In 1991, a team of researchers linked familial ALS to chromosome 21. Two years later, the SOD1 gene was identified as being associated with many cases of familial ALS. The enzyme coded for by SOD1 carries out a very important function in cells: it removes dangerous superoxide radicals by converting them into non-harmful substances. Defects in the action of this enzyme mean that the superoxide radicals attack cells from the inside, causing their death. Several different mutations in this enzyme all result in ALS, making the exact molecular cause of the disease difficult to ascertain.
Recent research has suggested that treatment with drugs called antioxidants may benefit ALS patients. However, since the molecular genetics of the disease are still unclear, a significant amount of research is still required to design other promising treatments for ALS.
- ALS Therapy Development Foundation
- MDA ALS Research
- ALS Association
- The Forbes Norris MDA/ALS Research Center
- The Eleanor and Lou Gehrig MDA/ALS Center
- The Robert Packard Center for ALS Research at Johns Hopkins
- CytRx Corporation
- The National Institute of Neurological Disorders and Stroke
~Best viewed with a positive attitude~