Journal
ANNUAL REVIEW OF NEUROSCIENCE
Volume 31, Issue -, Pages 91-123Publisher
ANNUAL REVIEWS
DOI: 10.1146/annurev.neuro.30.051606.094302
Keywords
mitochondrial DNA; maternal inheritance; oxidative stress; apoptosis; oxidative phosphorylation; aging
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Funding
- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT [P01HD032062] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [P50NS011766, P01NS011766] Funding Source: NIH RePORTER
- NICHD NIH HHS [HD32062] Funding Source: Medline
- NINDS NIH HHS [NS 11766] Funding Source: Medline
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Mitochondrial diseases (encephalomyopathies) have traditionally been ascribed to defects of the respiratory chain, which has helped researchers explain their genetic and clinical complexity. However, other mitochondrial functions are greatly important for the nervous system, including protein importation, organellar dynamics, and programmed cell death. Defects in genes controlling these functions are attracting increasing attention as causes not only of neurological (and psychiatric) diseases but also of age-related neurodegenerative disorders. After discussing some pathogenic conundrums regarding the neurological manifestations of the respiratory chain defects, we review altered mitochondrial dynamics in the etiology of specific neurological diseases and in the physiopathology of more common neurodegenerative disorders.
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