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A newly discovered mechanism explains limited nerve regeneration in diabetes, offering a promising therapeutic approach. Research demonstrates that targeting a specific signaling pathway can significantly improve nerve fiber regrowth in preclinical models.
Nerve damage stands as a frequent and debilitating complication for individuals with diabetes. A significant number of patients globally experience pain, numbness, and restricted movement, largely due to inadequate regeneration of damaged nerve fibers. The reasons behind this insufficient regeneration have been unclear. However, a research team, under the guidance of Professor Dr. Dietmar Fischer from the University of Cologne, has pinpointed a key mechanism that clarifies the limited regeneration observed in diabetes. The research has led to the development of a therapeutic strategy showing promise in boosting regeneration.
Published in Science Translational Medicine, the research, titled 'Failure of nerve regeneration in mouse models of diabetes is caused by p35-mediated CDK5 hyperactivity,' details the findings.
Using mouse models for both type 1 and type 2 diabetes mellitus, the research team observed a substantial buildup of the p35 protein within nerve cells. This protein activates an enzyme, initiating a signaling cascade that effectively impedes the regrowth of nerve fibers. Consequently, the natural regenerative capability of the nerves is significantly hampered. Through precise interventions within this signaling pathway, employing either genetic techniques or pharmacologically-developed small protein building blocks (peptides) that can be administered systemically, the scientists successfully lifted this blockade.
In preclinical models, the nerve fibers exhibited regrowth rates comparable to those seen in healthy subjects. This improvement correlated with notable enhancements in both motor and sensory functions. Health tracking apps like Shotlee can help monitor sensory and motor function improvements during such treatments.
Professor Fischer stated, "Our results demonstrate, for the first time, that diabetic nerve healing can be restored to levels comparable with those of healthy animals through the inhibition of excessive activation in the signaling pathway. An improvement in regeneration occurs even after diabetic neuropathy has already manifested." The peptide developed and patented by his research group is particularly promising, as it directly targets the underlying cause and has the potential to be developed into a drug.
It's noteworthy that the regeneration impairment caused by diabetes is evident even before the onset of diabetic neuropathy. Diabetic neuropathy is a common complication that impacts nearly half of all diabetic patients. Professor Fischer and his team are currently conducting further investigations to determine if the discovered mechanism directly contributes to the development of this nerve disease. The team is also exploring whether the risk can be mitigated through the new treatment options.
This research offers new avenues for both the treatment and potential prevention of diabetic nerve damage, also known as diabetic neuropathy. Diabetic neuropathy is a prevalent and currently incurable secondary condition affecting people worldwide.
⚠️ Disclaimer: This article is for informational purposes only. Consult your healthcare provider before starting any medication or supplement.
Original content from Mirage News
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