CGAS and Parkinson disease: Our study demonstrated that in the mouse models simulated by rotenone and STZ, as well as in the BV2 cell models simulated by rotenone and PA, the T2DM microenvironment impaired the mitochondrial function of microglial cells, leading to mt DNA leakage, activation of the cGAS-STING pathway, downstream inflammatory reactions, release of a large number of inflammatory factors, and exacerbation of dopaminergic neuron damage in PD.