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How chronic pain may be caused by signals from skin itself

June 9, 2011 - Washington

A new study has found that certain types of chronic pain may be caused by signals from the skin itself, rather than damage to nerves within the skin, as previously thought.

The study may explain why only 50 percent of patients experiencing chronic nerve pain achieve even partial relief from existing therapeutics.

For years, researchers have known that increased amounts of a molecule called Calcitonin Gene-Related Peptide (CGRP) is found in the skin of chronic pain patients.

The source of the increased CGRP was thought to be certain types of sensory nerve fibres in the skin that normally make and release a type or "isoform" called CGRP-alpha.

Curiously, however, the authors found that nerve fibres containing CGRP-alpha are actually reduced under painful conditions - leading them to investigate where the increased CGRP in the skin came from.

The answer, surprisingly, was that the skin cells themselves generate increased amounts of a lesser-known "beta" isoform of CGRP.

This skin cell-derived CGRP-beta is increased in painful conditions and may be sending pain signals to remaining sensory nerve fibres in the skin.

The discovery of CGRP-beta as a therapeutic target presents a potentially important new treatment approach.

"Since CGRP-alpha normally plays an important role in both the regulation of blood flow and normal inflammatory responses, targeting this molecule as a treatment for chronic pain could cause undesired side-effects on circulation," the paper's corresponding author, Phillip J. Albrecht, Ph.D., Assistant Professor of Neuroscience at Albany Medical College and Vice President at Integrated Tissue Dynamics, LLC, whose team conducted the research, said.

"However, since we know that these two forms of CGRP are derived from separate genes, we may be able to selectively manipulate the beta isoform without affecting the alpha, and dramatically reduce unwanted toxicities-a common problem limiting the successful development of novel pain therapeutics.

"This is really a two-for-one discovery: a novel mechanism we can specifically target in a novel skin location," he stated.

The study has been published in the June 6 online version of the international research journal PAIN.


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