In dogs, Aβ immunotherapy could reduce the presence of amyloid plaques and astroglial reaction in aged individuals (Neus Bosch et al., 2015). A vaccine directed against fibrillary Aβ (anti-Aβ42) reduced the presence of Aβ plaques in canine prefrontal cortex and improved the function of the frontal cortex, thus resulting in cognitive benefits (Head et al., 2008). Anti-Aβ42 vaccination of dogs with CCD, in combination with behavioral enrichment, resulted in reduced presence of Aβ plaques in the brain, a significant maintenance of learning abilities over time and cognitive maintenance with no improvement in cognition (Davis et al., 2017). This anti-Aβ vaccine, however, also increased the frequency of brain microhemorrhages (Davis et al., 2017) which is commonly observed in the development of these immunotherapies also in human trials and could be very serious side effect. Similarly to pharmacological compounds, immunotherapies in both dogs and humans have provided modest improvements at most, yet similarities between human and canine patients again highlight the parallels between diseases and usefulness of dogs as a preclinical model for AD.