These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Upregulation of calpain correlates with increased neurodegeneration in acute experimental auto-immune encephalomyelitis.
    Author: Guyton MK, Wingrave JM, Yallapragada AV, Wilford GG, Sribnick EA, Matzelle DD, Tyor WR, Ray SK, Banik NL.
    Journal: J Neurosci Res; 2005 Jul 01; 81(1):53-61. PubMed ID: 15952172.
    Abstract:
    Although calpain up-regulation is well established in experimental auto-immune encephalomyelitis (EAE), a link between increased calpain expression and activity and neurodegeneration has not been examined. Therefore, spinal cord tissue from Lewis rats with EAE was examined to test the hypothesis that increased calpain expression in neurons would correlate with increased cell death and axonal damage in a time-dependent manner following EAE induction. We found that increased calpain expression in EAE corresponded to increased TUNEL-positive neurons and to increased expression of dephosphorylated neurofilament protein, markers of cell death and axonal degeneration, respectively. An increase in internucleosomal DNA fragmentation in EAE spinal cord suggested that cell death was, at least partially, due to apoptosis. Axonal damage was further demonstrated in EAE spinal cord compared with control via morphological analysis, revealing granular degeneration of filament and microtubule integrity, loss of myelin, and mitochondrial damage. Calcium (Ca2+) influx, which is required for calpain activation, was also increased in EAE spinal cord. From these findings, we conclude that increases in Ca2+-induced calpain activity may play a crucial role in neurodegeneration in acute EAE.
    [Abstract] [Full Text] [Related] [New Search]