The investigation of the molecular pathways underlying the neuroprotection mechanisms of quercetin in in vitro and in the mouse model of Parkinson’s Disease (PD) has shown that the activation of PKD1–Akt pathway via the upregulation of PPAR-gamma coactivator 1-alpha (PGC-1a) and the transcription factor A, mitochondrial (TFAM) represents a mechanism to restore mitochondrial function and decrease the progression of dopaminergic neurodegeneration [29,30]. This evidence concerns the gene AKT1 and Parkinson disease.