Role of Calcium in Familial Alzheimer’s Disease Clarified

In a recent study published in the Journal of Neuroscience, researchers from the Perelman School of Medicine at the University of Pennsylvania found mutations in two proteins associated with familial Alzheimer’s disease (FAD). The two proteins interact with a calcium release channel in an intracellular compartment. Mutant forms of these proteins that cause FAD, but not the normal proteins, result in exaggerated calcium signaling in the cell. Currently therapies for Alzheimer’s disease include drugs that treat the symptoms of cognitive loss and dementia, and drugs that address that pathology of Alzheimer’s are experimental. The new research suggests that approaches based on modulating calcium signaling could be explored. The two proteins, called PS1 and PS2 (presenilin 1 and 2), interact with a calcium release channel, the inositol trisphosphate receptor (IP3R), in the endoplasmic reticulum. “We set out to answer the question: Is increased calcium signaling, as a result of the presenilin-IP3R interaction, involved in the development of familial Alzheimer’s disease symptoms, including dementia and cognitive deficits?” said the lead author of the study. “And looking at the findings of these experiments, the answer is a resounding ‘yes.’“ To read more about this study, click here.