Cognitive, behavioral, neuroimaging and inflammatory biomarkers after hospitalization for COVID-19 in Brazil

Kenji Sudo, Felipe; Pinto, Talita P.; G. Q. Barros-Aragão, Fernanda; Bramati, Ivanei; Marins, Theo F.; Monteiro, Marina; Meireles, Fernanda; Soares, Rejane; Erthal, Pilar; Calil, Victor; Assuncao, Naima; Oliveira, Natalia; Bondarovsky, Joana; Lima, Camila; Chagas, Beatriz; Batista, Alana; Lins, Julia; Pinheiro, Thaís L.; Mendonca, Felippe; Silveira de Souza, Andrea; Rodrigues, Fernanda C.; de Freitas, Gabriel R.; Kurtz, Pedro; Mattos, Paulo; Rodrigues, Erika C.; De Felice, Fernanda G.; Tovar-Moll, Fernanda

doi:10.1016/j.bbi.2023.10.020

Cited by 3 publications

(2 citation statements)

References 85 publications

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“…We have recently established that brain TNFα upregulation triggers microglial-mediated synaptic engulfing in a mouse model of CNS viral infection leading to memory impairment ( Figueiredo et al, 2019 ). In a COVID-19 longitudinal cohort, we showed that acute and persistent blood TNFα is associated with persistent neuroimaging and memory alterations up to one-year post-COVID ( Sudo et al, 2024 ). Infliximab treatment, an anti-TNFα monoclonal antibody, alleviated memory deficits and synapse pathology in infected mice.…”

Section: Discussionmentioning

confidence: 99%

Changes in neuroinflammatory biomarkers correlate with disease severity and neuroimaging alterations in patients with COVID-19 neurological complications

Barros-Aragão,

Pinto,

Carregari

et al. 2024

Brain, Behavior, & Immunity - Health

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Section: Discussionmentioning

confidence: 99%

Changes in neuroinflammatory biomarkers correlate with disease severity and neuroimaging alterations in patients with COVID-19 neurological complications

Barros-Aragão,

Pinto,

Carregari

et al. 2024

Brain, Behavior, & Immunity - Health

Self Cite

View full text Add to dashboard Cite

“…We have recently established that brain TNFα upregulation triggers microglial-mediated synaptic engul ng in a mouse model of CNS viral infection leading to memory impairment(Figueiredo et al, 2019). In a COVID-19 longitudinal cohort, we showed that acute and persistent blood TNFα is associated with persistent neuroimaging and memory alterations up to one-year post-COVID(Sudo et al, 2024). In iximab treatment, an anti-TNFα monoclonal antibody, alleviated memory de cits and synapse pathology in infected mice.…”

mentioning

confidence: 86%

Changes in neuroinflammatory biomarkers correlate with disease severity and neuroimaging alterations in patients with COVID-19 neurological complications.

Barros-Aragão,

Pinto,

Carregari

et al. 2024

Preprint

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COVID-19 induces acute and persistent neurological symptoms in mild and severe cases. Proposed concomitant mechanisms include direct viral infection and strain, coagulopathy, hypoxia, and neuroinflammation. However, underlying molecular alterations associated with multiple neurological outcomes in both mild and severe cases are majorly unexplored. To illuminate possible mechanisms leading to COVID-19 neurological disease, we retrospectively investigated in detail a cohort of 35 COVID-19 mild and severe hospitalized patients presenting neurological alterations subject to clinically indicated cerebrospinal fluid (CSF) sampling. Clinical and neurological investigation, brain imaging, viral sequencing, and cerebrospinal CSF analyses were carried out. We found that COVID-19 patients presented heterogeneous neurological symptoms dissociated from lung burden. Nasal swab viral sequencing revealed a dominant strain at the time of the study, and we could not detect traces of SARS-CoV-2’s spike protein in patients’ CSF by multiple reaction monitoring analysis. Patients presented ubiquitous systemic hyper-inflammation and broad alterations in CSF proteomics related to inflammation, innate immunity, and hemostasis, irrespective of COVID-19 severity or neuroimaging alterations. Elevated CSF interleukin-6 (IL6) correlated with disease severity (sex-, age-, and comorbidity-adjusted mean Severe 24.5 pg/ml, 95% confidence interval (CI) 9.62–62.23 vs. Mild 3.91 pg/mL CI 1.5–10.3 patients, p = 0.019). CSF tumor necrosis factor-alpha (TNFα) and IL6 levels were higher in patients presenting pronounced neuroimaging alterations compared to those who did not (sex-, age-, and comorbidity-adjusted mean TNFα Pronounced 3.4, CI 2.4–4.4 vs. Non-Pronounced 2.0, CI 1.4–2.5, p = 0.022; IL6 Pronounced 33.11, CI 8.89-123.31 vs Non-Pronounced 6.22, CI 2.9-13.34, p = 0.046). Collectively, our findings put neuroinflammation as a possible driver of COVID-19 acute neurological disease in mild and severe cases.

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Neurological Complications of COVID-19: Unraveling the Pathophysiological Underpinnings and Therapeutic Implications

Vashisht,

Singh

et al. 2024

Viruses

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease (COVID-19), induced a global pandemic with a diverse array of clinical manifestations. While the acute phase of the pandemic may be waning, the intricacies of COVID-19′s impact on neurological health remain a crucial area of investigation. Early recognition of the spectrum of COVID-19 symptoms, ranging from mild fever and cough to life-threatening respiratory distress and multi-organ failure, underscored the significance of neurological complications, including anosmia, seizures, stroke, disorientation, encephalopathy, and paralysis. Notably, patients requiring intensive care unit (ICU) admission due to neurological challenges or due to them exhibiting neurological abnormalities in the ICU have shown increased mortality rates. COVID-19 can lead to a range of neurological complications such as anosmia, stroke, paralysis, cranial nerve deficits, encephalopathy, delirium, meningitis, seizures, etc., in affected patients. This review elucidates the burgeoning landscape of neurological sequelae associated with SARS-CoV-2 infection and explores the underlying neurobiological mechanisms driving these diverse manifestations. A meticulous examination of potential neuroinvasion routes by SARS-CoV-2 underscores the intricate interplay between the virus and the nervous system. Moreover, we dissect the diverse neurological manifestations emphasizing the necessity of a multifaceted approach to understanding the disease’s neurological footprint. In addition to elucidating the pathophysiological underpinnings, this review surveys current therapeutic modalities and delineates prospective avenues for neuro-COVID research. By integrating epidemiological, clinical, and diagnostic parameters, we endeavor to foster a comprehensive analysis of the nexus between COVID-19 and neurological health, thereby laying the groundwork for targeted therapeutic interventions and long-term management strategies.

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Cognitive, behavioral, neuroimaging and inflammatory biomarkers after hospitalization for COVID-19 in Brazil

Cited by 3 publications

References 85 publications

Changes in neuroinflammatory biomarkers correlate with disease severity and neuroimaging alterations in patients with COVID-19 neurological complications

Changes in neuroinflammatory biomarkers correlate with disease severity and neuroimaging alterations in patients with COVID-19 neurological complications

Changes in neuroinflammatory biomarkers correlate with disease severity and neuroimaging alterations in patients with COVID-19 neurological complications.

Neurological Complications of COVID-19: Unraveling the Pathophysiological Underpinnings and Therapeutic Implications

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