Mechanism of axonal transport dysfuction of mitochondria in Alzheimer's disease
10.3760/cma.j.cn115354-20221209-00898
- VernacularTitle:阿尔茨海默病中线粒体轴突转运障碍的发生机制
- Author:
Yihan SHEN
1
;
Hanxiao XU
;
Linhao JIANG
;
Minhui XU
;
Tianjiao XIA
Author Information
1. 南京大学医学院，南京 210008
- Keywords:
Alzheimer's disease;
Mitochondrial axonal transport;
Beta-amyloid;
Tau protein;
Presenilin-1
- From:
Chinese Journal of Neuromedicine
2023;22(5):476-479
- CountryChina
- Language:Chinese
-
Abstract:
Alzheimer's disease (AD) is a central neurodegenerative disease with still unclear pathogenesis. Recent studies have shown that axonal transport dysfuction of mitochondria may contribute to AD progression. Normal mitochondrial axonal transport mainly involves microtubules, molecular motors and connexins, while AD early pathological changes can damage mitochondrial axonal transport by interfering with these proteins: accumulated β-amyloid (Aβ) impairs the function of molecular motors; abnormally modified Tau protein reduces microtubule stability; mutant presenilin-1 (PS1) can induce phosphorylation of some related proteins by activating glycogen synthase kinase-3β (GSK-3β); all these processes can damage mitochondrial axonal transport, leading to synaptic dysfunction. This review aims to clarify the possible mechanisms of axonal transport dysfuction of mitochondria in AD and provides new ideas for AD treatment.
