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Neurochem Res. 2009 Oct;34(10):1824-9. doi: 10.1007/s11064-009-9960-5. Epub 2009 Apr 1.

Dysregulation of calcium homeostasis in Alzheimer's disease.

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Menzies Research Institute, University of Tasmania, Private Bag 24, Hobart, TAS 7001, Australia.


The accumulation of oligomeric species of beta-amyloid protein in the brain is considered to be a key factor that causes Alzheimer's disease (AD). However, despite many years of research, the mechanism of neurotoxicity in AD remains obscure. Recent evidence strongly supports the theory that Ca2+ dysregulation is involved in AD. Amyloid proteins have been found to induce Ca2+ influx into neurons, and studies on transgenic mice suggest that this Ca2+ influx may alter neuronal excitability. The identification of a risk factor gene for AD that may be involved in the regulation of Ca2+ homeostasis and recent findings which suggest that presenilins may be involved in the regulation of intracellular Ca2+ stores provide converging lines of evidence that support the idea that Ca2+ dysregulation is a key step in the pathogenesis of AD.

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