The new perspective of Alzheimer's Disease Research: Mechanism and therapeutic strategy of neuronal senescence.

Ageing Res Rev

Department of Physiology and Neurobiology, School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang 453003, China. Electronic address:

Published: December 2024

AI Article Synopsis

  • Alzheimer's disease (AD) is a progressive neurodegenerative disorder linked to neuronal senescence, which plays a key role in its development, though the exact connection remains unclear.
  • Neuronal senescence involves a permanent halt in the cell cycle, leading to changes that contribute to AD's progression, highlighting the need for further research in this area.
  • Despite recent therapeutic strategies focusing on Aβ and Tau proteins, effective treatments for AD are still lacking due to the disease's complex nature, prompting a need for new insights into its pathogenesis and potential therapies.

Article 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.

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Source
http://dx.doi.org/10.1016/j.arr.2024.102593DOI Listing

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