Increases in BDNF levels, observed in male SAMP-8 [13] and in transgenic mice model for Alzheimer’s disease [14], synaptic and neuronal maintenance in hippocampal areas of CA1, CA3 and GrDG, as well as inhibition of GSK-3β (all seen in the present work), reduction of neuroinflammation observed in SAMP-8 ex vivo hippocampus [36] and reduction of senile plaques (also observed in this and previous works), are some of the observed effects that may, altogether, contribute to long-term behavioral observations. The gene discussed is BDNF; the disease is early-onset autosomal dominant Alzheimer disease.