Hyper/neuroinflammation in COVID-19 and suicide etiopathogenesis: Hypothesis for a nefarious collision?
Hyper/neuroinflammation in COVID-19 and suicide etiopathogenesis: Hypothesis for a nefarious collision?
复制标题
DOI：
10.1016/j.neubiorev.2022.104606
复制
发表时间：
2022-05
影响因子：
8.2
通讯作者：
Nguyen KD
中科院分区：
文献类型：
--
作者：
Costanza A;Amerio A;Aguglia A;Serafini G;Amore M;Hasler R;Ambrosetti J;Bondolfi G;Sampogna G;Berardelli I;Fiorillo A;Pompili M;Nguyen KD
越来越多的科学和临床证据表明，病理性高炎症是SARS-CoV-2感染和COVID-19急性疾病的主要特征。随着COVID-19长期综合征的出现，包括神经精神后遗症在内的几种慢性健康后果引起了公众和医学界的关注。由于炎症介质也被认为是自杀观念和行为的假定生物标志物，在COVID-19的背景下，过度炎症和神经炎症可能有一些碰撞点，重叠和相互关联。本文旨在总结当前对covid -19相关超/神经炎症的分子和细胞机制的了解，重点关注其与自杀发展的炎症假设的相关性。随后，还提到了通过免疫调节剂（其中许多处于实验阶段）以及精神药理学/心理治疗方法缓解COVID-19过度/神经炎症的策略。虽然COVID-19幸存者的自杀风险（迄今为止知之甚少）需要通过纵向研究进一步分析，但目前的观察和机制假设值得对这一可能出现的心理健康问题给予更多关注。
Accumulating scientific and clinical evidence highlighted pathological hyperinflammation as a cardinal feature of SARS-CoV-2 infection and acute COVID-19 disease. With the emergence of long COVID-19 syndrome, several chronic health consequences, including neuropsychiatric sequelae, have gained attention from the public and medical communities. Since inflammatory mediators have also been accredited as putative biomarkers of suicidal ideations and behaviors, hyper- and neuroinflammation might share some colliding points, overlapping and being interconnected in the context of COVID-19. This review aims to provide a summary of current knowledge on the molecular and cellular mechanisms of COVID-19-associated hyper/neuroinflammation with focus on their relevance to the inflammatory hypothesis of suicide development. Subsequently, strategies to alleviate COVID-19 hyper/neuroinflammation by immunomodulatory agents (many of which at experimental stages) as well as psychopharmacologic/psychotherapeutic approaches are also mentioned. While suicide risk in COVID-19 survivors - until now little known - needs further analysis through longitudinal studies, current observations and mechanistic postulates warrant additional attention to this possibly emerging mental health concern.
登录
查看更多内容
影响因子：
158.5
作者：
Boulware, David R.;Pullen, Matthew F.;Hullsiek, Kathy H.
通讯作者：
Hullsiek, Kathy H.
炎症反应导致 COVID-19 患者死后大脑皮层神经元死亡
影响因子：
5
作者：
Boroujeni, Mahdi Eskandarian;Simani, Leila;Aliaghaei, Abbas
通讯作者：
Aliaghaei, Abbas
DOI：
10.1016/j.ijid.2020.09.016
发表时间：
2020-11
期刊：
International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases
影响因子：
--
作者：
Afrin LB;Weinstock LB;Molderings GJ
通讯作者：
Molderings GJ
DOI：
10.1126/science.abc6261
发表时间：
2020-09-04
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Arunachalam PS;Wimmers F;Mok CKP;Perera RAPM;Scott M;Hagan T;Sigal N;Feng Y;Bristow L;Tak-Yin Tsang O;Wagh D;Coller J;Pellegrini KL;Kazmin D;Alaaeddine G;Leung WS;Chan JMC;Chik TSH;Choi CYC;Huerta C;Paine McCullough M;Lv H;Anderson E;Edupuganti S;Upadhyay AA;Bosinger SE;Maecker HT;Khatri P;Rouphael N;Peiris M;Pulendran B
通讯作者：
Pulendran B
影响因子：
10.6
作者：
Black, Carmen;Miller, Brian J.
通讯作者：
Miller, Brian J.