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2015 Grants - Storr
Toxicity Pathways and Catalytic Potential of Cu-Containing Aß Oligomers
Tim Storr, Ph.D.
Simon Fraser University
Burnaby, British Columbia, Canada
2015 New Investigator Research Grant
How do copper-containing beta-amyloid clumps promote the development of Alzheimer’s disease?
The protein fragment beta-amyloid has long been a key suspect in Alzheimer’s disease. Beta-amyloid molecules have a normal function, but in Alzheimer’s they form clumps called oligomers and plaques that may be toxic to nerve cells. Recent studies indicate that beta-amyloid is more likely to form toxic clumps when it interacts with charged metal particles called ions, especially copper ions. Researchers do not know exactly how this harmful interaction takes place, but it may result from copper ions becoming improperly regulated in the Alzheimer’s brain. More research is needed to understand how copper-containing oligomers exert their toxicity in the brain after they have formed.
Tim Storr, Ph.D., and colleagues will perform a series of experiments to examine how copper-containing amyloid oligomers affect nerve cell health. They will administer these oligomers to nerve cells grown in laboratory dishes and determine if they inhibit nerve cell function and cell-to-cell communication. They will also explore if these copper-containing oligomers could be used to help detect early brain changes associated with Alzheimer’s disease or targeted for the development of new treatments.
The results of these studies may provide new information on the biological factors underlying beta-amyloid’s toxicity in Alzheimer’s disease. If successful, the results of Dr. Storr’s effort could shed light on novel avenues for developing targeted therapies to slow or stop the progression of Alzheimer’s disease at its earliest stages.
Co-funded by the Alzheimer’s Association and Brain Canada Foundation