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Dysregulation of Calcium Homeostasis in Alzheimer's Disease

Citation

Small, DH, Dysregulation of Calcium Homeostasis in Alzheimer's Disease, Neurochemical Research, 34, (10) pp. 1824-1829. ISSN 0364-3190 (2009) [Refereed Article]

DOI: doi:10.1007/s11064-009-9960-5

Abstract

The accumulation of oligomeric species of b-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.

Item Details

Item Type:Refereed Article
Keywords:Amyloid; Calcium; Toxicity; Alzheimer’s disease; Dementia
Research Division:Medical and Health Sciences
Research Group:Neurosciences
Research Field:Neurosciences not elsewhere classified
Objective Division:Health
Objective Group:Clinical Health (Organs, Diseases and Abnormal Conditions)
Objective Field:Neurodegenerative Disorders Related to Ageing
Author:Small, DH (Professor David Small)
ID Code:61401
Year Published:2009
Web of Science® Times Cited:50
Deposited By:Menzies Institute for Medical Research
Deposited On:2010-03-03
Last Modified:2010-04-16
Downloads:0

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