AQP4 and synucleinopathy: The A53T-LDclns and AQP4+/−-PFFs mice models showed the highest AQP4 depolarisation, alpha-synuclein aggregation, dopaminergic neurodegeneration and inflammatory activity compared to the other mice models, indicating that impaired glymphatic flow is a powerful progression factor in a developing synucleinopathy [32,33].