More MS news articles for Nov 2001

Gene therapy shields neurons from disease, injury

http://www.reutershealth.com/archive/2001/11/12/eline/links/20011112elin002.html

By E. J. Mundell

NEW YORK, Nov 12 (Reuters Health) - By delivering a specific gene to nerve tissues, scientists say they were able to prevent the paralyzing, potentially lethal death of nervous system cells in young, injured rats.

The finding may someday pave the way for similar treatments in humans that could help patients with spinal injuries or conditions such as Huntington's disease or amyotrophic lateral sclerosis (ALS, also known as Lou Gehrig's disease).

The gene in question triggers production of a compound called heat shock protein 27, which works to "rescue immature neurons from injury-related death," according to Dr. Susanna Benn of Massachusetts General Hospital and Harvard Medical School in Boston. She presented the findings Sunday in San Diego, California, at the annual meeting of the Society for Neuroscience.

Paralysis and death due to neurologic injury or disease is caused by the death of millions of nerve cells, such as those found in the spinal cord. Finding ways to prevent these cells from dying is key to helping these patients survive and retain normal motor function.

In an interview with Reuters Health, Benn explained that heat shock protein 27 (Hsp27) protects and preserves nerve cells whenever they are placed under stress. She and her colleague Dr. Clifford Woolf speculated that the introduction into nerve tissue of a gene that triggers production of Hsp27 could help cells survive in the face of injury.

To test this theory, the researchers "piggybacked" the gene onto a harmless, inactivated herpes virus, which acted as a vehicle to deliver the gene to the injured nerve cells of rat pups. The pups used in the experiment were subjected to nerve injuries roughly comparable to human injuries following a "car accident or deep tissue wound," according to Benn.

The Harvard team reports that, as expected, the gene "switched on" production of Hsp27 and effectively prevented the death of injured nerve cells in the pups.

The research could have "important clinical and therapeutic implications," Benn explained, including treatments that could "prevent both sensory and motor neuron loss in patients with nerve damage associated with diabetes or AIDS, or in degenerative motor neuron diseases such as ALS."

She said further research needs to be done to determine whether Hsp27 can protect neurons lying deep within the brain, as well. If those results proved positive, therapies might someday be developed that could slow or prevent the degenerative brain cell loss associated with Alzheimer's and Parkinson's disease.