Hence, it has been found that the expression of uPA, but not of its receptor (uPAR), is decreased in the synapses of AD patients and 5XFAD mice (express human APP with the Swedish (KM670/671NL), Florida (I716V) and London (V717I) mutations together with a mutant presenilin 1 (M146L, L286V) under the control of the murine Thy-1 promoter), by the ability of Aβ to halt the transcription of uPA mRNA in neurons but not in astrocytes [68]. The gene discussed is PLAU; the disease is Alzheimer disease.