Peripheral neuropathy is a common long-term complication of both type 1 and type 2 diabetes affecting about 50% of all patients.
Diabetic neuropathy can lead to loss of sensation, paresthesia and pain, and can affect the function of feet, hands and arms. These patients may also develop autonomic neuropathy which is a devastating complication. Hyperglycaemia is one of the main factors behind the development of diabetic peripheral neuropathy, but the underlying cellular mechanisms are unclear.
Our hypothesis is that impaired ability of the Schwann cell and axons to digest their own damaged components, i.e. impaired autophagy, may contribute to the development of diabetic neuropathy. Therefore, the focus of our research is to study if stimulation of autophagy can inhibit/delay the development of diabetic neuropathy.
Nerve damage may also occur after a physical trauma. Despite improvement of the methods used in nerve repair, the functional recovery is poor and many patients suffer from disability. We study the effect of autophagy stimulation in nerve healing process after nerve transection.
The results of our projects will provide insight into fundamental biological processes involved in development of peripheral neuropathy. It may also open a window to new preventive measures and treatment strategies for peripheral neuropathy.
