{"id":1506,"date":"2021-07-13T14:14:54","date_gmt":"2021-07-13T17:14:54","guid":{"rendered":"https:\/\/petrusraulino.com.br\/?p=1506"},"modified":"2024-11-11T17:15:12","modified_gmt":"2024-11-11T20:15:12","slug":"covid-19-affects-the-neurobiology-of-suicide","status":"publish","type":"post","link":"https:\/\/petrusraulino.com.br\/en\/covid-19-affects-the-neurobiology-of-suicide\/","title":{"rendered":"Does COVID-19 affect the neurobiology of suicide?"},"content":{"rendered":"

By Dr. Petrus Raulino<\/strong><\/em><\/p>\n

A review published in the journal Current Psychiatry Reports analyzed the effect of COVID-19<\/a> on the biological characteristics of vulnerability to suicide and their interaction with the biological pathways related to suicide.<\/span><\/p>\n

The hypothesis is that SARS-CoV-2 interacts with various biological processes underlying suicidal behavior, such as the renin-angiotensin system, nicotinic receptors (dysregulation of the cholinergic anti-inflammatory pathway) and central and systemic inflammation.<\/span><\/p>\n

In addition, social distancing measures can also worsen objective (physical distancing) or subjective (loneliness) social disconnection, increasing the risk especially in people with a predisposition to mental disorders.<\/span><\/p>\n

As for the renin-angiotensin system, recent research on COVID-19 has shown that the virus enters host cells through the interaction of its \"spike\" protein with the angiotensin-converting enzyme 2 (ACE-2) receptor, decreasing its activity.<\/span><\/p>\n

By unbalancing the ACE\/ACE-2 metabolic pathways, COVID-19 could theoretically affect vulnerability to suicide in individuals who carry the ACE \"risk\" genotypes.<\/span><\/p>\n

Patients at risk of suicide may be more susceptible to dysregulation of the hypothalamic-pituitary-adrenal axis following SARS-CoV-2 infection because the virus targets ACE-2 and may affect the ACE\/ACE-2 balance that is associated with dysregulation of the hypothalamic-pituitary-adrenal axis in depressed individuals.<\/span><\/p>\n

COVID-19-related inflammation can also extend to the Central Nervous System through blood-brain barrier breakdown, viral neuroinvasion and cytokine secretion.<\/span><\/p>\n

In viral infections, several mechanisms may be related to neuroinflammation: retrograde axonal transport of the virus from the respiratory mucosa, peripheral inflammation that modulates brain function and migration of mononuclear cells transporting the virus across the blood-brain barrier.<\/span><\/p>\n

In the brain, SARS-CoV-2 infection can theoretically initiate chronic low-grade inflammation that alters cognitive functions and induces neurotoxicity and neurodegeneration, thus setting the stage for psychiatric disorders.<\/span><\/p>\n

Knowledge of the interactions between COVID-19 and the neurobiology of suicide could bring benefits for the development of suicide prevention treatments in the context of the pandemic.<\/span><\/p>\n

In addition, it can help to demystify the search for treatment with a psychiatrist. medicines against Covid<\/a>.<\/span><\/p>\n

References<\/h4>\n

Conejero, I., Nobile, B., Oli\u00e9, E., & Courtet, P. (2021). How does COVID-19 affect the neurobiology of suicide? Current psychiatry reports, 23(4), 1-13.<\/span><\/p>\n

Lan, J., Ge, J., Yu, J., Shan, S., Zhou, H., Fan, S., ... & Wang, X. (2020). Structure of the SARS-CoV-2 spike receptor-binding domain bound to the ACE2 receptor. Nature, 581(7807), 215-220.<\/span><\/p>\n

Zheng, Y. Y., Ma, Y. T., Zhang, J. Y., & Xie, X. (2020). COVID-19 and the cardiovascular system. Nature Reviews Cardiology, 17(5), 259-260.<\/span><\/p>\n

Hoffmann, M., Kleine-Weber, H., Schroeder, S., Kr\u00fcger, N., Herrler, T., Erichsen, S., ... & P\u00f6hlmann, S. (2020). SARS-CoV-2 cell entry depends on ACE2 and TMPRSS2 and is blocked by a clinically proven protease inhibitor. cell, 181(2), 271-280.<\/span><\/p>\n

Farsalinos, K., Niaura, R., Le Houezec, J., Barbouni, A., Tsatsakis, A., Kouretas, D., ... & Poulas, K. (2020). Nicotine and SARS-CoV-2: COVID-19 may be a disease of the nicotinic cholinergic system. Toxicology reports, 7, 658.<\/span><\/p>\n

Mamdani, M., Gomes, T., Greaves, S., Manji, S., Juurlink, D. N., Tadrous, M., ... & Antoniou, T. (2019). Association between angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and suicide. JAMA network open, 2(10), e1913304-e1913304.<\/span><\/p>\n

Ancelin, M. L., Carri\u00e8re, I., Scali, J., Ritchie, K., Chaudieu, I., & Ryan, J. (2013). Angiotensin-converting enzyme gene variants are associated with both cortisol secretion and late-life depression. Translational psychiatry, 3(11), e322-e322.<\/span><\/p>\n

Sparks, D. L., Hunsaker III, J. C., Amouyel, P., Malafosse, A., Bellivier, F., Leboyer, M., ... & Helbecque, N. (2009). Angiotensin I?converting enzyme I\/D polymorphism and suicidal behaviors. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics, 150(2), 290-294.<\/span><\/p>\n

Hishimoto, A., Shirakawa, O., Nishiguchi, N., Hashimoto, T., Yanagi, M., Nushida, H., ... & Maeda, K. (2006). Association between a functional polymorphism in the renin-angiotensin system and completed suicide. Journal of neural transmission, 113(12), 1915-1920.<\/span><\/p>\n

Baghai, T. C., Schule, C., Zwanzger, P., Minov, C., Zill, P., Ella, R., ... & Rupprecht, R. (2002). Hypothalamic-pituitary-adrenocortical axis dysregulation in patients with major depression is influenced by the insertion\/deletion polymorphism in the angiotensin I-converting enzyme gene. Neuroscience letters, 328(3), 299-303.<\/span><\/p>","protected":false},"excerpt":{"rendered":"

By Dr. Petrus Raulino A review published in the journal Current Psychiatry Reports analyzed the effect of COVID-19 on the biological characteristics of vulnerability to suicide and its interaction with biological pathways related to suicide. 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