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Article: The Neural Correlates of COVID-19 induced Erectile Dysfunction in Males

TitleThe Neural Correlates of COVID-19 induced Erectile Dysfunction in Males
Authors
Issue Date30-May-2023
PublisherOAE Publishing
Citation
Ageing and Neurodegenerative Diseases, 2023, v. 3, n. 8, p. 1-9 How to Cite?
Abstract

Emerging evidence suggests that there are long-term complications after recovery from COVID-19, which involve multiple systems and lead to deterioration of the quality of life. Among these different complications, male sexual dysfunction, in particular erectile dysfunction, is one of the complications being identified recently. It was initially hypothesized that due to the presence of Angiotensin-converting enzyme II (ACE2) and transmembrane protease serine 2 (TMPRSS 2) in testes and Leydig cells, the male reproductive system is vulnerable to the infection of COVID-19, which may lead to a decrease in testosterone production and sexual dysfunction. However, evidence from a recent neurological study suggests that COVID-19 may be directly associated with dysregulation of the nervous systems at the central level in regions including the limbic system (e.g., hippocampus and amygdala), hypothalamus, brainstem, and the peripheral system (e.g., sympathetic nerves, olfactory bulb). As these affected regions are crucial for sexual behaviors, these observations may provide an alternate explanation for sexual dysfunction in COVID-19 survivors. To explore the potential involvement of the nervous system in sexual dysfunction induced by COVID-19, this review discusses the recent findings from the neurological perspective and states the possible research work that may be needed to delineate the underlying pathology.


Persistent Identifierhttp://hdl.handle.net/10722/357178
ISSN

 

DC FieldValueLanguage
dc.contributor.authorLau, Benson Wui-Man-
dc.contributor.authorLee, Jada Chia-Di-
dc.contributor.authorChan, Dalinda-Isabel Sanchez-Vidaña,Jackie Ngai-Man-
dc.contributor.authorLau, Way Kwok-Wai-
dc.contributor.authorSo, Kwok-Fai-
dc.date.accessioned2025-06-23T08:53:49Z-
dc.date.available2025-06-23T08:53:49Z-
dc.date.issued2023-05-30-
dc.identifier.citationAgeing and Neurodegenerative Diseases, 2023, v. 3, n. 8, p. 1-9-
dc.identifier.issn2769-5301-
dc.identifier.urihttp://hdl.handle.net/10722/357178-
dc.description.abstract<p>Emerging evidence suggests that there are long-term complications after recovery from COVID-19, which involve multiple systems and lead to deterioration of the quality of life. Among these different complications, male sexual dysfunction, in particular erectile dysfunction, is one of the complications being identified recently. It was initially hypothesized that due to the presence of Angiotensin-converting enzyme II (ACE2) and transmembrane protease serine 2 (TMPRSS 2) in testes and Leydig cells, the male reproductive system is vulnerable to the infection of COVID-19, which may lead to a decrease in testosterone production and sexual dysfunction. However, evidence from a recent neurological study suggests that COVID-19 may be directly associated with dysregulation of the nervous systems at the central level in regions including the limbic system (e.g., hippocampus and amygdala), hypothalamus, brainstem, and the peripheral system (e.g<em>.</em>, sympathetic nerves, olfactory bulb). As these affected regions are crucial for sexual behaviors, these observations may provide an alternate explanation for sexual dysfunction in COVID-19 survivors. To explore the potential involvement of the nervous system in sexual dysfunction induced by COVID-19, this review discusses the recent findings from the neurological perspective and states the possible research work that may be needed to delineate the underlying pathology.</p>-
dc.languageeng-
dc.publisherOAE Publishing-
dc.relation.ispartofAgeing and Neurodegenerative Diseases-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.titleThe Neural Correlates of COVID-19 induced Erectile Dysfunction in Males-
dc.typeArticle-
dc.identifier.doi10.20517/and.2023.09-
dc.identifier.volume3-
dc.identifier.issue8-
dc.identifier.spage1-
dc.identifier.epage9-
dc.identifier.eissn2769-5301-

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