AQP4, predominantly situated in the perivascular astrocyte end-feet, functions as a pivotal element of the glymphatic system.25 In mice overexpressing human A53T-ɑ-synuclein, the absence of AQP4 hastened the accumulation of ɑ-synuclein, exacerbated the depletion of dopaminergic neurons and accelerated the manifestation of Parkinson's disease-like symptoms.26 Furthermore, the upregulation of A53T-ɑ-synuclein decreased AQP4 expression and inhibited glymphatic activity in mice, thereby establishing a detrimental feedback loop. This evidence concerns the gene AQP4 and Parkinson disease.