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Study reveals potential for new treatment of paralysis and brain disease

Helsinki, Finland, July 25, 2005 A study released today could reveal the key to treating nearly 140 million people worldwide who suffer from spinal cord injuries, Alzheimer's disease, ALS and other devastating neurological diseases.

The study, published in the online version of the Journal of Neuroscience Research, shows how a protein called KDI tri-peptide (KDI) can block the harmful effects of a substance called glutamate that is present in all degenerative brain diseases and spinal cord injuries, causing permanent cell death and preventing the repair of damaged nerve connections. Glutamate is produced as part of the body's natural reaction to central nervous system damage.

In the new study, researchers at the Brain Laboratory at the University of Helsinki (www.brainlab.fi) and at the Johnnie B. Byrd, Sr., Alzheimer's Center & Research Institute in Tampa, Fla., show KDI to be a potent and wide-ranging blocker of glutamate's damaging chemical processes. It therefore has a tremendous ability to protect the brain and spinal cord from cell death and even enable regrowth.

Human clinical trials are expected to begin as soon as next year. No toxic side effects have been seen in studies so far, and the Finnish researchers do not expect any since KDI occurs naturally in the human body, including in the central nervous system. An added advantage is that KDI can be easily synthesised, therefore avoiding the problems associated with human cell donation.

Paralysis reversal in rats offered clues to wide-ranging applications

The new findings follow from previous studies in which KDI, when injected into the spines of paralyzed rats, produced dramatic results. The rats were able to bear weight and walk again after only 3 months. Further laboratory experiments showed that KDI also had the ability to promote regrowth of nerves in damaged areas and to prevent brain cell death. These results paved t
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Contact: Todd Ringler
todd.ringler@edelman.com
781-599-7542
Edelman Public Relations
25-Jul-2005


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