Genetic profiles of familial late-onset Alzheimer's disease in China: The Shanghai FLOAD study
返回论文页
Full-length article|更新时间:2022-11-09
|
Genetic profiles of familial late-onset Alzheimer's disease in China: The Shanghai FLOAD study
Genetic profiles of familial late-onset Alzheimer's disease in China: The Shanghai FLOAD study
Genes & Diseases2022年9卷第6期
作者机构:
1. Department of Neurology and Institute of Neurology, Ruijin Hospital Affiliated with Shanghai Jiao Tong University School of Medicine,Shanghai,PR China,200025
2. Institute of Neurology, Huashan Hospital, Fudan University,Shanghai,PR China,200040
3. National Clinical Research Center for Aging and Medicine, Huashan Hospital, Fudan University,Shanghai,PR China,200040
4. Department of Biochemistry, Center for Neurodegenerative Disease, Emory University School of Medicine,GA,Atlanta,USA,30322
Genetic profiles of familial late-onset Alzheimer's disease in China: The Shanghai FLOAD study[J]. Genes & Diseases, 2022,9(6).
Xin-Yi Xie, Qian-Hua Zhao, Qiang Huang, et al. Genetic profiles of familial late-onset Alzheimer's disease in China: The Shanghai FLOAD study[J]. Genes & Diseases, 2022,9(6).
Genetic profiles of familial late-onset Alzheimer's disease in China: The Shanghai FLOAD study[J]. Genes & Diseases, 2022,9(6). DOI: 10.1016/j.gendis.2021.05.001.
Xin-Yi Xie, Qian-Hua Zhao, Qiang Huang, et al. Genetic profiles of familial late-onset Alzheimer's disease in China: The Shanghai FLOAD study[J]. Genes & Diseases, 2022,9(6). DOI: 10.1016/j.gendis.2021.05.001.
Genetic profiles of familial late-onset Alzheimer's disease in China: The Shanghai FLOAD study
摘要
Abstract
Compared with early-onset familial AD (FAD)
the heritability of most familial late-onset Alzheimer's disease (FLOAD) cases still remains unclear. However
there are few reported genetic profiles of FLOAD to date. In the present study
targeted sequencing of selected candidate genes was conducted for each of 90 probands with FLOAD and 101 unrelated matched normal controls among Chinese Han population. Results show a significantly lower rate of mutation in APP and PSENs
and
APOE
ε4 genetic risk is higher for FLOAD. Among the Chinese FLOAD population
the most frequent variant was
CR1
rs116806486 [5.6%
95% CI (1.8%
12.5%)]
followed by coding variants of
TREM2
(4.4%
95%CI (1.2%
10.9%)) and novel mutations of
ACE
[3.3%
95%CI (0.7%
9.4%)]. Next
we found that novel pathogenic mutations in
ACE
including frame-shift and nonsense mutations were in association with FLOAD regardless of
APOE
ε4 status. Evidence from the Alzheimer's disease Neuroimaging Initiative (ADNI) database also supported this finding in different ethnicities. Results of
in vitro
analysis suggest that frame-shift and nonsense mutations in
ACE
may be involved in LOAD through decreased ACE protein levels without affecting direct processing of APP.