Experimental Treatments In ALS

Main Category: Neurology / Neuroscience
Also Included In: Huntingtons Disease;  Alzheimer's / Dementia
Article Date: 21 Apr 2006 - 14:00 PDT

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Two experimental treatments in animal models of amyotrophic lateral sclerosis (ALS, or Lou Gehrig's disease), may point the way to future clinical therapies of this disease. ALS destroys the nerve cells (neurons) in the brain and spinal cord that control muscles. A mutated enzyme called SOD1 has been shown to cause some cases of the disease. Researchers showed that by removing SOD1 not in neurons, but in neighboring cells called microglia, they could improve survival in a mouse model of the disease. Microglia may be much easier to target, or to replace, than neurons, making this finding potentially significant.

Antisense oligonucleotides stimulate the body's own cells to destroy selected genetic messages before they can become harmful. Researchers who used antisense oligonucleotides against SOD1 showed they could treat wide areas of the brain in both rats and monkeys, decreasing SOD1 and increasing survival. This therapeutic strategy may be useful against other targets in other neurodegenerative diseases as well, such as Huntington's disease and Alzheimer's disease.

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American Academy of Neurology 58th Annual Meeting

The American Academy of Neurology, an association of more than 19,000 neurologists and neuroscience professionals, is dedicated to improving patient care through education and research. A neurologist is a doctor with specialized training in diagnosing, treating and managing disorders of the brain and nervous system such as Alzheimer's disease, epilepsy, multiple sclerosis, Parkinson disease, and stroke.

Contact: Robin Stinnett
rstinnett@aan.com
American Academy of Neurology

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