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2016 Grants - Dallas
Carbon Monoxide Suppression of Alzheimer’s Disease Pathology
Mark Dallas, Ph.D.
University of Reading
Reading, United Kingdom
2016 Alzheimer’s Association Research Grant (AARG)
Can carbon monoxide help protect nerve cells in the brain from toxic effects of beta-amyloid?
A hallmark of Alzheimer’s disease is the accumulation of the protein fragment beta-amyloid into plaques in the brain. Amyloid plaques are thought to interfere with nerve cell function and potentially contribute to impaired thinking and memory. Carbon monoxide (CO) is widely recognized as a toxic gas; however, small amounts of CO are naturally produced by the body’s cells. Recent studies by Mark Dallas, Ph.D., and colleagues found that CO could suppress the toxic effects of beta-amyloid in nerve cells growing in laboratory dishes. More research is needed to determine the mechanisms that may underlie the potentially protective effects of CO in the brain.
For their current work, Dr. Dallas and colleagues will determine if carbon monoxide may protect nerve cells and supporting cells called astrocytes in the brain. They hypothesize that CO may prevent calcium imbalances in the cells that can be triggered by beta-amyloid. Calcium is essential for cellular function, but must be tightly regulated since excessively high levels are toxic to cells. The researchers will expose nerve cells and astrocytes to beta-amyloid and then treat them with CO. They will measure changes in calcium levels, energy balance and cellular function.
If successful, this research may reveal the ability of carbon monoxide to protect brain cells against toxic effects of beta-amyloid. Importantly, these studies could lead to the development of new therapies that optimize the amount of carbon monoxide in the brain to help prevent or slow the progression of Alzheimer’s disease.