Rb1, the Primary Active Ingredient in Panax ginseng C.A. Meyer, Exerts Antidepressant-Like Effects via the BDNF-Trkb-CREB Pathway.

Panax ginseng C.A. Meyer (Araliaceae), a popular tonic and dietetic herbal medicine, has been traditionally prescribed in China and other countries to treat affective disorders. The medicinal parts of ginseng, the roots and flower buds, have become increasingly popular as dietary supplements due to the current holistic healthcare trend. We have investigated for the first time the antidepressive actions of the different medicinal parts, namely, the main roots, fibrous roots, and flower buds (in water extract and powder), of garden-cultivated ginseng through behavioral and drug-induced tests in mice. The water extracts, but not the powders of ginseng fibrous roots, flower buds, and main roots (1.5 g of crude drug per kilogram, p.o.), significantly reduced the immobility time in the forced swim test (FST) and tail suspension test (TST); moreover, the water extracts enhanced the 5-hydroxytryptophan (5-HTP)-induced head-twitch response and antagonized the action of reserpine in the mouse. We then explored the antidepressive mechanism of action of the ginsenoside Rb1 (Rb1) related to the brain-derived neurotrophic factor (BDNF) and its downstream proteins in mice exposed to chronic unpredictable mild stress (CUMS). Treatment with Rb1 (20 mg/kg, p.o.) for 21 days significantly attenuated the CUMS-induced decrease in the activities of BDNF, tropomyosin-related kinase B (TrkB), protein kinase B (AKT), extracellular regulatory protein kinase (ERK), and cyclic adenosine monophosphate (cAMP) response element binding protein (CREB) in the mouse hippocampal CA3 region and prefrontal cortex (PFC). Interestingly, treatment with the novel TrkB antagonist ANA-12 (0.5 mg/kg, i.p.) did not alter the level of BDNF but significantly blocked the antidepressive effects of Rb1 on proteins downstream of BDNF in CUMS-treated mice. These results suggest that BDNF-TrkB-CREB signaling may be involved in the antidepressive mechanism of the action of Rb1.

Antidepressive Effects of Exercise / 신경정신의학

Exercise is considered as one of the therapeutic options. in many major treatment guidelines for depression In terms of the underlying neurobiological mechanisms, it has been suggested that the antidepressive effects of exercise can be explained by the increased hippocampal volume associated with an increased level of brain-derived neurotrophic factor (BDNF). However, there have been no significant effects of exercise on cognitive functions in depression. Exercise has been used based on substantial evidence in the context of its therapeutic efficacy in depression. In personalized medicine, various potential mediators for the relationship between exercise and depressive symptoms should be controlled. Since it has been consistently reported that exercise has no significant therapeutic effects on cognitive domains in depression, it is necessary that the efficacy of exercise on cognitive domains should be evaluated with rigorous methodology. Furthermore, it has been suggested that exercise has potentially positive effects in the prevention of depression. Despite the controversies regarding supporting evidence, it is concluded that exercise may be regarded as a “safe and broad-spectrum antidepressant” and used in the context of “prevention and treatment of depression.”

Antidepressive response of inpatients with major depression to adjuvant occupational therapy: a case-control study.

BACKGROUND: Despite marked costs and limited evidence regarding effectiveness, occupational therapy (OT) is widely applied in psychiatric settings and financed by health insurance companies in European countries. This pilot study investigated the antidepressive effects of adjuvant OT for patients with major depression in a 6-week inpatient setting, stratified for females and males. METHODS: A total of 114 inpatients with major depression were assigned to either a standard OT group (using basic handcraft) or an active control group that played board games (2 h daily, 5 days a week). HAMD-21 scores were assessed as the primary outcome parameter after 3-6 weeks. RESULTS: The OT intervention was not superior to "board game" (BG) activities in reducing depressive symptoms. However, significant interaction effects were found in favor of the OT group regarding anxiety measures and other variables. Male participants displayed more significant interaction effects than female participants. CONCLUSIONS: OT as an adjuvant short-term treatment for inpatients with major depression may be more efficacious than game interventions in terms of reducing anxiety and other symptoms, particularly in males. Trial registration The study was registered in the EU Clinical Trials Register as a multicenter trial (EudraCT Number 2009-016463-10; https://www.clinicaltrialsregister.eu/ctr-search/trial/2009-016463-10/DE#A) However, because of the elaborate setting requirements, the original study design with four centers was transformed into a solution with those two centers facilitating the pertinent resources. Furthermore, "mono-therapy with mirtazapine" was changed into "preferably mono-therapy with any antidepressant drug".