Cellular senescence induced by cholesterol accumulation is mediated by lysosomal ABCA1 in APOE4 and AD.

Shaowei Wang, Boyang Li, Jie Li, Zhiheng Cai, Cristelle Hugo, Yi Sun, Lu Qian, Julia Tcw, Helena C Chui, Dante Dikeman, Isaac Asante, Stan G Louie, David A Bennett, Zoe Arvanitakis, Alan T Remaley, Bilal E Kerman, Hussein N Yassine

Keck School of Medicine, University of Southern California, Los Angeles, CA, 90033, USA.Keck School of Medicine, University of Southern California, Los Angeles, CA, 90033, USA. · pubmed

Paper

Abstract

Cellular senescence, a hallmark of aging, has been implicated in Alzheimer's disease (AD) pathogenesis. Cholesterol accumulation is known to drive cellular senescence; however, its underlying mechanisms are not fully understood. ATP-binding cassette transporter A1 (ABCA1) plays an important role in cholesterol homeostasis, and its expression and trafficking are altered in APOE4 and AD models. However, the role of ABCA1 trafficking in cellular senescence associated with APOE4 and AD remains unclear.

The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.

Research summary

The paper claims that cholesterol accumulation induces cellular senescence through lysosomal ABCA1 in the context of APOE4 and Alzheimer's disease. This research is relevant as it explores the mechanisms underlying cellular senescence, which is a key aspect of aging and age-related diseases, potentially contributing to our understanding of the root causes of these conditions.

Author of this paper? Send a correction.