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The Intersection between COVID-19, the Gene Family of ACE2 and Alzheimer’s Disease
Author(s) -
Mahdi Montazer Haghighi,
Erfan Ghani Kakhki,
Christine Sato,
Mahdi Ghani,
Ekaterina Rogaeva
Publication year - 2020
Publication title -
neuroscience insights
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.735
H-Index - 17
ISSN - 2633-1055
DOI - 10.1177/2633105520975743
Subject(s) - disease , inflammation , immune dysregulation , gene , covid-19 , angiotensin converting enzyme 2 , biology , immunology , genetics , medicine , infectious disease (medical specialty)
We reviewed factors that might influence COVID-19 outcomes (eg, neurological symptoms), including the link to Alzheimer’s disease. Since the virus triggers COVID-19 infection through binding to ACE2, we focused on the ACE2 gene family, including ACE. Both ACE2 and ACE are involved in the renin–angiotensin system (RAS). In general, ACE causes inflammation and vasoconstriction, while ACE2 leads to anti-inflammation activity and vasodilation. The disturbed balance between these counter-regulatory pathways could influence susceptibility to COVID-19. Notably, dysregulation of the RAS-equilibrium contributes to Alzheimer’s disease. Differences in the incidence and symptoms of COVID-19 in diverse populations could be attributed to variability in the human genome. For example, ACE and ACE2 variations could modify the outcome of COVID-19 in different populations. It would be important to conduct genome-wide studies to detect variants influencing COVID-19 presentation, with a special focus on variants affecting immune-related pathways and expression of RAS-related genes.

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