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The Characterisation Of The Mechanism Of Beta Amyloid Toxicity In Alzheimer's Disease
Funder
National Health and Medical Research Council
Funding Amount
$94,430.00
Summary
Alzheimer�s disease (AD) is the most common form of dementia and is characterised by the beta amyloid peptide (A_) found in plaques in the brain. A structural transition to aggregated/ oligomeric forms of A_ is accompanied by a gain of toxicity. In this study the biological and biophysical characterisation of a variety of A_ peptides will be performed. The study will also use oligomers from cell culture media and brain tissue that have been influential in AD research but poorly characterised.
Most normal cells naturally cease their growth because their chromosomes erode from repeated cell division. The erosion takes place at the ends of the chromosomes, or telomeres. All cancer cells avoid this erosion, and thus fail to cease their growth. About 85% of all cancers achieve this by activating an enzyme called telomerase, an enzyme that allows cancer cells to avoid the natural ageing process. This project aims to understand how this enzyme gets recruited to chromosome ends.