As for the molecular mechanisms underlying the pro-cognitive effects of GEBR-32a in AD mice, it can be hypothesised that our PDE4D inhibitor reverses the Aβ-mediated inhibition of the cAMP/PKA/CREB pathway, as it happens with rolipram42, 48, thus leading to the rescue of hippocampal LTP and memory deficits. The gene discussed is PDE4D; the disease is memory.