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Mitochondria and beta-amyloid in brain ischemia/reperfusion

Obiettivo

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.

Campo scientifico (EuroSciVoc)

Parole chiave

Argomento(i)

Invito a presentare proposte

FP6-2004-MOBILITY-11
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Meccanismo di finanziamento

ERG - Marie Curie actions-European Re-integration Grants

Coordinatore

LITHUANIAN UNIVERSITY OF HEALTH SCIENCES
Contributo UE
Nessun dato
Costo totale
Nessun dato