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