INTERRELATED MECHANISMS OF CELLULAR INFLAMMATION AND DEMYELINIZATION IN DIABETIC NEUROPATHY

Abstract

Diabetic neuropathy is one of the most common and disabling complications of diabetes mellitus, leading to progressive nerve damage and dysfunction. The mechanisms underlying diabetic neuropathy are complex and include metabolic disturbances, oxidative stress, and changes in blood vessels. However, recent research has increasingly emphasized the critical roles of cellular inflammation and the loss of myelin in the development and progression of this disease. This paper examines the interconnected mechanisms of cellular inflammation and the loss of myelin in diabetic neuropathy. It discusses how inflammation, triggered by high blood sugar levels, activates immune cells and promotes the release of pro-inflammatory molecules that damage Schwann cells and disrupt the protective layer around nerves. This damage leads to problems with nerve function, including sensory loss and muscle weakness. Furthermore, the loss of myelin initiates a harmful cycle, in which demyelination further promotes inflammation, leading to more severe nerve damage.