine levels.
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PMID:Association of apolipoprotein E genotype and cerebrovascular disease risk factors in a Turkish population. 1857 10

Factors predisposing to and associated with atherosclerosis may impact the onset and progression of Alzheimer disease (AD). The high prevalence of atherosclerosis and associated risk factors in American Indians makes them ideal subjects to test this association. We compared frequency of history of hypertension, myocardial infarction, stroke, diabetes, and high cholesterol in 34 American Indians with AD with 34 age-matched American Indian controls, and 34 age-matched whites with probable AD. We also measured waist size, height, and weight, and acquired blood for determination of plasma homocysteine and apolipoprotein E genotype. The 3 groups did not differ significantly in age or sex. History of hypertension and diabetes was significantly more common among American Indian AD patients than Indian controls or whites with AD. The 3 groups did not differ in history of stroke or myocardial infarction. Body mass index was significantly greater in both Indian groups than the white AD group. Plasma homocysteine levels were greater, but not significantly so, in the Indian AD than the Indian control group. Thus, there is preliminary evidence of a modest association between history of hypertension and diabetes and AD in a small sample of American Indians. This suggests that changes in lifestyle factors could influence the expression of AD in American Indians.
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PMID:Atherosclerosis risk factors in American Indians with Alzheimer disease: preliminary findings. 1858 May 94

Cerebral amyloid angiopathy (CAA) is cerebrovascular amyloid deposition and is related to stroke and dementia. CAA is classified into 6 types according to the biochemical properties of amyloid proteins, and among 6 types, the sporadic CAA of amyloid beta protein (Abeta) type is most frequently found in elderly people or patients with Alzheimer's disease (AD). In sporadic CAA of the Abeta type, the epsilon4 allele of the apolipoprotein E gene is associated with increased vascular Abeta deposition, while the epsilon2 allele is associated with CAA-related intracerebral hemorrhage. We have also reported that the genetic polymorphisms of presenilin-1, neprilysin, transforming growth factor beta-1, and alpha1-antichymotrypsin are associated with CAA. In the case of hereditary CAA of the Abeta type, mutations in the genes of amyloid precursor protein (APP) and presenilins have been reported. Interestingly, the missense mutations associated with CAA are located in the middle portion of Abeta, while those associated with familial AD (FAD) are near the N- or C- terminals of Abeta. Individuals with FAD with APP duplication have been reported to present with severe CAA. Some of the FAD patients with mutations in the presenilin genes and patients with Down syndrome also show CAA as a complication. Besides sporadic or hereditary CAA of the Abeta type, hereditary CAA with cerebrovascular deposition of cystatin C, transthyretin, gelsolin, prion protein, and ABri/ADan have also been reported in association with mutations in the genes of the precursor proteins. Better understanding of the genetic factors influencing CAA will lead to identification of novel diagnostic markers and the development of preventive for CAA and CAA-related disorders.
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PMID:[Genetic factors for cerebral amyloid angiopathy]. 1906 61

Subarachnoid hemorrhage (SAH) strikes individuals at a young age with devastating neurologic consequences. Classic formulations that correlate complications and outcome with clinical variables do not explain all the heterogeneity that is usually found in clinical practice. The role of genetic predisposition has recently been investigated. Particular attention has been paid to the apolipoprotein E (APOE) genotype that encodes for a polymorphic protein existing as 3 isoforms (apoE2, apoE3, apoE4), products of alleles E2, E3, and E4 at a single gene locus. ApoE is produced by astrocytes and exerts complex neuroprotective functions that make it a hub of the biochemical network of SAH. The neuroprotective effectiveness of the apoE4 isoform is reduced with respect to the others and this has made the E4 allele a risk factor candidate. Recently published observational studies and meta-analyses suggested that the APOE genotype may strongly improve the usual predictive model with the possibility of optimizing clinical decisions according to the individual's needs. Furthermore, the clinical results, together with new biological insights, suggest that SAH may be a possible candidate for the ongoing research on apoE-based neuroprotective therapy. This article reviews the clinical studies, analyzes their methodology, and surveys the biological links between the physiopathology of SAH and apoE and the possible prospects.
J Stroke Cerebrovasc Dis
PMID:Significance of apolipoprotein E in subarachnoid hemorrhage: neuronal injury, repair, and therapeutic perspectives--a review. 1925 Nov 87


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