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Literature DB >> 25846864

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

Polina Egorova¹, Elena Popugaeva¹, Ilya Bezprozvanny².

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.

Entities: CellLine Chemical Disease Gene Mutation Species

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

Mesh：

Year: 2015 PMID： 25846864 PMCID： PMC4433580 DOI： 10.1016/j.semcdb.2015.03.010

Source DB: PubMed Journal: Semin Cell Dev Biol ISSN： 1084-9521 Impact factor: 7.727

97 in total

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Authors: Adebimpe W Kasumu; Xia Liang; Polina Egorova; Daria Vorontsova; Ilya Bezprozvanny
Journal: J Neurosci Date: 2012-09-12 Impact factor: 6.167

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6. A store-operated Ca(2+) influx pathway in the bag cell neurons of Aplysia.

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8. Abnormalities in the climbing fiber-Purkinje cell circuitry contribute to neuronal dysfunction in ATXN1[82Q] mice.

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2. Nicotinamide Pathway-Dependent Sirt1 Activation Restores Calcium Homeostasis to Achieve Neuroprotection in Spinocerebellar Ataxia Type 7.

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Journal: Cerebellum Date: 2019-12 Impact factor: 3.847

4. In vivo analysis of cerebellar Purkinje cell activity in SCA2 transgenic mouse model.

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5. In Vivo Analysis of the Climbing Fiber-Purkinje Cell Circuit in SCA2-58Q Transgenic Mouse Model.

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6. P2X receptor overexpression induced by soluble oligomers of amyloid beta peptide potentiates synaptic failure and neuronal dyshomeostasis in cellular models of Alzheimer's disease.

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