Role of PrPC Expression in Tau Protein Levels and Phosphorylation in Alzheimer¿s Disease Evolution
Springer Science+Business Media New York 2014 Abstract Alzheimer’s disease (AD) is characterized by the presence of amyloid plaques mainly consisting of hydrophobic β-amyloid peptide (Aβ) aggregates and neurofibrillary tangles (NFTs) composed principally of hyperphosphorylated tau.Aβ oligomers have...
| Autores: | , , , , , |
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| Tipo de recurso: | otro |
| Estado: | Versión publicada |
| Fecha de publicación: | 2014 |
| País: | España |
| Institución: | Consejo Superior de Investigaciones Científicas (CSIC) |
| Repositorio: | DIGITAL.CSIC. Repositorio Institucional del CSIC |
| OAI Identifier: | oai:digital.csic.es:10261/140268 |
| Acceso en línea: | http://hdl.handle.net/10261/140268 |
| Access Level: | acceso abierto |
| Palabra clave: | Aβ oligomers Cellular prion protein Alzheimer’s disease Microtubule-associated protein tau |
| Sumario: | Springer Science+Business Media New York 2014 Abstract Alzheimer’s disease (AD) is characterized by the presence of amyloid plaques mainly consisting of hydrophobic β-amyloid peptide (Aβ) aggregates and neurofibrillary tangles (NFTs) composed principally of hyperphosphorylated tau.Aβ oligomers have been described as the earliest effectors to negatively affect synaptic structure and plasticity in the affected brains, and cellular prion protein (PrPC) has been proposed as receptor for these oligomers. The most widely accepted theory holds that the toxic effects ofAβ are upstream of change in tau, a neuronal microtubule-associated protein that promotes the polymerization and stabilization of microtubules. However, tau is considered decisive for the progression of neurodegeneration, and, indeed, tau pathology |
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