Calcium signaling and molecular mechanisms underlying neurodegenerative diseases

Ekaterina Pchitskaya, Elena Popugaeva, Ilya Bezprozvanny

Research output: Contribution to journalArticle

40 Citations (Scopus)

Abstract

Calcium (Ca2+) is a ubiquitous second messenger that regulates various activities in eukaryotic cells. Especially important role calcium plays in excitable cells. Neurons require extremely precise spatial-temporal control of calcium-dependent processes because they regulate such vital functions as synaptic plasticity. Recent evidence indicates that neuronal calcium signaling is abnormal in many of neurodegenerative disorders such as Alzheimer's disease (AD), Huntington's disease (HD) and Parkinson's disease (PD). These diseases represent a major medical, social, financial and scientific problem, but despite enormous research efforts, they are still incurable and only symptomatic relief drugs are available. Thus, new approaches and targets are needed. This review highlight neuronal calcium-signaling abnormalities in these diseases, with particular emphasis on the role of neuronal store-operated Ca2+ entry (SOCE) pathway and its potential relevance as a therapeutic target for treatment of neurodegeneration.

Original languageEnglish (US)
JournalCell Calcium
DOIs
StateAccepted/In press - 2017

Fingerprint

Calcium Signaling
Neurodegenerative Diseases
Calcium
Neuronal Plasticity
Huntington Disease
Second Messenger Systems
Eukaryotic Cells
Parkinson Disease
Alzheimer Disease
Neurons
Research
Pharmaceutical Preparations
Therapeutics

Keywords

  • Alzheimer disease
  • Ca homeostasis
  • Ca signaling
  • Huntington disease
  • Neurodegeneration
  • Neuronal store-operated Ca2+ entry
  • Neuronal store-operated Ca channels
  • Parkinson disease

ASJC Scopus subject areas

  • Physiology
  • Molecular Biology
  • Cell Biology

Cite this

Calcium signaling and molecular mechanisms underlying neurodegenerative diseases. / Pchitskaya, Ekaterina; Popugaeva, Elena; Bezprozvanny, Ilya.

In: Cell Calcium, 2017.

Research output: Contribution to journalArticle

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