Fig. 3.

The pathophysiologic model involving oxidative stress and thermal regulation in PD in this study. Mitochondria are responsible for maintaining the cellular energy reserves with heat production. Mitochondrial dysfunction is involved in activated neuroinflammation and increased oxidative stress. The injury from oxidative stress might induce cell apoptosis or death, which would in turn result in the loss of heat production and the associated relatively low T_v (pathway B). However, in the condition of cell damage but survival, the resulting hyper-metabolism under oxidative stress would promote heat generation and the associated relatively high T_v (pathway A). The dynamic regulation of pro- and anti-inflammatory cytokines could potentially promote neuroprotection and lead to the initiation of thermal modulation. Other etiologies, such as autonomic dysfunction and dopamine agonists, might also be related to thermal dysregulation in PD (pathways C and D)