This suggests that, in Drosophila, combining the two key pathogenic hallmarks of Alzheimer’s disease is not sufficient to induce tau spread, although evidence from other studies shows you can still gain useful insights on the impacts of Aβ and tau on neuronal toxicity and synaptic function.62,63 Indeed, in Fig. 2C, post-synaptic Aβ expression does appear to lower hTau expression in pre-synaptic neurons compared to conditions without Aβ, which suggests post-synaptic Aβ toxicity is leading to reduced pre-synaptic hTau levels. The gene discussed is MAPT; the disease is early-onset autosomal dominant Alzheimer disease.