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10.1007/s13760-021-01748-5

http://scihub22266oqcxt.onion/10.1007/s13760-021-01748-5
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34327666!8321009!34327666
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suck abstract from ncbi

pmid34327666      Acta+Neurol+Belg 2021 ; 121 (5): 1117-1122
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  • Is there a common pathophysiological mechanism between COVID-19 and depression? #MMPMID34327666
  • da Silva Lopes L; Silva RO; de Sousa Lima G; de Araujo Costa AC; Barros DF; Silva-Neto RP
  • Acta Neurol Belg 2021[Oct]; 121 (5): 1117-1122 PMID34327666show ga
  • COVID-19 is a disease caused by SARS-CoV-2 and was initially considered to cause serious damage to the respiratory system. Over time, it has been found to affect other organs due to its ability to bind to the ACE2 receptor (type 2 angiotensin-converting enzyme), which can be found in various tissues, including the central nervous system. In addition, a large formation of pro-inflammatory cytokines responsible for various lesions was observed during the evolution of this disease. Our objective was to demonstrate the molecular mechanisms involved in the infection that may demonstrate the relationship between COVID-19 and the development of depressive conditions. Based on the main medical databases (LiLacs, SciELO, Bireme, Scopus, EBSCO, and PubMed) and using the terms 'coronavirus infections' AND 'Inflammation' AND 'depression' AND 'cytokines', we conducted an integrative review of articles published in 2020. Considering this stage of Covid-19 and the inflammatory component of depression, this review showed a relationship between these two conditions based on common pathophysiological mechanisms indicating possible depressive disorders in surviving patients, especially in the most severe cases. The role of inflammatory cytokines and the presence of ACE-2 receptors on the cell surface appear to be the common pathophysiological mechanism between COVID-19 and depression.
  • |COVID-19/*complications/*physiopathology[MESH]
  • |Depression/*etiology/*physiopathology[MESH]
  • |Humans[MESH]


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