The Aβ25–35 mouse model only relies on the amyloid hypothesis wherein Aβ triggers AD pathology due to accumulation and oligomerization, which in turn trigger tau phosphorylation, neuroinflammation, oxidative stress and synaptic dysfunction, common features described in patients with AD (Heneka et al., 2015; Selkoe and Hardy, 2016; Jackson et al., 2019; Ayton and Bush, 2021). Here, MAPT is linked to Alzheimer disease.