There have been speculations on the reasons for the lack of NFTs in the canine brain and in the brains of other animals (Kuroki et al., 1997; Youssef et al., 2016). First possibility is the dissimilarity between canine TAU protein sequence in comparison to human’s. Secondly, the lifespan of dogs might be too short to develop NFTs, as Aβ deposition precedes NTFs formation. Thirdly, although the amyloid protein sequence is highly conserved between species, its N-terminal part is not, which might influence TAU phosphorylation and its subsequent aggregation into NFTs. Therefore, it seems that only humans develop the full blown AD pathology with amyloid plaques, NFTs and dementia. There have been few reports of possible AD in aged great apes (Rosen et al., 2008; Perez et al., 2013, 2016), although also in these the TAU pathology was very limited. Several reasons for this exceptional vulnerability of humans to develop AD have been proposed (Arendt et al., 2017; Walker and Jucker, 2017). Predisposition to develop AD might arise as early as during embryonic development over the period of neurogenesis, this was inferred from the modular deposition of AD related cerebral deposits which mirrors the formation and migration of neurons and on a larger scale development of brain regions (Arendt et al., 2017). In humans, the relative brain size is much larger than in any other animal and this expansion is due to longer duration of brain development as well as higher number of neuronal progenitor cell division cycles, the latter giving rise to genomic aberrations, which in turn can be the origin of AD (Arendt et al., 2017). Furthermore, the neurons display genomic mosaicism, which was detected in neurons of approximately 10% of normally aged people. These neurons were shown to preferentially undergo apoptosis in AD (Arendt et al., 2010). The extent of neuronal genomic mosaicism is brain region specific and correlates with differential vulnerability to neurofibrillary pathology (Arendt et al., 2015). Moreover, the pathological TAU conversion might commence as early as in children (Braak and Del Tredici, 2012), although it has not been firmly established if these processes are transient in nature. The canine model would therefore serve as an accessible and suitable model to further delineate why, except for humans, are other species less susceptible to develop tauopathies.