转录组
疾病
生物
神经科学
电池类型
小胶质细胞
神经退行性变
亨廷顿病
细胞
表型
阿尔茨海默病
基因
医学
炎症
病理
遗传学
基因表达
免疫学
作者
Hansruedi Mathys,José Dávila-Velderrain,Zhuyu Peng,Fan Gao,Shahin Mohammadi,Jennie Z. Young,Madhvi Menon,Liang He,Fatema Abdurrob,Xueqiao Jiang,Anthony J. Martorell,Richard M. Ransohoff,Brian P. Hafler,David A. Bennett,Manolis Kellis,Li‐Huei Tsai
出处
期刊:Nature
[Nature Portfolio]
日期:2019-05-01
卷期号:570 (7761): 332-337
被引量:1998
标识
DOI:10.1038/s41586-019-1195-2
摘要
Alzheimer's disease is a pervasive neurodegenerative disorder, the molecular complexity of which remains poorly understood. Here, we analysed 80,660 single-nucleus transcriptomes from the prefrontal cortex of 48 individuals with varying degrees of Alzheimer's disease pathology. Across six major brain cell types, we identified transcriptionally distinct subpopulations, including those associated with pathology and characterized by regulators of myelination, inflammation, and neuron survival. The strongest disease-associated changes appeared early in pathological progression and were highly cell-type specific, whereas genes upregulated at late stages were common across cell types and primarily involved in the global stress response. Notably, we found that female cells were overrepresented in disease-associated subpopulations, and that transcriptional responses were substantially different between sexes in several cell types, including oligodendrocytes. Overall, myelination-related processes were recurrently perturbed in multiple cell types, suggesting that myelination has a key role in Alzheimer's disease pathophysiology. Our single-cell transcriptomic resource provides a blueprint for interrogating the molecular and cellular basis of Alzheimer's disease.
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