Targeting calpain in synaptic plasticity

Michel Baudry1, Maggie M Chou, Xiaoning Bi

  • 1Western University of Health Sciences, Graduate College of Biomedical Sciences, Basic Medical Sciences, COMP , 309 E 2nd St, Pomona, CA 91766, USA. mbaudry@westernu.edu

Abstract

Insights

Calpains, calcium-dependent proteases, are involved in cell functions and neurodegeneration. Inhibiting calpain activity may offer therapeutic benefits for conditions linked to synaptic plasticity deregulation.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Biochemistry

Background:

  • Calpains are calcium-dependent proteases crucial for various cellular functions, including cell division, migration, and death.
  • In the central nervous system (CNS), µ-calpain and m-calpain isoforms are linked to synaptic plasticity and neurodegeneration.
  • This review focuses on the role of calpains in synaptic plasticity and their therapeutic potential.

Purpose of the Study:

  • To review the literature on calpain involvement in synaptic plasticity.
  • To explore the connection between calpain activity and learning impairments.
  • To discuss the potential for developing calpain-targeting therapeutics.

Main Methods:

  • Literature review of studies on calpains and synaptic plasticity.
  • Analysis of research linking calpains to learning and memory deficits.
  • Evaluation of therapeutic strategies targeting calpain activity.

Main Results:

  • Calpain activation is implicated in neurodegenerative processes and cancer.
  • A peptide targeting calpain demonstrated neuroprotective effects in neonatal hypoxia/ischemia models.
  • Calpain dysregulation is associated with altered synaptic plasticity.

Conclusions:

  • Therapeutic strategies involving calpain inhibition are of significant interest.
  • Development of selective calpain inhibitors or substrate-targeting drugs is needed.
  • Targeting calpains offers potential for treating conditions related to synaptic plasticity deregulation.

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