Affiliations 

  • 1 Department of Physiology and Neurobiology, School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang 453003, China; Department of Toxicology, Advanced Medical and Dental Institute, Universiti Sains Malaysia, Penang 13200, Malaysia
  • 2 Henan International Joint Laboratory of Cardiovascular Remodeling and Drug Intervention, School of Pharmacy, Xinxiang 453003, China
  • 3 Department of Toxicology, Advanced Medical and Dental Institute, Universiti Sains Malaysia, Penang 13200, Malaysia; Dementia Multidisciplinary Research Program of IPPT (DMR-IPPT), Advanced Medical and Dental Institute, Universiti Sains Malaysia, Penang 13200, Malaysia. Electronic address: niksyazni@usm.my
  • 4 Department of Toxicology, Advanced Medical and Dental Institute, Universiti Sains Malaysia, Penang 13200, Malaysia. Electronic address: vlim@usm.my
  • 5 Henan International Joint Laboratory of Cardiovascular Remodeling and Drug Intervention, School of Pharmacy, Xinxiang 453003, China. Electronic address: pengli@xxmu.edu.cn
  • 6 Department of Physiology and Neurobiology, School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang 453003, China. Electronic address: yalingyin@xxmu.edu.cn
Ageing Res Rev, 2024 Dec;102:102593.
PMID: 39566741 DOI: 10.1016/j.arr.2024.102593

Abstract

Alzheimer's disease (AD), commonly known as senile dementia, is a neurodegenerative disease with insidious onset and gradually worsening course. The brain is particularly sensitive to senescence, and neuronal senescence is an important risk factor for the occurrence of AD. However, the exact pathogenesis between neuronal senescence and AD has not been fully elucidated so far. Neuronal senescence is characterized by the permanent stagnation of the cell cycle, and the changes in its structure, function, and microenvironment are closely related to the pathogenesis and progression of AD. In recent years, studies such as the Aβ cascade hypothesis and Tau protein phosphorylation have provided new strategies for the therapy of AD, but due to the complexity of the etiology of AD, there are still no effective treatment measures. This article aims to deeply analyze the pathogenesis between AD and neuronal senescence, and sort out various existing therapeutic methods, to provide new ideas and references for the clinical treatment of AD.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.