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Interaction Between the Glymphatic System and α-Synuclein in Parkinson's Disease
Yu Zhang # 1, Cui Zhang # 1, Xu-Zhong He 1, Zhen-Hua Li 1, Jing-Cai Meng 1, Rui-Ting Mao 1, Xin Li 1, Rong Xue 1, Qian Gui 2, Guo-Xing Zhang 1, Lin-Hui Wang 3
...In mice receiving the intranigral injection of recombinant human α-syn, we found that the glymphatic suppression via aquaporin-4 (AQP4) gene deletion or acetazolamide treatment reduced the clearance of injected α-syn from the brain. In mice overexpressing the human A53T-α-syn, we revealed that AQP4 deficiency accelerated the accumulation of α-syn, facilitated the loss of dopaminergic neurons, and accelerated PD-like symptoms. We also found that the overexpression of A53T-α-syn reduced the expression/polarization of AQP4 and suppressed the glymphatic activity of mice. The study demonstrates a close interaction between the AQP4-mediated glymphatic system and parenchymal α-syn, indicating that restoring the glymphatic activity is a potential therapeutic target to delay PD progression.