Role of mitochondrial homeostasis and dynamics in Alzheimer's disease. Neurobiol Dis 2013 Mar;51:3-12
Date
01/24/2012Pubmed ID
22266017Pubmed Central ID
PMC3337963DOI
10.1016/j.nbd.2011.12.057Scopus ID
2-s2.0-84871417031 (requires institutional sign-in at Scopus site) 133 CitationsAbstract
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 mitochondrial 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.
Author List
Selfridge JE, E L, Lu J, Swerdlow RHAuthor
Lezi E PhD Assistant Professor in the Cell Biology, Neurobiology and Anatomy department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
Alzheimer DiseaseAnimals
Homeostasis
Humans
Mitochondria
Mitochondrial Dynamics
