Prion protein and Abeta-related synaptic toxicity impairment.
EMBO Mol Med
; 2(8): 306-14, 2010 Aug.
Article
en En
| MEDLINE
| ID: mdl-20665634
ABSTRACT
Alzheimer's disease (AD), the most common neurodegenerative disorder, goes along with extracellular amyloid-beta (Abeta) deposits. The cognitive decline observed during AD progression correlates with damaged spines, dendrites and synapses in hippocampus and cortex. Numerous studies have shown that Abeta oligomers, both synthetic and derived from cultures and AD brains, potently impair synaptic structure and functions. The cellular prion protein (PrP(C)) was proposed to mediate this effect. We report that ablation or overexpression of PrP(C) had no effect on the impairment of hippocampal synaptic plasticity in a transgenic model of AD. These findings challenge the role of PrP(C) as a mediator of Abeta toxicity.
Texto completo:
1
Bases de datos:
MEDLINE
Asunto principal:
Sinapsis
/
Priones
/
Péptidos beta-Amiloides
/
Enfermedad de Alzheimer
/
Hipocampo
Tipo de estudio:
Prognostic_studies
Límite:
Animals
/
Humans
Idioma:
En
Revista:
EMBO Mol Med
Asunto de la revista:
BIOLOGIA MOLECULAR
Año:
2010
Tipo del documento:
Article
País de afiliación:
Suiza