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Review
. 2022;20(4):738-750.
doi: 10.2174/1570159X19666210609162809.

Potential Mechanisms and Clinical Effectiveness of Acupuncture in Depression

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Review

Potential Mechanisms and Clinical Effectiveness of Acupuncture in Depression

Na-Na Yang et al. Curr Neuropharmacol. 2022.

Abstract

Major depressive disorder is the most common mental disorder with significant economic burden and limited treatments. Acupuncture has emerged as a promising non-pharmacological treatment for reducing depressive symptoms. However, the potential mechanisms and clinical effectiveness of acupuncture are not fully understood. This review aimed to: (1) summarize the available evidence on the mechanisms and clinical effectiveness of acupuncture for depression, and then (2) compare with pharmacological interventions, guiding future studies. Studies with animal models of depression and patients have shown that acupuncture could increase hippocampal and network neuroplasticity and decrease brain inflammation, potentially to alleviating depressive disorders. Overall clinical studies indicated that acupuncture could relieve primary depression, particularly milder cases, and was helpful in the management of post-stroke depression, pain-related depression, and postpartum depression both as an isolated and adjunct treatment. It was emphasized that acupuncture combined with antidepressant pharmacological treatment not only enhanced the improvement of primary and secondary depressive symptoms but also reduced the side effects of the medical treatment, which is the main cause for high dropout rates with drug treatment. In summary, substantial evidence from animal and human researches supported the beneficial effect of acupuncture in depression. However, most clinical trials of acupuncture were small, and it is unclear whether their findings can be generalized, so more studies are needed.

Keywords: Depression; acupuncture; inflammation; neuroplasticity; non-pharmacological treatment; pharmacological treatments.

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Figures

Fig. (1)
Fig. (1)
Hypothesis of neuroplasticity and immune involvement in the pathophysiology of major depressive disorder. The reduction in hippocampal volume was related to the duration of depression (A). The synaptic contacts and processions between neurons were decreased in major depressive disorder, which can be reversed by upregulating the expression of 5-HT and BDNF (B). Activated microglia produce inflammatory cytokines and nitric oxide that can contribute to depression through hyper-activation of the HPA axis and IDO (C). Gut microbiotic permeability accelerated the production of inflammatory cytokines in peripheral tissues (D), which act directly on the CNS via leaky regions of the brain-brain barrier (E). 5-HT, serotonin; BDNF, Brain-derived neurotrophic factor; HPA, the hypothalamic-pituitary-adrenal axis; IDO, the enzyme indoleamine-2,3-deoxygenase.

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