Published Paper Details:

It is becoming more widely acknowledged that chronic diabetes mellitus (DM) increases the incidence of neurodegenerative illnesses, including Parkinson's disease (PD). Oxidative stress as well as neuroinflammation stand highlighted as important, interconnected drivers for dopaminergic neurodegeneration among the major mechanisms connecting these two disorders. Diabetes-related chronic hyper glycemia results in a compromised antioxidant defense system, increased generation in reactive oxygen molecules (ROS) and compromised mitochondrial activity. Due to their great susceptibility to oxidative insults, dopamine-producing neurons of the substantia nigra are especially affected by the prolonged oxidative stress caused by these alterations. Furthermore, neuroprotective pathways may be disrupted by poor insulin transmission in the brain, making neurons even more susceptible to oxidative & inflammatory assaults. Oxidative stress & neuroinflammation are key and perhaps changeable pathways in diabetes-induced neurodegeneration, even though other elements like mitochondrial malfunction and protein aggregation (like ?-synuclein) also contribute to Parkinson's disease pathogenesis. ?-synuclein aggregation & dopaminergic cell death are two classic PD diseases that are caused by the synergistic combination of oxidative stress and neuroinflammation, which upsets neuronal homeostasis. These results highlight how crucial it is to target oxidative & inflammatory pathways in diabetic populations help prevent or delay the emergence of Parkinson's disease. One promising approach to risk reduction and therapeutic intervention is to address these pathways.