We have selected APP-PS1 mice with the age of 14 months, as at this time point the animals present a full spectrum of pathology, showing severe amyloid plaque deposition in the hippocampus and cortex, high levels of microgliosis and astrogliosis, vascular alterations, and cognitive deficits (Jankowsky et al., 2004; Lalonde et al., 2005; Janota et al., 2015; Unger et al., 2016). The gene discussed is APP; the disease is amyloidosis.