Crosstalk between calpain and calcineurin in excitotoxic neurodegeneration; therapeutic targets for the treatment of excitotoxic neurodegeneration

Hai Yan Wu, Hideki Matsui, Kazuhito Tomizawa

Research output: Contribution to journalReview article

2 Citations (Scopus)

Abstract

The accumulation of high local concentrations of excitatory amino acids, particularly glutamate, is involved in neuronal cell death in neurodegenerative diseases such as stroke, trauma, Huntington's disease, and amyotrophic lateral sclerosis. Accumulation of glutamate leads to excessive Ca2+ influx into the neuron. The molecules involved in neuronal degeneration following intracellular Ca2+ overload have been identified. Calcineurin and calpain, a Ca2+/calmodulin-dependent protein phosphatase and Ca 2+-dependent cysteine protease, respectively, are two of the most important Ca2+-dependent effectors during neuronal degeneration. These two molecules have been thought to mediate neuronal degeneration through independent cascades. However, recent studies have shown that a cross-talk pathway exists between calcineurin and calpain in neurons and the pathway plays a critical role in excitotoxic neuronal degeneration. This review covers recent findings regarding the cross-talk pathway involved in neuronal degeneration and novel neuroprotective reagents that block the signal pathway.

Original languageEnglish
Pages (from-to)207-216
Number of pages10
JournalCurrent Medicinal Chemistry - Central Nervous System Agents
Volume5
Issue number3
DOIs
Publication statusPublished - Sep 2005
Externally publishedYes

Keywords

  • Alzheimer's disease
  • Calcineurin
  • Calpain
  • Neuronal apoptosis
  • Neuronal degeneration

ASJC Scopus subject areas

  • Neuroscience(all)
  • Neuropsychology and Physiological Psychology
  • Molecular Medicine

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