Mitochondrial aging and dysfunction in Alzheimer's disease.
Prog Neuropsychopharmacol Biol Psychiatry
; 29(3): 407-10, 2005 Mar.
Article
em En
| MEDLINE
| ID: mdl-15795049
ABSTRACT
Disruptions in energy metabolism have been suggested to be a prominent feature, perhaps even a fundamental component, of Alzheimer's disease (AD). These abnormalities in cerebral metabolism precede the onset of neurological dysfunction as well as gross neuropathology of AD. These changes may stem from inhibition of mitochondrial enzymes including pyruvate dehydrogenase, cytochrome c oxidase, and alpha-ketoglutarate dehydrogenase. Several lines of evidence also suggest a role for oxidative stress in the neuropathology associated with the disease state. Because mitochondria are the major site of free radical production in cells, they are also a primary target for oxidative damage and subsequent dysfunction. This link between mitochondrial dysfunction and the pathophysiology of AD is supported by several lines of evidence.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Envelhecimento
/
Doença de Alzheimer
/
Mitocôndrias
Limite:
Animals
/
Humans
Idioma:
En
Revista:
Prog Neuropsychopharmacol Biol Psychiatry
Ano de publicação:
2005
Tipo de documento:
Article
País de afiliação:
Estados Unidos