( Researchers from the University of Cali...)Molecular Therapy Holds Promise in the Treatment of Amyotrophic Lateral Sclerosis,Health

Researchers from the University of California, San Diego (UCSD) School of Medicine, the Center for Neurologic Study and Isis Pharmaceutical Corporation have created// and tested molecular therapy in animals which they feel will assist in the treatment of amyotrophic lateral sclerosis (ALS), or Lou Gehrig's disease. The study has shown that it is possible to ensure the delivery of therapeutic molecules known as antisense oligonucleotides to the brain and spinal cord through the cerebrospinal fluid in relatively small doses, which when tested on rats, showed a marked decline in the progression of ALS.

The study will be published July 27 in advance of publication in the August issue of Journal of Clinical Investigation.With colleagues Timothy Miller, M.D., Ph.D., UCSD Department of Neurosciences, and Richard A. Smith, M.D., of the Center for Neurologic Study, Cleveland found that when effective doses of the antisense therapy were delivered, far less of a protein that causes a hereditable form of amyotrophic lateral sclerosis was produced.

ALS is a progressive disease that attacks motor neurons that reach from the brain to the spinal cord and from the spinal cord to the muscles throughout the body. Estimated to affect some 30,000 Americans, most people are diagnosed with ALS between the ages of 40 and 70. Typically, ALS patients live only three to five years after initial diagnosis.

Neurotoxicity from an accumulation of mutant proteins is believed to be at the root of many neurodegenerative diseases. ALS can be caused by a mutation in a protein called SOD1, and the antisense drug effectively silences the gene that codes for this mutant protein – found in the cells of patients with inherited forms of ALS.

In this disease, selective killing of spinal cord "motor neurons" occurs. Motor neurons are long and complex nerve cells that control voluntary movement. Degeneration of motor neurons in ALS leads to progressive loss of musc
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