For example, social isolation in genetically determined symptoms of an Alzheimer’s disease mouse model (APP/PS1 double mutant, i.e., amyloid precursor protein/presenilin 1) prolonged latency in the working memory test (Huang et al., 2011), increased the Aβ42/Aβ40 ratio in the hippocampus, increased the number of manganese-superoxide-dismutase-positive neurons in the CA1, CA2, and CA3 hippocampal areas, amygdala, and locus coeruleus, and decreased the number of ChAT-positive neurons in the vertical and horizontal diagonal bands of Broca (Huang et al., 2011). The gene discussed is PSEN1; the disease is early-onset autosomal dominant Alzheimer disease.