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2015 Grants - Stutzmann
Intracellular Ca2+ Channels as a Therapeutic Target for Alzheimer’s Drug Discovery
Grace E. Stutzmann, Ph.D.
Rosalind Franklin University of Medicine and Science
North Chicago, Illinois
2015 Discovery-Validation of Therapeutic Targets for Developing Novel Interventions of Alzheimer’s Disease Grant
Could drugs that stabilize calcium levels inside nerve cells be developed as a treatment for Alzheimer’s disease?
Calcium is essential for the normal function of all cells and is particularly important for the unique functions of nerve cells. However, calcium levels inside of cells must be regulated very closely, since excessively high calcium levels are toxic to cells. In Alzheimer’s disease, there is evidence that calcium levels inside nerve cells become too high. This can impair the ability of the cells to function properly and ultimately lead to loss of memory and other cognitive abilities.
One way cells regulate their own calcium levels is by storing it inside specialized compartments and releasing it only at controlled times. Calcium is released from these compartments by calcium channels inside the cell that can open and close. Some evidence suggests that these channels may be dysregulated in Alzheimer’s disease and drugs aimed at restoring the function of calcium channels could be used to help treat Alzheimer’s disease.
Grace E. Stutzmann, Ph.D., and colleagues have developed several novel drug candidates that stabilize calcium channels and prevent calcium levels from reaching toxic levels. They have proposed a series of experiments to further develop these drug candidates and test their ability to prevent cell damage in nerve cells growing in laboratory dishes and in mice that have been genetically engineered to have an Alzheimer’s-like condition. The researchers will test if these drug candidates can regulate calcium levels in the brain and preserve nerve cell structure and function.
These studies represent the initial steps in the development of drugs to stabilize calcium levels in nerve cells during the early stages of Alzheimer’s disease. If successful, the results of this work could provide the foundation for moving these potential drug candidates into human clinical trials for the treatment of Alzheimer’s disease.