Mechanism of myelin breakdown in experimental demyelination: A putative role for calpain

Citation
Ke. Schaecher et al., Mechanism of myelin breakdown in experimental demyelination: A putative role for calpain, NEUROCHEM R, 26(6), 2001, pp. 731-737
Citations number
53
Categorie Soggetti
Neurosciences & Behavoir
Journal title
NEUROCHEMICAL RESEARCH
ISSN journal
03643190 → ACNP
Volume
26
Issue
6
Year of publication
2001
Pages
731 - 737
Database
ISI
SICI code
0364-3190(200106)26:6<731:MOMBIE>2.0.ZU;2-U
Abstract
Although calpain has been extensively studied, its physiological function i s poorly understood. In contrast, its role in the pathophysiology of variou s diseases has been implicated, including that of experimental allergic enc ephalomyelitis (EAE), an animal model of the demyelinating disease multiple sclerosis (MS). In EAE, calpain degrades myelin proteins, including myelin basic protein (MBP), suggesting a role for calpain in the breakdown of mye lin in this disease. Subsequent studies revealed increased calpain activity and expression in the glial and inflammatory cells concomitant with loss o f axon and myelin proteins. This suggested a crucial role for calpain in de myelinating diseases.