Are dopamine and serotonin involved in COVID-19 pathophysiology?

Are dopamine and serotonin involved in COVID-19 pathophysiology?
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DOI:
10.1016/j.ejpsy.2020.10.004
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发表时间:
2021-01
期刊:
The European journal of psychiatry
影响因子:
--
通讯作者:
Bernardini F
Bernardini F
中科院分区:
其他
文献类型:
--
作者:
Attademo L;Bernardini F

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全世界都受到 SARS-CoV-2 引起的 COVID-19 的影响,给所有国家的健康、社会和经济系统带来了前所未有的后果。 COVID-19 大流行不仅威胁身体健康,也威胁心理健康。 1 事实上,越来越多的科学证据表明,COVID-19 对感染者的心理健康以及对被隔离者、精神疾病患者和医护人员的心理影响具有潜在的直接影响。 1, 2 关于第一点(即感染对心理健康的直接影响)的讨论似乎相当有趣。临床证据表明,COVID-19 患者可能会遇到短期和长期的心理健康问题。 COVID-19 患者出现谵妄、精神错乱、烦躁和意识改变,以及抑郁、焦虑、创伤性应激和失眠的情况并不罕见。 1, 2 冠状病毒感染的神经精神后遗症的假定病因学机制可能具有多因素基础,但仍不明确。病毒感染对中枢神经系统的直接影响、脑血管疾病、生理损伤、炎症反应和免疫系统反应、医疗干预、社会隔离、身体不适、新型严重和潜在致命疾病的心理影响、对感染他人的担忧以及临床/社会耻辱,都可能独立或更可能协同地参与病因过程。 1, 2有趣的是,最近有人推测多巴胺和血清素合成途径的改变可能与 COVID-19 的病理生理学有关。 3 血管紧张素 I 转换酶 2(ACE2,编码 SARS-CoV-2 的主要受体)和多巴脱羧酶(DDC,编码催化多巴胺、血清素和组胺生物合成的酶)之间的显着联系表明这些神经递质可能参与其中,基于与基因共表达、共调节和功能相关的相似性。事实上,有证据表明 ACE2 和 DDC 在非神经元细胞类型中共同表达和共同调节。此外,已经证明 ACE2 受体在多巴胺神经元中高度表达,而在帕金森病(以多巴胺缺乏为特征)中表达减少。 4 因此,
The whole world is being affected by COVID-19 caused by SARS-CoV-2, with unprecedented consequences on health, social and economic systems in all countries. The COVID-19 pandemic is not only a threat to physical health but mental health as well. 1 In fact, scientific evidence is emerging on the potential direct effects of COVID-19 on mental health of people infected, as well as on the psychological impact on people quarantined, on patients with psychiatric disorders and on the health-care workforce. 1, 2 Discussion on the first of these points (ie the direct effects of the infection on mental health) appears to be rather interesting. Clinical evidence is showing that patients with COVID-19 might experience short-and long-term mental health problems. Delirium, confusion, agitation, and altered consciousness, as well as depression, anxiety, traumatic stress, and insomnia, have been described not rarely in patients with COVID-19. 1, 2 Putative aetiological mechanisms of the neuropsychiatric sequelae of coronavirus infection have a likely multifactorial basis but are still poorly established. The direct effects of viral infection on CNS, cerebrovascular disease, physiological impairments, the inflammatory response and the immune system reaction, medical interventions, social isolation, physical discomfort, the psychological impact of a novel severe and potentially fatal illness, concerns about infecting others, and clinical/social stigma, might be all involved in the aetiological process, independently or more likely synergistically. 1, 2Interestingly, it has been recently postulated that alterations of both the dopamine and serotonin synthetic pathways might be involved in COVID-19 pathophysiology. 3 The possible involvement of these neurotransmitters is suggested by a significant link---based on similarities related to gene co-expression, co-regulation and function---between Angiotensin I Converting Enzyme 2 (ACE2, encoding the main receptor to SARS-CoV-2) and Dopa Decarboxylase (DDC, encoding the enxyme that catalyzes the biosynthesis of dopamine, serotonin and histamine). In fact, evidence shows that ACE2 and DDC co-express and co-regulate in nonneuronal cell types. Furthermore, it has been demonstrated that ACE2 receptors are highly expressed in dopamine neurons and that they are reduced in Parkinson’s disease (characterized by dopamine deficiency). 4 Hence, a