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Lack of association between LGMN and Alzheimer’s disease in the Southern Han Chinese population
European Journal of Neuroscience ( IF 2.7 ) Pub Date : 2020-06-07 , DOI: 10.1111/ejn.14857
Xinyue Zhang 1 , Bin Jiao 1, 2, 3 , Ling Weng 1 , Yafang Zhou 1 , Lina Guo 1 , Xin Wang 1 , Lu Zhou 1 , Xixi Liu 1 , Xuewen Xiao 1 , Hui Liu 1 , Xiangyu Zhu 1 , Chenping Li 1 , Yuan Zhu 1 , Qijie Yang 1 , Zhuojie Lin 1 , Yaling Jiang 1 , Yafei Wen 1 , Hui Zhou 1 , Lu Shen 1, 2, 3, 4 , Xinxin Liao 2, 3, 5
Affiliation  

Recently, functional studies have demonstrated that legumain (LGMN) cleaves both amyloid β‐protein precursor and tau, promoting senile plaques and formation of neurofibrillary tangles, which may play a crucial role in the pathogenesis of Alzheimer's disease (AD). However, the genetic role of LGMN in AD has not been clearly elucidated. Here, we used Sanger sequencing to investigate the single independent (single‐variant association test) and cumulative (gene‐based association test) effects of variants in the LGMN gene as potential susceptibility factors for AD, in a cohort comprising 676 AD cases and 365 elderly controls from the Han population of South China. In single‐variant association analysis, none of the common variants in LGMN were statistically significant. In gene‐based analysis, the LGMN gene also showed no association with AD. The results of our replication study in the Alzheimer's Disease Neuroimaging Initiative cohort also showed no association between LGMN and AD. These findings suggest that the LGMN gene may not be a critical factor for AD development.
更新日期:2020-06-07
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