New Research Suggests A New Therapeutic Approach for Diabetic Neuropathy

A Glycation End-Product receptor associated with activation of NF-kappaB plays a key role in the loss of pain perception experienced by many patients with diabetes.

Inhibiting the interactions between the receptor for advanced glycation end products (RAGE) and NF-kappaB could provide a new therapeutic approach for diabetic neuropathy, lead author Dr. Angelika Bierhaus, from the University of Heidelberg in Germany, and colleagues note.

In sural nerve biopsies, RAGE, ligands of the receptor, activated NF-kappaBp65, and IL-6 were identified together in the microvasculature of patients with diabetic neuropathy, according to the report in The Journal of Clinical Investigation for December.

Testing in diabetic mice showed that advanced glycation end products promoted the activation of NF-kappaB and led to an increase in NF-kappaB-dependent gene expression. Moreover, RAGE blockade prevented these effects and mice lacking RAGE showed blunted NF-kappaB activation.

Treatment with soluble RAGE restored pain perception in wild type mice with diabetic neuropathy, the investigators note. In contrast, RAGE knockout mice were largely protected from losing pain perception in the first place.

By delineating the interaction between advanced glycation end products and RAGE "as a discrete target impacting on neuronal function, the current work suggests the potential utility of therapeutic approaches focused on RAGE in neuropathy, an area where few therapeutic options are currently available," the authors note.

J Clin Invest 2004;114:1741-1751.
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