Disturbed calcium signaling in spinocerebellar ataxias and Alzheimer's disease

Polina Egorova; Elena Popugaeva; Ilya Bezprozvanny

doi:10.1016/j.semcdb.2015.03.010

Disturbed calcium signaling in spinocerebellar ataxias and Alzheimer's disease

Semin Cell Dev Biol. 2015 Apr:40:127-33. doi: 10.1016/j.semcdb.2015.03.010. Epub 2015 Apr 4.

Authors

Polina Egorova¹, Elena Popugaeva¹, Ilya Bezprozvanny²

Affiliations

¹ Laboratory of Molecular Neurodegeneration, St. Petersburg State Polytechnical University, St. Petersburg, Russia.
² Laboratory of Molecular Neurodegeneration, St. Petersburg State Polytechnical University, St. Petersburg, Russia; Department of Physiology, University of Texas Southwestern Medical Center at Dallas, Dallas, TX, USA. Electronic address: Ilya.Bezprozvanny@UTSouthwestern.edu.

Abstract

Neurodegenerative disorders, such as spinocerebellar ataxias (SCAs) and Alzheimer's disease (AD) represent a huge scientific and medical question, but the molecular mechanisms of these diseases are still not clear. There is increasing evidence that neuronal calcium signaling is abnormal in many neurodegenerative disorders. Abnormal neuronal calcium release from the endoplasmic reticulum may result in disturbances of cell homeostasis, synaptic dysfunction, and eventual cell death. Neuronal loss is observed in most cases of neurodegenerative diseases. Recent experimental evidence supporting the role of neuronal calcium signaling in the pathogenesis of SCAs and AD is discussed in this review.

Keywords: Alzheimer's disease; Ataxia; Calcium; Polyglutamine expansion disorders; Store-operated calcium entry; Synapse.

Publication types

Research Support, Non-U.S. Gov't
Review

MeSH terms

Alzheimer Disease / metabolism*
Alzheimer Disease / pathology
Animals
Calcium Signaling*
Humans
Spinocerebellar Ataxias / metabolism*
Spinocerebellar Ataxias / pathology
Synapses / pathology

Abstract

Publication types

MeSH terms

Grants and funding