Review Article
Roles of Sodium-Calcium Exchanger Isoform-3 toward Calcium Ion Regulation in Alzheimers Disease
Henok KA1,3*, Tongmei Zhang2,3, Hao Li2,3 and Youming Lu2,31Department of Pathology and Pathophysiololgy, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
2Department of Physiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
3Institute for Brain Research, Collaborative Innovation Center for Brain Science, Huazhong University of Science and Technology, Wuhan, China
- *Corresponding Author:
- Henok Kessete Afewerky
Department of Pathology and Pathophysiology
Tongji Medical College, Huazhong University of Science and Technology
Wuhan, Hubei, 430030, China
Tel: 0086-13260654649
E-mail: henokessete@hust.edu.cn
Received date: December 01, 2016; Accepted date: December 12, 2016; Published date: December 19, 2016
Citation: Henok KA, Zhang T, Li H, Lu Y(2016) Roles of Sodium-Calcium Exchanger Isoform-3 toward Calcium Ion Regulation in Alzheimers Disease. J Alzheimers Dis Parkinsonism 6:291. doi:10.4172/2161-0460.1000291
Copyright: © 2016 Henok KA, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Alzheimer’s disease (AD) is a late-onset progressive neurodegenerative disorder that leads to cognitive, memory and behavioural impairments. Substantial evidence indicates that disrupted neuronal calcium homeostasis is an early event in AD that could mediate synaptic dysfunction and neuronal toxicity. Sodium calcium exchangers (NCXs) play important roles in regulating intracellular calcium, and accumulated data suggests that reduced NCX function, following aberrant proteolytic cleavage of these exchangers, may contribute to neurodegeneration. This review, characterizes the expression and activity of NCX as a prominent feature of AD brain, identifies the molecular mechanisms underlying the effects of NCX isoforms, and pinpoints the molecular determinants responsible for the effects of NCX. Our findings suggest that calpain mediates cleavage of NCX3 in AD brain and therefore that reduced NCX3 activity contributes to the sustained increases in intraneuronal calcium concentrations that are associated with caspase-12 activation and neuronal death in AD.
