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Published Online: 29 January 2009

Mechanisms of Calpain Proteolysis Following Traumatic Brain Injury: Implications for Pathology and Therapy: A Review and Update

Publication: Journal of Neurotrauma
Volume 14, Issue Number 3

ABSTRACT

Much recent research has focused on the pathological significance of calcium accumulation in the central nervous system (CNS) following cerebral ischemia, spinal cord injury (SCI), and traumatic brain injury (TBI). Disturbances in neuronal calcium homeostasis may result in the activation of several calcium-sensitive enzymes, including lipases, kinases, phosphatases, and proteases. One potential pathogenic event in a number of acute CNS insults, including TBI, is the activation of the calpains, calcium-activated intracellular proteases. This article reviews new evidence indicating that overactivation of calpains plays a major role in the neurodegenerative cascade following TBI in vivo. Further, this article presents an overview from in vivo and in vitro models of CNS injuries suggesting that administration of calpain inhibitors during the initial 24-h period following injury can attenuate injury-induced derangements of neuronal structure and function. Lastly, this review addresses the potential contribution of other proteases to neuronal damage following TBI.

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cover image Journal of Neurotrauma
Journal of Neurotrauma
Volume 14Issue Number 3MARCH 1997
Pages: 121 - 134
PubMed: 9104930

History

Published online: 29 January 2009
Published in print: MARCH 1997

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