Format

Send to

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

Disturbed calcium signaling in spinocerebellar ataxias and Alzheimer's disease.

Author information

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

PMID:
25846864
PMCID:
PMC4433580
DOI:
10.1016/j.semcdb.2015.03.010
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Elsevier Science Icon for PubMed Central
Loading ...
Support Center