Ahmed, Z; Doward, AI; Pryce, G; Taylor, DL; Pocock, JM; Leonard, JP; ... Cuzner, ML; + view all Ahmed, Z; Doward, AI; Pryce, G; Taylor, DL; Pocock, JM; Leonard, JP; Baker, D; Cuzner, ML; - view fewer (2002) A role for caspase-1 and-3 in the pathology of experimental allergic encephalomyelitis - Inflammation versus degeneration. AM J PATHOL , 161 (5) 1577 - 1586.
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Axonal loss, already present in the acute and first relapse phases of experimental allergic encephalomyelitis (EAE) in the ABH mouse, only becomes apparent in the third relapse in the interleukin-12 model of relapsing EAE in the Lewis rat. Caspase-1 immunostaining in the spinal cord of Lewis rats was mainly localized to inflammatory cuffs with the greatest proportion of active caspase-1-positive cells detected during the first and second relapses, correlating with enzyme activity and protein on Western blots. However, in the spinal cord of ABH mice during acute EAE, caspase-1 immunostaining was localized both on inflammatory and neuronal cells, again correlating with enzyme activity and protein production. In contrast, caspase-3 expression in the spinal cord of Lewis rats did not increase significantly until the third relapse when inflammatory and neuronal cells and axons became positive in line with a significant increase in caspase activity. In ABH mice active caspase-3 was already immunolocalized. on axons and apoptotic neurons in the spinal cord during the acute stage of EAE. Because caspase-3 is a downstream cell death signal it may be possible to reduce apoptosis by selectively blocking caspase-3 and therefore provide a therapeutic target for EAE and potentially, multiple sclerosis.
|Title:||A role for caspase-1 and-3 in the pathology of experimental allergic encephalomyelitis - Inflammation versus degeneration|
|Keywords:||NEURONAL APOPTOSIS, CHROMOGRANIN-A, SPINAL-CORD, LEWIS RAT, ENZYME, ACTIVATION, CELLS, PROTEASES, PATHWAYS, CLEAVAGE|
|UCL classification:||UCL > School of Life and Medical Sciences > Faculty of Brain Sciences > Institute of Neurology > IoN - Neuroinflammation|
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