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Conclusions

Since calpaun expression is upregulated in activated glial/inflammatory cells in EAE, increases in calpaun activity and expression may be a result of cell activation, and thus present in all inflammatory responses. Future studies employing calpaun-specific inhibitors are therefore needed to (1) elucidate the role(s) of calpaun in autoimmune demyelinating diseases and (2) evaluate the potential for possible therapeutic benefits associated therewith.

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Shields, D.C., Banik, N.L. (2002). Calcium Activated Neutral Proteinase in Demyelinating Diseases. In: Lajtha, A., Banik, N.L. (eds) Role of Proteases in the Pathophysiology of Neurodegenerative Diseases. Springer, Boston, MA. https://doi.org/10.1007/0-306-46847-6_3

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