A new study has identified a key molecule that contributes to painful diabetic neuropathy, an incurable nerve disease that affects some diabetic patients. A chemokine receptor- CXCR4, reversed pain and nerve degeneration in laboratory models and may provide relief to patients, according to Daniela Menichella, MD, PhD, assistant professor in the Ken and Ruth Davee Department of Neurology in the Division of Neuromuscular Disorders and senior author on the study.
Blocking CXCR4 can reverse the pain and the pathological degeneration of the nerves in the skin. Painful diabetic neuropathy (PDN) is caused by hyper-excitable nociceptors, and patients suffer severe pain while nerves in the skin degenerate. Current therapies include medications for pain relief but no treatments actually address the underlying cause of the disease.
Previous studies have shown that inflammation, commonly associated with diabetes, can trigger hyper-excitability of nociceptor neurons, and a particular class of protein messenger molecules called chemokines are associated with inflammation and excitability. Interrupting this disease pathway by inhibiting CXCR4-mediated hyper-excitability may lead to the first ever disease-modifying therapy for PDN.
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