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Maas BiolAB Announces That Cyclosporin Blocks Alzheimer's Model SAN DIEGO--(BW HealthWire)--Nov. 12, 2001--Maas BiolAB announced today that cyclosporin protected of the usually hardest hit cholinergic neurons in a rat model of Alzheimer's disease. Results from a new preclinical study were presented today at the 31st annual meeting of the Society for Neuroscience in San Diego by Cesar Borlongan Ph.D., neurodegeneration researcher at the National Institute of Health. Dr. Borlongan is Scientific Advisor to Maas BiolAB, and head of its Scientific Advisory Board. Maas is developing cyclosporin as a treatment for Alzheimer's and other neurodegenerative diseases. "CsA may promote better neuroprotection because of its multiple sites of action, such as preserving the integrity of calcium channels, blocking the mitochondria permeability transition pore, promoting neurotrophic factor support, and inhibiting free radicals," Borlongan explained. "Recent data have shown a direct correlation of increased tyrosine hydroxylase immunoreactivity in specific brain regions that display decreased calcineurin immunoreactivity. Similar correlations were noted between enhanced choline acetyltransferase immunoreactivity and decreased calcineurin," Dr. Borlongan reported. "Our observed cyclosporin enhancement of septal ChAT immunoreactivity suggests potential therapeutic utility of cyclosporin for brain disorders characterized by alterations of the cholinergic system." "Maas will develop cyclosporin neuroprotection for Alzheimer's, Parkinson's, Huntington's and ALS," said Marcus Keep, M.D., President and CEO of Maas. "Dr. Borlongan's innovative research and exciting results lead towards a cure for people suffering from Alzheimer's." "Unlike the briefly effective and transiently symptomatic dementia drugs like Aricept and Excelon, cyclosporin has the potential to stop the disease process itself by blocking massive neuronal apoptosis," said Eskil Elmer, Ph.D., Maas Scientific Director. "Dr. Borlongan has demonstrated that cyclosporin prevents the loss of the actual cells that make acetylcholine. No other drug does that."
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