ScienceDaily (July 17, 2008) — Researchers at the University of Pennsylvania School of Medicine have shown that mutations in two proteins associated with familial Alzheimer's disease disrupt the flow of calcium ions within neurons. The two proteins, called PS1 and PS2 (presenilin 1 and 2), interact with a calcium release channel in an intracellular cell compartment.
“The ‘calcium dysregulation’ hypothesis for inherited, early onset familial Alzheimer's disease has been suggested by previous research findings, but our current study identifies a molecular mechanism that makes this hypothesis very compelling,” says lead author J. Kevin Foskett, PhD, Professor of Physiology. “Mutated PS1 and PS2 caused exaggerated cellular calcium signaling in cells through a calcium channel in the endoplasmic reticulum called the inositol trisphosphate receptor [InsP3R], suggesting that it or other proteins in this calcium signaling pathway could be targets for new Alzheimer’s disease therapies.” The study appeared in the June 26 issue of Neuron.
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