疾病
推论
因果推理
梅德林
因果关系(物理学)
医学
认知心理学
认知科学
临床神经学
神经科学
心理学
退行性疾病
帕金森病
精神科
因果模型
功能连接
拉福拉病
人工智能
作者
Si‐Chun Gu,Q. Sun,Wen Zhang,Chang‐Yi Shen,Hang Su,Fang Xie,Can‐Xing Yuan,Zhi‐dong Zhou,Eng King Tan,Qing Ye
摘要
BACKGROUND: Parkinson's disease (PD) involves heterogeneous neurodegenerative processes across brain cell types. The cell-type-specific effects of genetic risk remain unclear. OBJECTIVE: We aimed to identify cell-type-specific causal genes for PD and to link genetic risk to molecular mechanisms and therapeutic opportunities. METHODS: We performed the first cell-stratified Mendelian randomization integrating single-cell expression quantitative trait loci data from eight brain cell types with large PD genome-wide association studies datasets, followed by validation, neuropathological correlation, and postmortem expression analyses. RESULTS: Thirteen significant causal associations for four genes (ARL17A, ARL17B, KANSL1, LRRC37A) were identified across seven cell types, with consistent replication. ARL17A increased risk, whereas ARL17B, KANSL1, and LRRC37A were protective. Gene expression correlated with disease severity and showed cell-type-specific dysregulation. Drug-gene interaction screen highlighted US Food and Drug Administration-approved agents including raloxifene and dorzolamide as potential therapeutic modulators. CONCLUSIONS: This study contributed to cell-type-specific genetic mechanisms in PD, linking risk variants to molecular alterations and nominating therapeutic targets. © 2026 International Parkinson and Movement Disorder Society.
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