New transgenic rat model of ALS expands research possibilities

human patients and SOD1 transgenic mice and rats, globs of faulty SOD1 proteins are found. Scientists know that loss of SOD1 function isn't to blame for the symptoms of ALS; instead, the faulty enzyme picks up a new, still unknown, function.

Finding the link between faulty SOD1 and the disappearing glutamate transporter should help clarify why the many SOD1 mutations appear in patients with inherited ALS and even in some non-inherited cases of the disease, says Rothstein.

The investigations were stimulated by The ALS Association, and funded by the National Institutes of Health, the Center for ALS Research at Johns Hopkins, the Spinal Cord Disease Foundation and the Ludwig Institute for Cancer Research. The Center for ALS Research at Johns Hopkins, formed in March 2000, is a collaboration of scientists worldwide rapidly working to develop new treatments and to find a cure for ALS.


Contact: Joanna Downer
Johns Hopkins Medical Institutions

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