Cognitive dysfunction has become a major health issue in the global aging society. For treating cognitive dysfunction or dementia, several small molecules or innovative drugs, including a monoclonal antibody against the amyloid β protein, have been prescribed. However, their adverse effects require the exploration of alternative treatments. Artemisia argyi (Asteraceae) has been used as traditional medicine for gastrointestinal disorders and inflammation. Recent reports suggest it has potential neuroprotective effects; however, evidence regarding its cognitive benefits and underlying mechanisms remains limited. We examined the memory-enhancing effects of an ethanolic extract of A . argyi (EAA) (10, 30, or 100 mg/kg, once per each behavioral test) in a mouse model of scopolamine-induced cognitive dysfunction and explored its mode of action on memory-related signaling pathways. Memory-related performance was assessed using the Y-maze, novel object recognition, Morris water maze, and passive avoidance tests. Next, Western blotting was used to evaluate changes in signaling molecules, such as CaMKII, ERK, CREB, and brain-derived neurotrophic factor (BDNF) in the hippocampus. EAA administration significantly improved cognitive performance across all tests. It restored the phosphorylation levels of CaMKII, ERK, and CREB, respectively, as well as the expression level of BDNF, after 12 h of treatment. Moreover, it enhanced long-term potentiation without altering basal synaptic transmission within the hippocampus. In summary, EAA facilitated cognitive enhancement during a cholinergic impaired state, attributable to its influence on synaptic plasticity and activation of the CaMKII–ERK–CREB–BDNF signaling cascade.
Byun et al. (Fri,) studied this question.