Topic: Painful diabetic neuropathy

Painful diabetic neuropathy (PDN), a chronic and often incurable syndrome, is one of the most common and unpleasant complications of diabetes. Effective clinical interventions for PDN are very limited and already developed approaches are characterized by lack of molecular or cellular target specificity and a short duration of therapeutic effects. Numerous investigations causally link upregulation of Cav3.2 T-type Ca2+ channels in peripheral nociceptive neurons to painful symptoms of PDN. Here we suggest an approach, based on implementation of virus-mediated cell-specific delivery of vectors ex

Peripheral diabetic neuropathy (DN) affects 50% of Diabetes Mellitus (DM) patients and approximately 40-50% progress to painful diabetic neuropathy (pDN). Risk factors for pDN include high alcohol consumption, obesity, and low vitamin D levels, all associated with impaired oligodendrocyte progenitor cell (OPC) differentiation. Additionally, studies indicate that depletion of mature myelinating oligodendrocytes induces nociceptive responses in mice. These findings suggest that DM might disrupt oligodendrocyte dynamics, causing defects in central nervous system (CNS) myelin and the onset of neur

Painful diabetic neuropathy (pDN) is a serious, chronic complication affecting about 10-20% of diabetes mellitus (DM) patients, but the underlying cause remains unknown. Hints from risk factor assessment and literature point towards a role of oligodendrocyte and myelin homeostasis. Along this line, the main aim of the project is to identify adaptations occurring in the oligodendrocyte lineage due to the metabolic imbalances triggered by DM and determine which of these adaptations are crucial for the development of neuropathic pain. The high-fat high-sugar diet-induced type 2 DM mouse model is