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2016 Grants - Zhu
Role of Aberrant Calcium Signaling in Mitochondrial Dynamics in Alzheimer’s Disease
Xiongwei Zhu, Ph.D.
Case Western Reserve University
2016 Alzheimer’s Association Research Grant (AARG)
Does beta-amyloid lead to excess calcium in nerve cells in Alzheimer’s disease?
Calcium is essential for the function of all cells and is particularly important for the unique functions of nerve cells in the brain. However, calcium levels inside of cells must be regulated very closely, since excessively high calcium levels are toxic to cells. Beta-amyloid, the protein fragment that forms plaques in the brains of people with Alzheimer’s, can trigger harmful changes in calcium levels which can damage nerve cells and may ultimately contribute to memory problems. One way in which abnormal levels of calcium can impact nerve cells is by leading to dysfunction of specialized structures called mitochondria which normally move around and provide energy to cells. More research is needed to better understand how beta-amyloid affects nerve cell calcium levels and mitochondrial function in Alzheimer’s disease.
Xiongwei Zhu, Ph.D. and colleagues have proposed a series of experiments using nerve cells grown in laboratory dishes to determine how beta-amyloid may alter calcium levels inside nerve cells, leading to loss of normal mitochondrial function. The researchers will examine the nerve cells under a microscope and measure changes in the shape, size and movement of mitochondria within the cells. They will also use manipulate the levels of calcium in the cells and explore how this impacts the activity of proteins that are critical to mitochondria function.
The results of this work could provide new insight into how beta-amyloid may lead to mitochondrial dysfunction and nerve cell loss during Alzheimer’s disease. The molecular mechanisms involved in this process could serve as novel targets for the development of treatments to slow or prevent Alzheimer’s disease.