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   <ref-type name="Journal Article">17</ref-type>
   <contributors>
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   <titles>
    <title></title>
   </titles>
   <dates>
    <year>2023</year>
    <pub-dates>
     <date>2023-04-05</date>
    </pub-dates>
   </dates>
   <doi>10.3390/jpm13010123</doi>
   <abstract>To date, multiple efforts have been made to use genome-wide association studies (GWAS) to untangle the genetic basis for SARS-CoV-2 infection susceptibility and severe COVID-19. However, data on the genetic-related effects of SARS-CoV-2 infection on the presence of accompanying and long-term post-COVID-19 neurological symptoms in younger individuals remain absent. We aimed to examine the possible association between SNPs found in a GWAS of COVID-19 outcomes and three phenotypes: SARS-CoV-2 infection, neurological complications during disease progression, and long-term neurological complications in young adults with a mild-to-moderate disease course. University students (N = 336, age 18–25 years, European ancestry) with or without COVID-19 and neurological symptoms in anamnesis comprised the study sample. Logistic regression was performed with COVID-19-related phenotypes as outcomes, and the top 25 SNPs from GWAS meta-analyses and an MR study linking COVID-19 and cognitive deficits were found. We replicated previously reported associations of the FURIN and SLC6A20 gene variants (OR = 2.36, 95% CI 1.31–4.24) and OR = 1.94, 95% CI 1.08–3.49, respectively) and remaining neurological complications (OR = 2.12, 95% CI 1.10–4.35 for SLC6A20), while NR1H2 (OR = 2.99, 95% CI 1.39–6.69) and TMPRSS2 (OR = 2.03, 95% CI 1.19–3.50) SNPs were associated with neurological symptoms accompanying COVID-19. Our findings indicate that genetic variants related to a severe COVID-19 course in adults may contribute to the occurrence of neurological repercussions in individuals at a young age. © 2023 by the authors.</abstract>
   <urls>
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     <url>https://repo.bashgmu.ru/publication/4226</url>
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     <url>https://repo.bashgmu.ru/files/4402</url>
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