Cortical structure and the risk for Alzheimer’s disease: a bidirectional Mendelian randomization study

孟德尔随机化 后扣带 库尼乌斯 萎缩 楔前 邦费罗尼校正 内科学 神经科学 医学 心理学 疾病 阿尔茨海默病 皮质(解剖学) 认知 生物 遗传学 基因型 遗传变异 统计 基因 数学
作者
Bang‐Sheng Wu,Ya-Ru Zhang,Hong‐Qi Li,Kevin H.M. Kuo,Shi-Dong Chen,Qiang Dong,Yong Liu,Jin‐Tai Yu
出处
期刊:Translational Psychiatry [Springer Nature]
卷期号:11 (1) 被引量:41
标识
DOI:10.1038/s41398-021-01599-x
摘要

Abstract Progressive loss of neurons in a specific brain area is one of the manifestations of Alzheimer’s disease (AD). Much effort has been devoted to investigating brain atrophy and AD. However, the causal relationship between cortical structure and AD is not clear. We conducted a bidirectional two-sample Mendelian randomization analysis to investigate the causal relationship between cortical structure (surface area and thickness of the whole cortex and 34 cortical regions) and AD risk. Genetic variants used as instruments came from a large genome-wide association meta-analysis of cortical structure (33,992 participants of European ancestry) and AD (AD and AD-by-proxy, 71,880 cases, 383,378 controls). We found suggestive associations of the decreased surface area of the temporal pole (OR (95% CI): 0.95 (0.9, 0.997), p = 0.04), and decreased thickness of cuneus (OR (95% CI): 0.93 (0.89, 0.98), p = 0.006) with higher AD risk. We also found a suggestive association of vulnerability to AD with the decreased surface area of precentral ( β (SE): –43.4 (21.3), p = 0.042) and isthmus cingulate ( β (SE): –18.5 (7.3), p = 0.011). However, none of the Bonferroni-corrected p values of the causal relationship between cortical structure and AD met the threshold. We show suggestive evidence of an association of the atrophy of the temporal pole and cuneus with higher AD risk. In the other direction, there was a suggestive causal relationship between vulnerability to AD and the decreased surface area of the precentral and isthmus cingulate. Our findings shed light on the associations of cortical structure with the occurrence of AD.
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