细胞衰老处于炎症和阿尔茨海默病的十字路口。

Cellular senescence at the crossroads of inflammation and Alzheimer's disease.

机构信息

UK Dementia Research Institute, Institute of Neurology, University College London, London WC1E 6BT, UK; The Francis Crick Institute, London NW1 1AT, UK.

UK Dementia Research Institute, Institute of Neurology, University College London, London WC1E 6BT, UK; The Francis Crick Institute, London NW1 1AT, UK; Department of Neurosciences, Leuven Brain Institute, Katholieke Universiteit (KU) Leuven, Leuven, Belgium; Vlaams Instituut voor Biotechnologie (VIB) Centre for Brain and Disease Research, Leuven, Belgium.

出版信息

Trends Neurosci. 2021 Sep;44(9):714-727. doi: 10.1016/j.tins.2021.06.007. Epub 2021 Aug 5.

DOI:10.1016/j.tins.2021.06.007

PMID:34366147

Abstract

Aging is a key risk factor for Alzheimer's disease (AD), but the reasons for this association are not well understood. Senescent cells accumulate in aged tissues and have been shown to play causal roles in age-related pathologies through their proinflammatory secretome. The question arises whether senescence-induced inflammation might contribute to AD and bridge the gap between aging and AD. Here, we highlight the role of cellular senescence as a driver of the aging phenotype, and discuss the current evidence that connects senescence with AD and neurodegeneration.

摘要

衰老是阿尔茨海默病（AD）的一个关键风险因素，但这种关联的原因尚不清楚。衰老细胞在衰老组织中积累，并通过其促炎分泌组在与年龄相关的病理中发挥因果作用。问题是衰老引起的炎症是否会导致 AD，并弥合衰老和 AD 之间的差距。在这里，我们强调细胞衰老作为衰老表型驱动因素的作用，并讨论将衰老与 AD 和神经退行性变联系起来的现有证据。