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Dysregulation of neural calcium signaling in Alzheimer disease, bipolar disorder and schizophrenia

Prion. 2013 Jan-Feb;7(1):2-13. doi: 10.4161/pri.21767. Epub 2012 Aug 16.

Abstract

Neurons have highly developed Ca(2+) signaling systems responsible for regulating a large number of neural functions such as the control of brain rhythms, information processing and the changes in synaptic plasticity that underpin learning and memory. The tonic excitatory drive, which is activated by the ascending arousal system, is particularly important for processes such as sensory perception, cognition and consciousness. The Ca(2+) signaling pathway is a key component of this arousal system that regulates the neuronal excitability responsible for controlling the neural brain rhythms required for information processing and cognition. Dysregulation of the Ca(2+) signaling pathway responsible for many of these neuronal processes has been implicated in the development of some of the major neural diseases in man such as Alzheimer disease, bipolar disorder and schizophrenia. Various treatments, which are known to act by reducing the activity of Ca(2+) signaling, have proved successful in alleviating the symptoms of some of these neural diseases.

Keywords: Alzheimer disease; bipolar disease; calcium; inositol trisphosphate; reactive oxygen species; schizophrenia.

Publication types

  • Review

MeSH terms

  • Alzheimer Disease / metabolism*
  • Alzheimer Disease / pathology
  • Animals
  • Bipolar Disorder / metabolism*
  • Bipolar Disorder / pathology
  • Brain-Derived Neurotrophic Factor / metabolism
  • Calcium / metabolism
  • Calcium Signaling*
  • Humans
  • Neurons / metabolism
  • Neurons / pathology
  • Receptors, N-Methyl-D-Aspartate / metabolism
  • Schizophrenia / metabolism*
  • Schizophrenia / pathology

Substances

  • Brain-Derived Neurotrophic Factor
  • Receptors, N-Methyl-D-Aspartate
  • Calcium