Centre for Preclinical Research and Technology (CEPT), Department of Experimental and Clinical Pharmacology, Medical University of Warsaw, 1B Banacha Street, 02-097 Warsaw, Poland.
Department of Neurochemistry, Institute of Psychiatry and Neurology, 9 Sobieskiego Street, 02-957 Warsaw, Poland.
Cells. 2021 Sep 23;10(10):2519. doi: 10.3390/cells10102519.
According to the World Health Organization (WHO), more than 700,000 people die per year due to suicide. Suicide risk factors include a previous suicide attempt and psychiatric disorders. The highest mortality rate in suicide worldwide is due to depression. Current evidence suggests that suicide etiopathogenesis is associated with neuroinflammation that activates the kynurenine pathway and causes subsequent serotonin depletion and stimulation of glutamate neurotransmission. These changes are accompanied by decreased BDNF (brain-derived neurotrophic factor) levels in the brain, which is often linked to impaired neuroplasticity and cognitive deficits. Most suicidal patients have a hyperactive hypothalamus-pituitary-adrenal (HPA) axis. Epigenetic mechanisms control the above-mentioned neurobiological changes associated with suicidal behaviour. Suicide risk could be attenuated by appropriate psychological treatment, electroconvulsive treatment, and drugs: lithium, ketamine, esketamine, clozapine. In this review, we present the etiopathogenesis of suicide behaviour and explore the mechanisms of action of anti-suicidal treatments, pinpointing similarities among them.
据世界卫生组织（WHO）统计，每年有超过 70 万人因自杀而死亡。自杀的危险因素包括之前的自杀企图和精神障碍。全球自杀的死亡率最高是由于抑郁症。目前的证据表明，自杀的发病机制与神经炎症有关，神经炎症会激活犬尿氨酸途径，导致随后的血清素耗竭和谷氨酸神经传递的刺激。这些变化伴随着大脑中脑源性神经营养因子（BDNF）水平的降低，这通常与神经可塑性受损和认知缺陷有关。大多数有自杀倾向的患者下丘脑-垂体-肾上腺（HPA）轴活动过度。表观遗传机制控制着与自杀行为相关的上述神经生物学变化。适当的心理治疗、电惊厥治疗和药物（锂、氯胺酮、艾司氯胺酮、氯氮平）可以降低自杀风险。在这篇综述中，我们介绍了自杀行为的发病机制，并探讨了抗自杀治疗的作用机制，指出了它们之间的相似之处。
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