In a surprising new study published online in Neurobiology of Disease, researchers in the lab of Dr. Robert Friedlander, a professor at the University of Pittsburg School of Medicine, found that melatonin delayed the onset of symptoms and prolonged survival in SOD1 G93A mice. The researchers reported that melatonin appears to work by preventing apoptosis through a multipronged-approach, including inhibiting cytochrome c release, inhibiting the activation of the Rip2/caspase-1 pathway, and by reducing the levels and activation of caspase-3. Furthermore, the group found that disease progression in these mice was associated with melatonin receptor 1A loss and low levels of melatonin in the spinal cord. This work raises intriguing questions around the role of apoptosis in ALS. Click here to read the full story.
Zhang Y, Cook A, Kim J, Baranov SV, Jiang J, Smith K, Cormier K, Bennett E, Browser RP, Day AL, Carlisle DL, Ferrante RJ, Wang X, Friedlander RM. Melatonin inhibits the caspase-1/cytochrome c/caspase-3 cell death pathway, inhibits MT1 receptor loss and delays disease progression in a mouse model of amyotrophic lateral sclerosis. Neurobiology of Disease, 2013, March 26. Abstract
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