Figure 7. The hypothesis model of the signaling pathways by which LEO regulates neuroplasticity in cognitive deficits. In the pathological state of AD, AChE marker protein is up-regulated in the CA1 pyramidal neuron of APP/PS1 mice. PSD95, Synaptophysin, Synaptophysin /PSD95 contacts is also decreased in APP/PS1 mice. After LEO treatment, both presynaptic marker, synaptophysin and postsynaptic marker, PSD95 in hippocampus were up-regulated. LEO was demonstrated to be important for activation of BDNF, AKT and GSK in the hippocampus of AD mice. LEO may increase hippocampal neuroplasticity via acting upon three signaling pathways: (1) LEO may up-regulate BDNF protein level in the hippocampus, BDNF binding to its high-affinity TrkB, associated with neuroplasticity, including persistence of cell survival, stimulation of synaptic plasticity; (2) LEO may activate AKT, which is the downstream of TrkB receptor stimulation and related to enhancement of synaptic plasticity. (3) LEO could improve cognitive impairment by decreasing the AChE contents. GSK-3β can regulate the AChE levels in pathological conditions. AD, Alzheimer’s disease; ACh, acetylcholine; AChE, choline acetyltransferase; TrkB, receptor tyrosine kinase; AKT, protein kinase B; ERK, extracellular signal-regulated kinase; LEO, lemon essential oil.