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Apr 24, 2007

Inactivation of Protein Reduces Damage from MS

  • Scientists found that deactivating a protein, cyclophilin D, protects nerve fibers from damage in a mouse model of multiple sclerosis.

    "While we can't genetically inactivate cyclophilin D in people, there are drugs out there that can block the protein,” notes Michael Forte, Ph.D., senior scientist at the Vollum Institute at Oregon Health & Science University (OHSU). “Our research predicts that drugs that block cyclophilin D should protect nerve fibers from damage in MS."

    Cyclophin D is a key regulator of molecular processes in the nerve cell's mitochondrion and can participate in nerve fiber death. Inactivating this protein strengthens the mitochondrion, helping to protect nerve fibers from injury.

    The researchers believe that cyclophilin D is responsible for causing the unregulated opening of a pore in the mitochondrion's membrane that allows the calcium overload seen in MS patients. The OHSU team showed that mice lacking cyclophilin D still developed an MS-like disease, but unlike their counterparts possessing the protein, they partially recovered. Scientists found their nerve fibers remained intact and they resisted the free radicals and calcium overload.

    The research was done by investigators at OHSU, Portland Veterans Affairs Medical Center, and the University of Padova in Italy. The findings are published in the April 24 issue of Proceedings of the National Academy of Sciences.



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Scientifically Studying Ecstasy

MDMA (commonly known as the empathogen “ecstasy”) is classified as a Schedule 1 drug, which is reserved for compounds with no accepted medical use and a high abuse potential. Two researchers from Stanford, however, call for a rigorous scientific exploration of MDMA's effects to identify precisely how the drug works, the data from which could be used to develop therapeutic compounds.

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