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.