Alzheimer's disease (AD) is a profoundly debilitating neurodegenerative disorder without effective treatment or determinative antemortem diagnostics. Improvements in diagnostic and treatment options will require a better understanding of the biological processes that drive AD onset and progression. The prevailing model to explain AD pathogenesis holds that neuronal degeneration and clinical demise are precipitated by the gradual accumulation, in brain centers controlling memory and cognition, of amyloid-? (A?) peptide, a catabolite of the transmembrane Amyloid Precursor Protein (APP).

Even though ketamine has been heralded as a significant advance in the development of novel and rapidtreatments for depression, the acute psychotomimetic and reinforcing effects of this drug limit its utility.Previously, we demonstrated that activation of a circuit from the ventral hippocampus to the medial prefrontalcortex is both necessary and sufficient for ketamine?s sustained antidepressant-like effects in rats.

Even though ketamine has been heralded as a significant advance in the development of novel and rapidtreatments for depression, the acute psychotomimetic and reinforcing effects of this drug limit its utility.Previously, we demonstrated that activation of a circuit from the ventral hippocampus to the medial prefrontalcortex is both necessary and sufficient for ketamine?s sustained antidepressant-like effects in rats.