Association Between Alzheimer’s Disease and the NOS3 gene Glu298Asp Polymorphism in Chinese

Wang, Binbin; Tan, Sainan; Yang, Ze; Xie, Yanyan; Wang, Jing; Zhou, Sirui; Li, Shu; Zheng, Chengchao; Ma, Xu

doi:10.1007/s12031-007-9026-6

Cited by 12 publications

(7 citation statements)

References 18 publications

(28 reference statements)

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“…1 ). 23 case-control studies from 21 publications 2 6 7 8 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 including 5,670 cases and 5,046 controls were used to evaluate the association of G894T polymorphism with AD risk ( Table 1 ). Sample sizes ranged from 102 to 1,369 (median 365).…”

Section: Resultsmentioning

confidence: 99%

The nitric oxide synthase 3 G894T polymorphism associated with Alzheimer’s disease risk: a meta-analysis

Liu

Zeng

Wang

et al. 2015

Sci Rep

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The association between the G894T polymorphism (Glu298Asp) of nitric oxide synthase 3 (NOS3) and risk of Alzheimer’s disease (AD) was explored by performing a meta-analysis of case-control studies. Bibliographical searches were conducted in the MEDLINE, EMBASE, and China National Knowledge Infrastructure (CNKI) databases without any language limitations. Two investigators independently assessed abstracts for relevant studies, and reviewed all eligible studies. We adopted regrouping in accordance with the most probably appropriate genetic model. Odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of this association. We performed a meta-analysis including 21 published articles with 23 case-control studies (5,670 cases and 5,046 controls). In the analyses, we found significant association between G894T polymorphism and AD risk under a complete overdominant model (GG + TT vs. GT) (OR = 1.18; 95%CI, 1.04–1.35; P = 0.010). When stratified by time of AD onset, we found the association between this polymorphism and AD susceptibility to be more substantial among late onset patients than among early onset patients (OR for late vs. early onset: 1.33 vs. 1.02, P interaction = 0.049). The meta-analysis showed that the polymorphism G894T of NOS3 was associated with risk of AD.

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Section: Resultsmentioning

confidence: 99%

The nitric oxide synthase 3 G894T polymorphism associated with Alzheimer’s disease risk: a meta-analysis

Liu

Zeng

Wang

et al. 2015

Sci Rep

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“…Association between AD and the NOS3 gene polymorphism 247 in Asians. Eight studies [7,12,14,15,19,[23][24][25] were included in the subgroup of LOAD and four studies [7,12,15,25] were included in the subgroup of EOAD.…”

Section: Study Characteristicsmentioning

confidence: 99%

“…Sensitivity analysis showed that the study of Dahiyat et al [12], Styczynska et al [21], and Wang et al [23] was the origin of the heterogeneity. When we excluded the report by Dahiyat et al, Styczynska et al, and Wang et al, the heterogeneity disappeared and still no significant association was observed between NOS3 Glu298Asp polymorphism and AD risk.…”

Section: Sensitivity Analysismentioning

confidence: 99%

Association between Alzheimer's disease and the NOS3 gene Glu298Asp polymorphism

Zhao

Kong

et al. 2013

International Journal of Neuroscience

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“…The homozygous Glu 298 genotype has been found significantly over-represented in late-onset sporadic AD patients compared with controls [145]. Very recently, Wang and coworkers [146] replicated this finding in a large Chinese cohort. This suggests that NOS3 Glu 298 homozygous genotype might be a risk factor for sporadic AD.…”

Section: Endothelial Nitric Oxide Synthasementioning

confidence: 82%

The Role of Vascular Factors in Late-Onset Sporadic Alzheimers Disease. Genetic and Molecular Aspects

Rocchi¹,

Orsucci²,

Tognoni

et al. 2009

CAR

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Alzheimer's disease (AD) is a late-onset progressive neurodegenerative disorder which results in the irreversible loss of cortical neurons, particularly in the associative neocortex and hippocampus. AD is the most common form of dementia in the elderly. Apart from the neuronal loss, the pathological hallmarks are extracellular senile plaques, containing the peptide beta-amyloid (Abeta), and neurofibrillary tangles. The Abeta cascade hypothesis remains the main pathogenetic model, as suggested by familiar AD, mainly associated to mutation in amyloid precursor protein and presenilin genes. The remaining 95% of AD patients are mostly sporadic late-onset cases, with a complex aetiology due to interactions between environmental conditions and genetic features of the individual. A relationship between genetic and acquired vascular factors and AD has been hypothesized. Many vascular risk factors for AD, such as atherosclerosis, stroke and cardiac disease in the aging individual, could result in cerebrovascular dysfunction and trigger AD pathology. A major vascular susceptibility factor gene is the apolipoprotein E gene, found to be associated with sporadic late-onset AD cases. Another interesting vascular susceptibility gene is angiotensin converting enzyme. Other possible genes include VLDL-R, LRP, NOS3, CST3, OLR1, MTHFR, PON1 and VEGF, but many of the related studies have shown conflicting results. In this paper, we review the role of molecular vascular abnormalities and of the "vascular risk" genes supposed to be involved in the pathogenesis of AD, in an attempt to provide a comprehensive picture of what is known about the mechanisms underlying the role of vascular factors in late-onset sporadic AD.

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Association Between Alzheimer’s Disease and the NOS3 gene Glu298Asp Polymorphism in Chinese

Cited by 12 publications

References 18 publications

The nitric oxide synthase 3 G894T polymorphism associated with Alzheimer’s disease risk: a meta-analysis

The nitric oxide synthase 3 G894T polymorphism associated with Alzheimer’s disease risk: a meta-analysis

Association between Alzheimer's disease and the NOS3 gene Glu298Asp polymorphism

The Role of Vascular Factors in Late-Onset Sporadic Alzheimers Disease. Genetic and Molecular Aspects

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