Hence, given that physiological activation of NMDA and AMPA receptors are essential for inducing long-term potentiation (LTP), memory consolidation via CREB-mediated transcription of pro-survival genes in neurons, and synaptogenesis, it is likely that an increase in cyclic AMP-dependent activity in the brain via intranasal delivery of Forskolin (or with CNS/CT-001) can lead to a maintenance of synaptic plasticity and reduce cognitive decline in PD. The gene discussed is CREB1; the disease is Mental deterioration.