Targeting necroptosis in Alzheimer's disease: can exercise modulate neuronal death?

IF 4.1 2区医学 Q2 GERIATRICS & GERONTOLOGY

Frontiers in Aging Neuroscience Pub Date : 2025-03-14 eCollection Date: 2025-01-01 DOI:10.3389/fnagi.2025.1499871

Donglei Lu, Wenyu Zhang, Ruiyu Li, Sijie Tan, Yan Zhang

引用次数: 0

Abstract

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by cognitive decline and neuronal degeneration. Emerging evidence implicates necroptosis in AD pathogenesis, driven by the RIPK1-RIPK3-MLKL pathway, which promotes neuronal damage, inflammation, and disease progression. Exercise, as a non-pharmacological intervention, can modulate key inflammatory mediators such as TNF-α, HMGB1, and IL-1β, thereby inhibiting necroptotic signaling. Additionally, exercise enhances O-GlcNAc glycosylation, preventing Tau hyperphosphorylation and stabilizing neuronal integrity. This review explores how exercise mitigates necroptosis and neuroinflammation, offering novel therapeutic perspectives for AD prevention and management.

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来源期刊

Frontiers in Aging Neuroscience GERIATRICS & GERONTOLOGY-NEUROSCIENCES

CiteScore

6.30

自引率

8.30%

发文量

1426

期刊介绍： Frontiers in Aging Neuroscience is a leading journal in its field, publishing rigorously peer-reviewed research that advances our understanding of the mechanisms of Central Nervous System aging and age-related neural diseases. Specialty Chief Editor Thomas Wisniewski at the New York University School of Medicine is supported by an outstanding Editorial Board of international researchers. This multidisciplinary open-access journal is at the forefront of disseminating and communicating scientific knowledge and impactful discoveries to researchers, academics, clinicians and the public worldwide.