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Review
. 2018 Mar:70:87-94.
doi: 10.1016/j.ceca.2017.06.008. Epub 2017 Jun 30.

Calcium signaling and molecular mechanisms underlying neurodegenerative diseases

Ekaterina Pchitskaya  1 , Elena Popugaeva  2 , Ilya Bezprozvanny  3
Affiliations
Review

Calcium signaling and molecular mechanisms underlying neurodegenerative diseases

Ekaterina Pchitskaya et al. Cell Calcium. 2018 Mar.

Abstract

Calcium (Ca2+) is a ubiquitous second messenger that regulates various activities in eukaryotic cells. Especially important role calcium plays in excitable cells. Neurons require extremely precise spatial-temporal control of calcium-dependent processes because they regulate such vital functions as synaptic plasticity. Recent evidence indicates that neuronal calcium signaling is abnormal in many of neurodegenerative disorders such as Alzheimer's disease (AD), Huntington's disease (HD) and Parkinson's disease (PD). These diseases represent a major medical, social, financial and scientific problem, but despite enormous research efforts, they are still incurable and only symptomatic relief drugs are available. Thus, new approaches and targets are needed. This review highlight neuronal calcium-signaling abnormalities in these diseases, with particular emphasis on the role of neuronal store-operated Ca2+ entry (SOCE) pathway and its potential relevance as a therapeutic target for treatment of neurodegeneration.

Keywords: Alzheimer disease; Ca(2+) homeostasis; Ca(2+) signaling; Huntington disease; Neurodegeneration; Neuronal store-operated Ca(2+) channels; Neuronal store-operated Ca2+ entry; Parkinson disease.

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Figures

Figure 1
Figure 1
SOCE in neurons.
Figure 2
Figure 2
SOCE impairment in AD.
Figure 3
Figure 3
SOCE impairment in HD.
See this image and copyright information in PMC

References

    1. Alzheimer's Association Calcium Hypothesis, W. Calcium Hypothesis of Alzheimer's disease and brain aging: A framework for integrating new evidence into a comprehensive theory of pathogenesis. Alzheimers Dement. 2017;13:178–182 e117. - PubMed
    1. Arispe N, Diaz JC, Simakova O. Abeta ion channels. Prospects for treating Alzheimer's disease with Abeta channel blockers. Biochim Biophys Acta. 2007;1768:1952–1965. - PubMed
    1. Arispe N, Rojas E, Pollard HB. Alzheimer disease amyloid beta protein forms calcium channels in bilayer membranes: blockade by tromethamine and aluminum. Proc Natl Acad Sci U S A. 1993;90:567–571. - PMC - PubMed
    1. Arshad A, Chen X, Cong Z, Qing H, Deng Y. TRPC1 protects dopaminergic SH-SY5Y cells from MPP+, salsolinol, and N-methyl-(R)-salsolinol-induced cytotoxicity. Acta Biochim Biophys Sin. 2014;46:22–30. - PubMed
    1. Bandara S, Malmersjo S, Meyer T. Regulators of Calcium Homeostasis Identified by Inference of Kinetic Model Parameters from Live Single Cells Perturbed by siRNA. Science signaling. 2013;6:ra56. - PMC - PubMed

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