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2008 Grants - Stutzmann
Neuronal Ca2+ Dysregulation as a Pathogenic Factor in Alzheimer's Disease
Grace Stutzmann, Ph.D.
Rosalind Franklin University of Medicine and Science
North Chicago, Illinois
2008 New Investigator Research Grant
Although amyloid plaque, neurofibrillary tangles and cognitive decline are recognized as hallmarks of Alzheimer's disease, researchers also recognize that other pathologic changes occur long before these hallmarks can be observed. One such early pathologic change may involve the regulation of ionized calcium (Ca2+) inside nerve cells (neurons).
Ca2+ levels inside cells are normally regulated very strictly. One mechanism for such strict regulation is controlled storage and release of Ca2+ from the endoplasmic reticulum (ER), an extensive structure inside living cells. In mice that have been genetically engineered to express Alzheimer-like pathology, however, there is evidence that Ca2+ release from the ER is increased. This effect would be expected to increase Ca2+ levels in the cell and alter many aspects of cell function, possibly contributing to cell dysfunction or death.
Grace Stutzmann, Ph.D., and colleagues are studying how increased Ca2+ release from the ER affects the function of cellular processes linked to Alzheimer pathology, especially the generation of neurofibrillary tangles, amyloid plaque and neuronal dysfunction. They will study these effects in brain slices from mice with genes expressing Alzheimer-like pathology. These studies may provide insight into the very early steps leading to the neuronal dysfunction and pathological features of Alzheimer's disease.