Department of Clinical Pharmacology, School of Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece.
School of Medicine, National and Kapodistrian University of Athens, Athens, Greece.
Front Immunol. 2021 May 20;12:677879. doi: 10.3389/fimmu.2021.677879. eCollection 2021.
Increased prevalence of depression has been observed among patients with multiple sclerosis (MS) and correlated with the elevated levels of proinflammatory cytokines and the overall deregulation of monoaminergic neurotransmitters that these patients exhibit. Antidepressants have proved effective not only in treating depression comorbid to MS, but also in alleviating numerous MS symptoms and even minimizing stress-related relapses. Therefore, these agents could prospectively prove beneficial as a complementary MS therapy.
This review aims at illustrating the underlying mechanisms involved in the beneficial clinical effects of antidepressants observed in MS patients.
Through a literature search we screened and comparatively assessed papers on the effects of antidepressant use both and MS models, taking into account a number of inclusion and exclusion criteria.
studies indicated that antidepressants promote neural and glial cell viability and differentiation, reduce proinflammatory cytokines and exert neuroprotective activity by eliminating axonal loss. studies confirmed that antidepressants delayed disease onset and alleviated symptoms in Experimental Autoimmune Encephalomyelitis (EAE), the most prevalent animal model of MS. Further, antidepressant agents suppressed inflammation and restrained demyelination by decreasing immune cell infiltration of the CNS.
Antidepressants were efficient in tackling numerous aspects of disease pathophysiology both and models. Given that several antidepressants have already proved effective in clinical trials on MS patients, the inclusion of such agents in the therapeutic arsenal of MS should be seriously considered, following an individualized approach to minimize the adverse events of antidepressants in MS patients.
多发性硬化症（MS）患者中观察到抑郁患病率增加，这与这些患者表现出的促炎细胞因子水平升高和单胺能神经递质整体失调有关。抗抑郁药不仅已被证明可有效治疗 MS 合并的抑郁症，还可缓解许多 MS 症状，甚至最小化与压力相关的复发。因此，这些药物可能作为一种补充性 MS 治疗方法具有前瞻性益处。
本综述旨在说明抗抑郁药在 MS 患者中观察到的有益临床效果的潜在机制。
通过文献检索，我们筛选并比较了评估抗抑郁药使用对 MS 模型和对照模型影响的研究，并考虑了一些纳入和排除标准。
临床研究表明，抗抑郁药可促进神经和神经胶质细胞的存活和分化，降低促炎细胞因子的水平，并通过消除轴索丢失发挥神经保护作用。实验性自身免疫性脑脊髓炎（EAE）是最常见的 MS 动物模型，临床前研究证实，抗抑郁药可延迟疾病发作并缓解 EAE 症状。此外，抗抑郁药可通过减少中枢神经系统免疫细胞浸润来抑制炎症和阻止脱髓鞘。
抗抑郁药在 MS 模型和对照模型中都能有效地解决疾病病理生理学的许多方面。鉴于几种抗抑郁药已在 MS 患者的临床试验中证明有效，应根据个体化方法考虑将此类药物纳入 MS 的治疗方案中，以最小化 MS 患者抗抑郁药的不良反应。
