Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2006 Summer;12(2):135-48.
doi: 10.1111/j.1527-3458.2006.00135.x.

Involvement of calpain activation in neurodegenerative processes

Antoni Camins  1 , Ester Verdaguer, Jaume Folch, Mercè Pallàs
Affiliations
Review

Involvement of calpain activation in neurodegenerative processes

Antoni Camins et al. CNS Drug Rev. 2006 Summer.

Abstract

One of the challenges in the coming years will be to better understand the mechanisms of neuronal cell death with the objective of developing adequate drugs for the treatment of neurodegenerative disorders. Caspases and calpains are among the best-characterized cysteine proteases activated in brain disorders. Likewise, during the last decade, extensive research revealed that the deregulation of calpains activity is a key cytotoxic event in a variety of neurodegenerative disorders. Moreover, interest in the role of calpain in neurodegenerative processes is growing due to implication of the involvement of cdk5 in neurodegenerative diseases. Since calpain inhibitors appear to not only protect brain tissue from ischemia, but also to prevent neurotoxicity caused by such neurotoxins as beta-amyloid or 3-nitropropionic acid, the currently available data suggest that calpain and cdk5 play a key role in neuronal cell death. It seems clear that the inappropriate activation of cysteine proteases occurs not only during neuronal cell death, but may also contribute to brain pathology in ischemia and traumatic brain disorders. Pharmacological modulation of calpain activation may, therefore, be useful in the treatment of neurodegenerative disorders. It is possible, although difficult, to develop synthetic inhibitors of cysteine proteases, specifically calpains. The inhibition of calpain activation has recently emerged as a potential therapeutic _target for the treatment of neurodegenerative diseases.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Alavez S, Moran J, Franco‐Cea A, Ortega‐Gomez A, Casaletti L, Cameron LC. Myosin Va is proteolysed in rat cerebellar granule neurons after excitotoxic injury. Neurosci Lett 2004;367(9):404–409. - PubMed
    1. Alvarez A, Toro R, Caceres A, Maccioni RB. Inhibition of tau phosphorylating protein kinase cdk5 prevents beta‐amyloid‐induced neuronal death. FEBS Lett 1999;459: 421–426. - PubMed
    1. Araujo IM, Verdasca MJ, Leal EC, et al. Early calpain‐mediated proteolysis following AMPA receptor activation compromises neuronal survival in cultured hippocampal neurons. J Neurochem 2004;91: 1322–1331. - PubMed
    1. Banay‐Schwartz M, DeGuzman T, Palkovits M, Lajtha A. Calpain activity in adult and aged human brain regions. Neurochem Res 1994;19: 563–567. - PubMed
    1. Bano D, Young KW, Guerin CJ, et al. C leavage of the plasma membrana Na+/Ca2+ exchanger in excitotoxicity. Cell 2005;120: 275–285. - PubMed

Publication types

  NODES
twitter 2