Aug 24, 2013

Role of calpains in the injury-induced dysfunction and degeneration of the mammalian axon

Neurobiology of Disease
Marek Ma

Abstract

Axonal injury and degeneration, whether primary or secondary, contribute to the morbidity and mortality seen in many acquired and inherited central nervous system (CNS) and peripheral nervous system (PNS) disorders, such as traumatic brain injury, spinal cord injury, cerebral ischemia, neurodegenerative diseases, and peripheral neuropathies. The calpain family of proteases has been mechanistically linked to the dysfunction and degeneration of axons. While the direct mechanisms by which transection, mechanical strain, ischemia, or complement activation trigger intra-axonal calpain activity are likely different, the downstream effects of unregulated calpain activity may be similar in seemingly disparate diseases. In this review, a brief examination of axonal structure is followed by a focused overview of the calpain family. Finally, the mechanisms by which calpains may disrupt the axonal cytoskeleton, transport, and specialized domains (axon initial segment, nodes, and terminals) are discussed.

Mentioned in this Paper

Post-Traumatic Myelopathy
Establishment and Maintenance of Localization
Ischemia
Calpain II
Brain Injuries
Mild Traumatic Brain Injury
Percussion
Nervousness
Biochemical Pathway
Calpain Activity

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