APOE ε4 polymorphism has been recently described as a possible association with cognitive deficits in COVID-19 patients. This research aimed to establish the correlation between COVID-19 and cognitive impairment, and the APOE gene polymorphism among outpatients. We performed a cross-sectional study with confirmed COVID-19 patients and neurological symptoms that persisted for more than three months from onset. APOE genotypes were determined. The final number of patients included in this study was 219, of which 186 blood samples were collected for APOE genotyping, evaluated 4.5 months after COVID-19. Among the participants, 143 patients (65.3%) reported memory impairment symptoms as their primary concern. However, this complaint was objectively verified through screening tests (Addenbrooke Cognitive Examination-Revised and Mini-Mental State Examination) in only 36 patients (16.4%). The group experiencing cognitive decline exhibited a higher prevalence of the APOE ε4 allele than the normal group (30.8% vs. 16.4%, respectively, p = 0.038). Furthermore, the APOE ε4 allele and anxiety symptoms remained significant after multivariate analysis. This study assessed an outpatient population where cognitive changes were the primary complaint, even in mild cases. Moreover, the ε4 allele, sleep disorders, and anxiety symptoms were more frequent in the cognitive decline group.

The new severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was first reported in China and is responsible for Coronavirus disease (COVID-19). Despite being well tolerated by most patients, a fraction of cases evolve into a potentially fatal condition requiring intensive care. In addition to respiratory complications, several studies have reported cases of patients who developed intense thrombosis, including acute myocardial infarction and ischemic stroke, as well as the presence of elevated coagulation markers. Evidence has shown that the virus can interact directly with platelets and modulate their thrombotic and inflammatory functions, with significant prognostic implications. It is important to highlight that the emerging literature shows that when hyperactive these cells can act as pro-viral infections both in transporting their particles and in increasing inflammation, leading to a hyperinflammatory state and consequent clinical worsening. In this review, we searched for studies available in public databases and discussed the interaction of platelet biomarkers in the pathogenesis of COVID-19. In this context, understanding the mechanism of SARS-CoV-2 and these cells in different clinical conditions could help us to understand the coagulation and inflammation profiles of critically ill patients with the disease, guiding faster clinical management and enabling the reuse and targeting of more efficient therapies.

Angiotensin-converting enzyme 2 (ACE2) and the transmembrane serine protease 2 (TMPRSS2) are recognized as entry proteins of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and recently their Single Nucleotide Polymorphisms (SNP) have been studied in different populations to elucidate the impact on disease. The aim of this study was to evaluate the genetic SNP of ACE2 (rs35803318) and TMPRSS2 (rs2070788) genes in COVID-19 patients from Northeast Brazil compared with global populations, as well as the expression quantitative trait locus (eQTL). For ACE2 (rs35803318), we found 92.6% CC, 3.4% CT, and 4.0% TT genotype carriers in SARS-CoV-2-positive patients. Surprisingly, only the genotype frequencies of ACE2 SNP were not in Hardy-Weinberg equilibrium. For TMPRSS2 rs2070788, we found 22.3% GG, 50.7% AG, and 27% AA genotype carriers in SARS-CoV-2-positive patients. The expression quantitative trait loci (eQTLs) revealed that rs35803318 was associated with an altered PIR gene expression, and rs2070788 was found eQTLs association only with lung tissue. No significant association was identified between the genotype distribution of SNPs and the 'patient's outcome. In conclusion, our results suggest that ACE2 and TMPRSS2 may not be protective factors for global populations, including the Brazilian population, since the presence of SNPs does not affect the 'patient's outcome as described by other studies.