Abstract
BackgroundThe association between polymorphisms rs6265 and rs2030324 in brain-derived neurotrophic factor (BDNF) and Alzheimer’s disease (AD) has been widely reported, but the results remain controversial.MethodsA comprehensive search of Pubmed, Web of Science, China National Knowledge Infrastructure (CNKI), Wanfang Med Online and China Biology Medical literature database (CBM) was performed. Pooled odds ratios (ORs) with 95% confidence intervals (CIs) were calculated using fixed or random-effects models. We excluded the studies with OR>3.0 or OR<0.3 for sensitive analysis. Subgroup analysis by ethnicity, form of AD and gender was carried out. Meta-regression was conducted to explore the potential sources of between-study heterogeneity.Results29 articles with 7548 cases and 7334 controls concerning rs6265 and 22 articles with 5796 cases and 5706 controls concerning rs2030324 were included in this meta-analysis. The combined evidence suggested rs6265 contributing significantly to the increased risk of AD in females (codominant: fixed-effects model (FEM): OR = 1.13, 95% CI = 1.04–1.23; dominant: FEM: OR = 1.17, 95% CI = 1.05–1.31), especially for Caucasian females (codominant: FEM: OR = 1.18, 95% CI = 1.03–1.34; dominant: FEM: OR = 1.18, 95% CI = 1.01–1.37) and female late-onset Alzheimer’s disease (LOAD) patients (codominant: FEM: OR = 1.22, 95% CI = 1.05–1.41; dominant: FEM: OR = 1.23, 95% CI = 1.03–1.46). No evidence indicated an association between rs2030324 with AD in codominant (random-effects model (REM): OR = 1.06, 95% CI = 0.89–1.26) and dominant (REM: OR = 1.05, 95% CI = 0.86–1.27) models.ConclusionThis meta-analysis suggested A allele of rs6265 might increase the risk of AD in Caucasian females and female LOAD patients. In addition, no evidence indicated an association between rs2030324 with AD. Further studies are needed to confirm these results.
Highlights
Alzheimer’s disease (AD) is an age-associated neurodegenerative disorder characterized by progressive decline in cognitive function, which typically begins with deterioration in memory [1]
There have been many genetic polymorphisms reported to be associated with AD, such as amyloid precursor protein (APP), presenilin-1(PSEN1), presenilin2(PSEN2) [6], apolipoprotein E (APOE) [7,8] and sortilin-related receptor 1 (SORL1) [9]
Search Strategy A literature search was performed for available articles that were published in English or Chinese from the following databases: (1) Pubmed; (2) Web of Science; (3) China National Knowledge Infrastructure (CNKI); (4) Wanfang Med Online; (5) China Biology Medical literature database (CBM)
Summary
Alzheimer’s disease (AD) is an age-associated neurodegenerative disorder characterized by progressive decline in cognitive function, which typically begins with deterioration in memory [1]. The number of people with dementia worldwide in 2010 is estimated at 35.6 million and is projected to nearly double every 20 years to 65.7 million in 2030 and 115.4 million in 2050. The neuropathological etiology of AD remains unclear, but are probably related with the combined interaction between gene variants and environmental factors [5]. There have been many genetic polymorphisms reported to be associated with AD, such as amyloid precursor protein (APP), presenilin-1(PSEN1), presenilin2(PSEN2) [6], apolipoprotein E (APOE) [7,8] and sortilin-related receptor 1 (SORL1) [9]. The association between polymorphisms rs6265 and rs2030324 in brain-derived neurotrophic factor (BDNF) and Alzheimer’s disease (AD) has been widely reported, but the results remain controversial
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