May 6, 2002 (The Associated Press) -- An ordinary antibiotic slowed the progression of Lou Gehrig's disease in mice, suggesting a potential new approach for treating people, researchers report.
The disease, formally known as amyotrophic lateral sclerosis or ALS, attacks nerve cells that control movement. As these cells degenerate, an affected person becomes progressively paralyzed. Most cases appear between the ages of 40 and 70, and death follows an average of four years after symptoms appear.
The antibiotic, minocycline, was shown recently to prolong the lives of mice with a version of Huntington's disease, another neurodegenerative disorder. It is now being tested against Huntington's in people.
Minocycline has been used as an antibiotic for 30 years in people and has a good track record for safety, even when taken for long periods, said Dr. Robert Friedlander of Brigham and Women's Hospital in Boston, senior author of the new study.
The work is reported in the May 2 issue of the journal Nature. Researchers studied mice with a version of ALS created by genetic mutations.
Daily injections of minocycline delayed appearance of the disease and prolonged life. Treated mice lived about 137 days, compared to 126 days for untreated mice.
The drug's effect has nothing to do with its antibiotic ability. Rather, researchers found that minocycline treatment reduces production of a protein within nerve cells that can lead to cell death. That discovery should help in finding more powerful and effective drugs, they said.
Friedlander said he believed minocycline or similarly actings drugs will eventually form part of a cocktail of medications used to treat ALS.
Minocycline looks promising as a potential ALS treatment, the Muscular Dystrophy Association said in a statement. While there had been prior evidence it might be effective, the new findings provide more direct support for the idea, said Sharon Hesterlee, the MDA's director of research development.
The research was funded by Project A.L.S., the MDA, other groups and the federal government.
Copyright 2002 The Associated Press. All rights reserved.
