生物
神经科学
小胶质细胞
疾病
阿尔茨海默病
因果关系(物理学)
神经退行性变
淀粉样蛋白(真菌学)
炎症
免疫学
病理
医学
物理
量子力学
植物
作者
Bart De Strooper,Eric Karran
出处
期刊:Cell
[Elsevier]
日期:2016-02-01
卷期号:164 (4): 603-615
被引量:1395
标识
DOI:10.1016/j.cell.2015.12.056
摘要
The amyloid hypothesis for Alzheimer's disease (AD) posits a neuron-centric, linear cascade initiated by Aβ and leading to dementia. This direct causality is incompatible with clinical observations. We review evidence supporting a long, complex cellular phase consisting of feedback and feedforward responses of astrocytes, microglia, and vasculature. The field must incorporate this holistic view and take advantage of advances in single-cell approaches to resolve the critical junctures at which perturbations initially amenable to compensatory feedback transform into irreversible, progressive neurodegeneration.
科研通智能强力驱动
Strongly Powered by AbleSci AI