Application of Fullerene Nanoparticles to Improve Brain Health and Prevent Neuronal Damages in Diabetes Mellitus; a Review Study

Chronic hyperglycemia during diabetes is the leading cause of nerve tissue damage and neuronal dysfunction, which is defined as diabetic neuropathy. This activation, through the activation of a wide range of destructive cellular markers in the brain and then a defect in the learning and memory process, leads to a kind of forgetfulness called diabetic dementia. Increased production and accumulation of free radicals that lead to oxidative damage in brain tissue is one of the key pathways to damage neurons and nerve tissue. In addition to damaging cellular structures, these radicals induce various brain pathways, including PI3-kinase, AKT, and ERK1/2, by inducing the production of various inflammatory cytokines and mTOR (mammalian target of rapamycin) proteins in the brain. It then plays a key role in the destruction of neurons and dementia caused by diabetes by hyper-phosphorylation of tau protein and accumulation of beta-amyloid proteins. Fluorine nanoparticles (C60), as a powerful antioxidant and free radical scavenger, can prevent the accumulation of a variety of free radicals in brain tissue during diabetes. The use of these nanoparticles can prevent neuronal damage and diabetic neuropathy by inhibiting destructive signaling pathways that are activated by increased production of free radicals. Therefore, due to the lack of significant toxicity of these nanoparticles in biological environments, the use of these agents can be considered as a new treatment to maintain brain health and prevent neuropathy and dementia during diabetes.