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Content archived on 2024-05-29

Mitochondria and beta-amyloid in brain ischemia/reperfusion

Objective

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.

Fields of science (EuroSciVoc)

Keywords

Topic(s)

Call for proposal

FP6-2004-MOBILITY-11
See other projects for this call

Funding Scheme

ERG - Marie Curie actions-European Re-integration Grants

Coordinator

LITHUANIAN UNIVERSITY OF HEALTH SCIENCES
EU contribution
No data
Total cost
No data