期刊
NEUROBIOLOGY OF DISEASE
卷 173, 期 -, 页码 -出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nbd.2022.105855
关键词
Alzheimer's disease; Transcription factor EB; Autophagy; Lysosome; A? plaque; Tau phosphorylation
资金
- National Key Research and Devel- opment Program of Hubei Province [2020BCA089]
- National Key Research and Development Program of China [2020YFC2006001]
- National Natural Science Foundation of China [81974218, 81671064]
This review focuses on the pathological mechanisms of Alzheimer's disease and highlights the research progress and therapeutic approaches related to TFEB, a transcription factor involved in autophagy regulation. It provides important insights into the treatment strategies and clinical management of AD.
Alzheimer's disease (AD), an age-dependent neurodegenerative disorder, is the most prevalent neurodegenera-tive disease worldwide. The primary pathological hallmarks of AD are the deposition of beta-amyloid plaques and neurofibrillary tangles. Autophagy, a pathway of clearing damaged organelles, macromolecular aggregates, and long-lived proteins via lysosomal degradation, has emerged as critical for proteostasis in the central nervous system (CNS). Studies have demonstrated that defective autophagy is strongly implicated in AD pathogenesis. Transcription factor EB (TFEB), a master transcriptional regulator of autophagy, enhances the expression of related genes that control autophagosome formation, lysosome function, and autophagic flux. The study of TFEB has greatly increased over the last decade, and the dysfunction of TFEB has been reported to be strongly asso-ciated with the pathogenesis of many neurodegenerative disorders, including AD. Here, we delineate the basic understanding of TFEB dysregulation involved in AD pathogenesis, highlighting the existing work that has been conducted on TFEB-mediated autophagy in neurons and other nonneuronal cells in the CNS. Additionally, we summarize the small molecule compounds that target TFEB-regulated autophagy involved in AD therapy. Our review may yield new insights into therapeutic approaches by targeting TFEB and provide a broadly applicable basis for the clinical treatment of AD.
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