Neurodegenerative diseases most likely occur in many other mammalian species, but there are very limited reports about these. The reports are focusing on the presence of Aβ deposits and phosphorylated TAU and/or NFTs, which are detected post mortem, not describing the cognitive deficit, this is of course more difficult to observe in wild life animals or in this aspect less characterized species. Diffuse deposits of Aβ were observed in the parietal cortex of dolphins and more compact senile plaques in their cerebellum (Di Guardo, 2018). Sheep and goats (Braak et al., 1994; Nelson et al., 1994; Nelson and Saper, 1995), cheetah (Serizawa et al., 2012), bison (Härtig et al., 2000, 2001), bears (Cork et al., 1988) and most species of nonhuman primates (Schultz et al., 2000a, b; Rosen et al., 2008; Oikawa et al., 2010; Perez et al., 2013, 2016; Rodriguez-Callejas et al., 2016; Reid et al., 2017) also develop amyloid plaques and/or harbor phosphorylated TAU laden neurons, but most of them do not have NFTs present in their central nervous systems (as reviewed in Youssef et al., 2016). However, AT8-immunostained pTAUSer202 and pTAUThr205 were found in the brains of brown lemur, rhesus monkey, baboons, rabbit, guanaco, and bison (Härtig et al., 2000). Furthermore, NFTs were revealed by Gallyas staining in aged bison (Härtig et al., 2001).