In combination with our findings that also the serotonin reuptake enhancer tianeptine and BDNF increase CA3- and CA1-FDSs and that the TrkB receptor antagonist ANA-12 prevents the effects of fluoxetine (10 μM), it is thus possible that the AD effects observed do not depend on enhanced monoaminergic neurotransmission, but, at least in part, on increased TrkB signaling. The gene discussed is NTRK2; the disease is Alzheimer disease.