Crosstalk between calcium, amyloid beta and the receptor for advanced glycation endproducts in Alzheimer's disease.
Rev Neurosci
; 20(2): 95-110, 2009.
Article
en En
| MEDLINE
| ID: mdl-19774788
Hallmarks of Alzheimer's disease (AD) include the accumulation of amyloid beta peptide (Abeta), hyperphosphorylation of tau protein, and increased inflammatory activity in the hippocampus and cerebral cortex. The receptor for advanced glycation endproducts (RAGE) has been shown to interact with Abeta and to modulate Abeta transport across the blood-brain barrier. Furthermore, RAGE is upregulated at sites of inflammation and its activation results in distinct intracellular signaling cascades in respect to Abeta conformers. Besides Abeta, RAGE interacts with several members of the calcium binding S100 protein family, amphoterin and advanced glycation endproducts. Mounting evidence suggests that RAGE is a key player in the signaling pathways triggered by Abeta and S100 proteins in AD. In this review, we discuss recent discoveries about the crosstalk between RAGE, Abeta and S100 proteins in the pathophysiology of AD.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Receptores Inmunológicos
/
Calcio
/
Péptidos beta-Amiloides
/
Enfermedad de Alzheimer
Tipo de estudio:
Prognostic_studies
Límite:
Animals
/
Humans
Idioma:
En
Revista:
Rev Neurosci
Asunto de la revista:
NEUROLOGIA
Año:
2009
Tipo del documento:
Article
País de afiliación:
Estados Unidos
Pais de publicación:
Alemania