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Hyper/neuroinflammation in COVID-19 and suicide etiopathogenesis: Hypothesis for a nefarious collision?
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 atten...
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Author(s). Published by Elsevier Ltd.
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8916836/ https://www.ncbi.nlm.nih.gov/pubmed/35289272 http://dx.doi.org/10.1016/j.neubiorev.2022.104606 |
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author | 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, K.D. |
author_facet | 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, K.D. |
author_sort | Costanza, A. |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-8916836 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | The Author(s). Published by Elsevier Ltd. |
record_format | MEDLINE/PubMed |
spelling | pubmed-89168362022-03-14 Hyper/neuroinflammation in COVID-19 and suicide etiopathogenesis: Hypothesis for a nefarious collision? 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, K.D. Neurosci Biobehav Rev Article 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. The Author(s). Published by Elsevier Ltd. 2022-05 2022-03-12 /pmc/articles/PMC8916836/ /pubmed/35289272 http://dx.doi.org/10.1016/j.neubiorev.2022.104606 Text en © 2022 The Authors Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active. |
spellingShingle | Article 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, K.D. Hyper/neuroinflammation in COVID-19 and suicide etiopathogenesis: Hypothesis for a nefarious collision? |
title | Hyper/neuroinflammation in COVID-19 and suicide etiopathogenesis: Hypothesis for a nefarious collision? |
title_full | Hyper/neuroinflammation in COVID-19 and suicide etiopathogenesis: Hypothesis for a nefarious collision? |
title_fullStr | Hyper/neuroinflammation in COVID-19 and suicide etiopathogenesis: Hypothesis for a nefarious collision? |
title_full_unstemmed | Hyper/neuroinflammation in COVID-19 and suicide etiopathogenesis: Hypothesis for a nefarious collision? |
title_short | Hyper/neuroinflammation in COVID-19 and suicide etiopathogenesis: Hypothesis for a nefarious collision? |
title_sort | hyper/neuroinflammation in covid-19 and suicide etiopathogenesis: hypothesis for a nefarious collision? |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8916836/ https://www.ncbi.nlm.nih.gov/pubmed/35289272 http://dx.doi.org/10.1016/j.neubiorev.2022.104606 |
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