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Contenido archivado el 2024-05-29

Mitochondria and beta-amyloid in brain ischemia/reperfusion

Objetivo

This project is to test whether beta-amyloid peptide accumulates in mitochondria during brain ischemia/reperfusion, whether it impairs mitochondrial functions and induces cell death in a mitochondrial permeability transition-dependent way, and whether estrogens and antioxidants can prevent these events. Accumulation of beta-amyloid peptide (Abeta is a key factor in Alzheimer's disease (AD). Increased levels of Abeta are observed in both ischemia/reperfusion- and AD-damaged brains, and ischemia often precedes AD.

Mitochondria are the primary target of ischemia and subsequent reperfusion, and they are both the source and the target of reactive oxygen species (ROS) generated under hypoxic and reoxygenated conditions. Recent evidence indicates that Abeta accumulates intraneuronally and intramitochondrially. In mitochondria, Abeta is shown to inhibit cytochrome c oxidase, to change mitochondrial membrane properties, mitochondrial capacity to accumulate calcium, and to stimulate mitochondria-related apoptosis.

Ámbito científico (EuroSciVoc)

Palabras clave

Tema(s)

Convocatoria de propuestas

FP6-2004-MOBILITY-11
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Régimen de financiación

ERG - Marie Curie actions-European Re-integration Grants

Coordinador

LITHUANIAN UNIVERSITY OF HEALTH SCIENCES
Aportación de la UE
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Coste total
Sin datos