title: Disturbed calcium signaling in spinocerebellar ataxias and Alzheimer's disease.
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.
authors.affiliation: Laboratory of Molecular Neurodegeneration, St. Petersburg State Polytechnical University, St. Petersburg, Russia.
authors.forename: Polina
authors.initials: P
authors.lastname: Egorova
authors.affiliation: Laboratory of Molecular Neurodegeneration, St. Petersburg State Polytechnical University, St. Petersburg, Russia.
authors.forename: Elena
authors.initials: E
authors.lastname: Popugaeva
authors.affiliation: 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.
authors.forename: Ilya
authors.initials: I
authors.lastname: Bezprozvanny
mesh_terms: D000544:Alzheimer Disease / Q000378:metabolism* / Q000473:pathology; D000818:Animals; D020013:Calcium Signaling; D006801:Humans; D020754:Spinocerebellar Ataxias / Q000378:metabolism* / Q000473:pathology; D013569:Synapses / Q000473:pathology
keywords: Alzheimer's disease; Ataxia; Calcium; Polyglutamine expansion disorders; Store-operated calcium entry; Synapse
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