Kennedy's Disease Press Releases

Production of a growth factor in the spinal cord drops just before the onset of symptoms in an animal model of a rare, hereditary motor neuron disease, scientists have found. The findings point to a potential new way of treating this disease, and possibly other neurodegenerative disorders as well.
Fact Sheet

Scientists have identified the gene altered in one of the most common hereditary ataxias, spinocerebellar ataxia 2 (SCA2). The discovery allows improved genetic testing and provides new clues about how genetic mutations cause several neurological disorders, including Huntington's disease. The findings are reported by three different groups in the November issue of Nature Genetics.

Scientists have identified a new type of trinucleotide repeat mutation that leads to Friedreich's ataxia (FA), a rare childhood neurodegenerative disease. The discovery allows accurate screening for carriers of the disease and may lead to the first effective treatments.

For the first time, scientists have linked a critical cellular enzyme to the gene defect found in Huntington's and several other hereditary neurological diseases. The finding provides important clues about how these diseases may develop and suggests that a single therapy eventually may be developed to treat them.

Scientists have discovered that another nervous system degenerative disorder, spinocerebellar ataxia type 1 (SCA1), has the same type of gene mutation occurring in Huntington's and Kennedy's diseases. In the disease, a normal three-base sequence in the genetic code — cytosine, adenine and guanine, or CAG — is abnormally repeated, according to Drs. Huda Y. Zoghbi, who led one team at the Baylor College of Medicine in Houston, Texas, and Harry T. Orr, who headed the other team at the University of Minnesota in Minneapolis. The same CAG repeat was reported earlier this year in Huntington's disease and in 1991 in the very rare Kennedy's disease, also called X-linked spinobulbar muscular atrophy.