Role of mitochondrial homeostasis and dynamics in Alzheimer's disease

NEUROBIOLOGY OF DISEASE

卷:51

Review

Selfridge, J. Eva¹  E, Lezi²  Lu, Jianghua³  Swerdlow, Russell H.^1,3,4 

[1] Univ Kansas, Sch Med, Dept Mol & Integrat Physiol, Kansas City, KS USA

[2] Univ Kansas, Sch Hlth Profess, Dept Phys Therapy & Rehabil Sci, Kansas City, KS USA

[3] Univ Kansas, Sch Med, Dept Neurol, Kansas City, KS USA

[4] Univ Kansas, Sch Med, Dept Biochem & Mol Biol, Kansas City, KS USA

关键词: Alzheimer's disease;    Autophagy;    Bioenergetics;    Biogenesis;    Fission;    Mitochondria;    Mitochondrial DNA;    Mitochondrial dysfunction;    Mitochondrial medicine;   

DOI  :  10.1016/j.nbd.2011.12.057

来源: Elsevier

【 摘 要 】

Alzheimer's disease (AD) is a progressive neurodegenerative disease that affects a staggering percentage of the aging population and causes memory loss and cognitive decline. Mitochondrial abnormalities can be observed systemically and in brains of patients suffering from AD, and may account for part of the disease phenotype. In this review, we summarize some of the key findings that indicate mitochondrial dysfunction is present in AD-affected subjects, including cytochrome oxidase deficiency, endophenotype data, and altered mitochondria! morphology. Special attention is given to recently described perturbations in mitochondrial autophagy, fission-fusion dynamics, and biogenesis. We also briefly discuss how mitochondrial dysfunction may influence amyloidosis in Alzheimer's disease, why mitochondria are a valid therapeutic target, and strategies for addressing AD-specific mitochondrial dysfunction. (C) 2012 Elsevier Inc. All rights reserved.

【 授权许可】

Free