In APP transgenic TgCRND8 mice, loss of Abi3-Gngt2 results in a gene dose- and age-dependent reduction in Aβ deposition, but in Abi3-Gngt2−/− mice, AAV-mediated expression of a pro-aggregating form of human tau exacerbates tauopathy and astrocytosis53. The gene discussed is GNGT2; the disease is tauopathy.