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La proteína priónica como receptor para el beta amiloide
Helmut W Kessels1, Louis N Nguyen, Sadegh Nabavi
1Center for Neural Circuits and Behavior, 9500 Gilman Drive 0634, University of California at San Diego, La Jolla, California 92093, USA.
Este estudio muestra que la proteína priónica celular (PrP(C)) no es necesaria para que el beta amiloide cause defectos sinápticos en modelos de la enfermedad de Alzheimer. La amiloide-beta perjudica la función cerebral independientemente de la PrP.
Área de la Ciencia:
- La neurociencia es la neurociencia.
- Biología Molecular Biología Molecular
- La bioquímica es la bioquímica.
Sus antecedentes:
- El aumento de los niveles de beta-amiloide (Aβ) en el cerebro está implicado en la etiología de la enfermedad de Alzheimer (EA).
- La Aβ está relacionada con la disfunción sináptica, incluida la depresión, la reducción de la densidad de la columna vertebral y el bloqueo de la potenciación a largo plazo (LTP).
- El receptor específico que media los efectos sinápticos de Aβ no ha sido claro.
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