Posted on Jun 10, 2013, 6 a.m.
Researchers find that a lack of the hormone melatonin is associated with the progression of an animal model of the neurodegenerative disease amyotrophic lateral sclerosis.
New research suggests that the sleep hormone melatonin may prove useful in the treatment of the fatal neurodegenerative disease amyotrophic lateral sclerosis (ALS). Robert Friedlander, M.D., Professor of neurosurgery and neurobiology at Pitt School of Medicine, and colleagues treated a mouse model of ALS-with injections of melatonin or with a placebo. Results showed that compared to untreated mice, mice treated with melatonin developed symptoms later, survived longer, and had less degeneration of motor neurons in the spinal cord. The study is the first to demonstrate that a lack of melatonin and/or its receptor, melatonin receptor 1 (MT1), is associated with the progression of ALS. The authors concluded that their findings show that melatonin is neuroprotective and that melatonin and modulation of MT1 pathways “may be promising therapeutic approaches for ALS”.
Yi Zhang, Anna Cook, Jinho Kim, Sergei V. Baranov, Jiying Jiang, Karen Smith, Kerry Cormier, Erik Bennett, Robert P. Browser, Arthur L Day, Diane L Carlisle, Robert J Ferrante, Xin Wang, Robert M Friedlander. 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. Neurobiol Dis. 2013;55C:26-35.