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Dysregulation of Calcium Homeostasis in Alzheimer’s Disease

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Abstract

The accumulation of oligomeric species of β-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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  1. Menzies Research Institute, University of Tasmania, Private Bag 24, Hobart, TAS, 7001, Australia

    David H. Small

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Correspondence to David H. Small.

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Special issue article in Honor of Dr. Graham Johnston.

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Small, D.H. Dysregulation of Calcium Homeostasis in Alzheimer’s Disease. Neurochem Res 34, 1824–1829 (2009). https://doi.org/10.1007/s11064-009-9960-5

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  • DOI: https://doi.org/10.1007/s11064-009-9960-5

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