Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8480466 | Seminars in Cell & Developmental Biology | 2015 | 7 Pages |
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
Aβ peptidesCaMKIICyt CPolyQmGluRSTIM1SOCEOPCARyRsDUBNMDARQuisqualateVDCCInsP3RInsP3SUMF1CAMTA1adcACaBPsIICRBACE1cGMPMCUAPPSCAOPTCa2+Inositol 1,4,5-triphosphateα-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptorAtaxiaspinocerebellar ataxiaOlivopontocerebellar atrophydeubiquitinating enzymeautosomal dominant cerebellar ataxiaMitolong-term depressionMRIFADAlzheimer's diseaseFamilial Alzheimer diseaseHuntington's diseaseMagnetic resonance imaginglong-term potentiationLTPknock-inPurkinje cellcytochrome cendoplasmic reticulumclimbing fiberparallel fiberMitochondrial calcium uniporterLTDStromal interaction molecule 1cyclic guanosine monophosphateCANMitochondriaSynapseStore-operated calcium entryParvalbuminPresenilincalcium-binding proteinsamyloid precursor proteincalcium/calmodulin-dependent protein kinase IIPolyglutamineAmyloid beta peptidesCalbindin D-28kStore-operated calcium channelsCalciumCalcineuringlutamineAMPA receptorInositol 1,4,5-triphosphate receptorN-methyl-d-aspartate receptorRyanodine receptorsMetabotropic glutamate receptor
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Authors
Polina Egorova, Elena Popugaeva, Ilya Bezprozvanny,