Cdk5 as a drug target for the treatment of Alzheimer's disease.
J Mol Neurosci
; 19(3): 267-73, 2002 Dec.
Article
em En
| MEDLINE
| ID: mdl-12540052
ABSTRACT
Cyclin-dependent kinase-5 (cdk5) is suggested to play a role in tau phosphorylation and contribute to the pathogenesis of Alzheimer's disease (AD). One of its activators, p25, is dramatically increased in AD brains where p25 and cdk5 are colocalized with neurofibrillary tangles. Several animal models have shown a correlation of p25/cdk5 activities with tau phosphorylation. Overexpression of p25/cdk5 in nueronal cultures not only leads to tau phosphorylation but also cytoskeletal abnormalities and neurodegeneration. Therefore, cdk5 kinase inhibitors are potential therapeutic agents for the treatment of AD. Availability of potent, selective, brain permeable cdk5 inhibitors and relevant animal models in which their efficacy can be treated will be critical in the development of these inhibitors.
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Base de dados:
MEDLINE
Assunto principal:
Quinases Ciclina-Dependentes
/
Inibidores Enzimáticos
/
Doença de Alzheimer
Limite:
Animals
/
Humans
Idioma:
En
Ano de publicação:
2002
Tipo de documento:
Article