Although an inverse temporal correlation between the appearance of the responsiveness of TrkB to systemic ADs and the robust reduction of BDNF-induced TrkB phosphorylation in ex vivo microslices cannot be taken as any evidence of causality, it is tempting to speculate that the same maturation processes that bring about the AD responsiveness, lead to developmental changes that restrict the effects of BDNF on TrkB. The gene discussed is BDNF; the disease is Alzheimer disease.