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2009 Grants - Norman
Functional Analysis of SEL-12/Presenilin on Calcium Release in C. elegans
Kenneth Norman, Ph.D.
Albany Medical College
Albany, New York
2009 New Investigator Research Grant
Presenilins are proteins strongly implicated in Alzheimer's disease. Indeed, about 40% of inherited cases of Alzheimer's disease can be attributed to a mutation in one of the presenilin genes. The function of presenilin proteins is not completely understood, although these proteins have been implicated in several processes that could explain their role in Alzheimer's disease.
A major reason for the difficulty in understanding the function of presenilins is the complexity of mammalian genes and cells. To overcome this difficulty, Kenneth Norman, Ph.D. and colleagues are studying the role of presenilins in a simple invertebrate organism, the nematode worm Caenorhabditis elegans (C. elegans). The researchers have already found evidence that the presenilin gene in these organisms is important for regulation of calcium signaling inside cells. Calcium signaling is a tightly regulated function of all cells, and dysfunction of calcium signaling can cause severe consequences, including cell death.
Dr. Norman and colleagues propose to study how presenilin proteins regulate calcium signaling in the cells of C. elegans. These organisms are a valuable model because their genetics are thoroughly understood, and can be manipulated experimentally. Therefore, Dr. Norman's team plans to use genetic techniques, as well as calcium imaging methods, to explore the role of presenilins in calcium signaling. It is known that calcium signaling pathways in a wide range of organisms operate in a similar fashion. Thus, these experiments will advance our understanding of how presenilin mutations affect calcium signaling in brain cells, improving our understanding of the mechanisms by which these mutations contribute to Alzheimer pathology.