Involvement of oxidative stress in post-acute sequelae of COVID-19: clinical implications DOI Creative Commons

Paola Mayara Valente Coronel,

Denise Caroline Luiz Soares Basilio,

Isabelly Teixeira Espinoça

et al.

Redox Report, Journal Year: 2025, Volume and Issue: 30(1)

Published: March 3, 2025

Oxidative stress (OS) plays a key role in the pathophysiology of COVID-19 and may be associated with sequelae after severe SARS-CoV-2 infection. This study evaluated OS inflammation biomarkers blood from individuals post-acute (PASC). 64 male female participants were distributed into three groups: healthy (n = 20), acute patients (symptoms for <3 weeks, n 15), PASC >12 29). Analyses included inflammatory cytokines, myeloperoxidase (MPO) activity, markers, such as superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST), gamma-glutamyl transferase (GGT), reduced (GSH), uric acid (UA), thiobarbituric reactive substances (TBARS), protein carbonyls (PC). Individuals showed increased IL-6 IL-8. Both groups exhibited decreased SOD CAT. GST only group. Elevated GGT GSH found High UA levels observed individuals. There no changes TBARS values ⁣⁣in However, PC concentrations elevated this Correlations identified between markers parameters. These findings suggest that pronounced OS, which potentially exacerbates disease complications. Monitoring could aid patient prognosis management.

Language: Английский

COVID-19, post-acute COVID-19 syndrome (PACS, “long COVID”) and post-COVID-19 vaccination syndrome (PCVS, “post-COVIDvac-syndrome”): Similarities and differences DOI Creative Commons
Felix Scholkmann,

Christian-Albrecht May

Pathology - Research and Practice, Journal Year: 2023, Volume and Issue: 246, P. 154497 - 154497

Published: May 3, 2023

Worldwide there have been over 760 million confirmed coronavirus disease 2019 (COVID-19) cases, and 13 billion COVID-19 vaccine doses administered as of April 2023, according to the World Health Organization. An infection with severe acute respiratory syndrome 2 (SARS-CoV-2) can lead an disease, i.e. COVID-19, but also a post-acute (PACS, "long COVID"). Currently, side effects vaccines are increasingly being noted studied. Here, we summarise currently available indications discuss our conclusions that (i) these specific similarities differences PACS, (ii) new term should be used refer (post-COVID-19 vaccination syndrome, PCVS, colloquially "post-COVIDvac-syndrome"), (iii) is need distinguish between (ACVS) (PACVS) - in analogy PACS ("long Moreover, address mixed forms caused by natural SARS-CoV-2 vaccination. We explain why it important for medical diagnosis, care research use terms (PCVS, ACVS PACVS) order avoid confusion misinterpretation underlying causes enable optimal therapy. do not recommend "Post-Vac-Syndrome" imprecise. The article serves current problem "medical gaslighting" relation PCVS raising awareness among professionals supplying appropriate terminology disease.

Language: Английский

Citations

87
The role of peripheral inflammatory insults in Alzheimer’s disease: a review and research roadmap DOI Creative Commons
Keenan A. Walker, Lydia M. Le Page, Niccolò Terrando

et al.

Molecular Neurodegeneration, Journal Year: 2023, Volume and Issue: 18(1)

Published: June 5, 2023

Abstract Peripheral inflammation, defined as inflammation that occurs outside the central nervous system, is an age-related phenomenon has been identified a risk factor for Alzheimer’s disease. While role of chronic peripheral well characterized in context dementia and other conditions, less known about neurologic contribution acute inflammatory insults take place system. Herein, we define immune challenge form pathogen exposure (e.g., viral infection) or tissue damage surgery) causes large, yet time-limited, response. We provide overview clinical translational research examined connection between disease, focusing on three categories have received considerable attention recent years: infection, critical illness, surgery. Additionally, review neurobiological mechanisms which facilitate neural response to discuss potential blood–brain barrier components neuro-immune axis After highlighting knowledge gaps this area research, propose roadmap address methodological challenges, suboptimal study design, paucity transdisciplinary efforts thus far limited our understanding how pathogen- damage-mediated may contribute Finally, therapeutic approaches designed promote resolution be used following preserve brain health limit progression neurodegenerative pathology.

Language: Английский

Citations

49
Proteomic and transcriptomic profiling of brainstem, cerebellum and olfactory tissues in early- and late-phase COVID-19 DOI
Josefine Radke, Jenny Meinhardt, Tom Aschman

et al.

Nature Neuroscience, Journal Year: 2024, Volume and Issue: 27(3), P. 409 - 420

Published: Feb. 16, 2024

Language: Английский

Citations

34
Cerebromicrovascular mechanisms contributing to long COVID: implications for neurocognitive health DOI Creative Commons
Mónika Fekete, Andrea Ceglédi,

Ágnes Szappanos

et al.

GeroScience, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 7, 2025

Abstract Long COVID (also known as post-acute sequelae of SARS-CoV-2 infection [PASC] or post-COVID syndrome) is characterized by persistent symptoms that extend beyond the acute phase infection, affecting approximately 10% to over 30% those infected. It presents a significant clinical challenge, notably due pronounced neurocognitive such brain fog. The mechanisms underlying these effects are multifactorial, with mounting evidence pointing central role cerebromicrovascular dysfunction. This review investigates key pathophysiological contributing cerebrovascular dysfunction in long and their impacts on health. We discuss how endothelial tropism direct vascular trigger dysfunction, impaired neurovascular coupling, blood–brain barrier disruption, resulting compromised cerebral perfusion. Furthermore, appears induce mitochondrial enhancing oxidative stress inflammation within cells. Autoantibody formation following also potentially exacerbates injury, chronic ongoing compromise. These factors collectively contribute emergence white matter hyperintensities, promote amyloid pathology, may accelerate neurodegenerative processes, including Alzheimer’s disease. emphasizes critical advanced imaging techniques assessing health need for targeted interventions address complications. A deeper understanding essential advance treatments mitigate its long-term consequences.

Language: Английский

Citations

2
The role of the blood–brain barrier during neurological disease and infection DOI Creative Commons
Adjanie Patabendige, Damir Janigro

Biochemical Society Transactions, Journal Year: 2023, Volume and Issue: 51(2), P. 613 - 626

Published: March 17, 2023

A healthy brain is protected by the blood–brain barrier (BBB), which formed endothelial cells that line capillaries. The BBB plays an extremely important role in supporting normal neuronal function maintaining homeostasis of microenvironment and restricting pathogen toxin entry to brain. Dysfunction this highly complex regulated structure can be life threatening. dysfunction implicated many neurological diseases such as stroke, Alzheimer's disease, multiple sclerosis, infections. Among other mechanisms, inflammation and/or flow disturbances are major causes infections diseases. In particular, ischaemic both contribute disruption, leading devastating consequences. While a transient or minor disruption could tolerated, chronic total breach result irreversible damage. It worth noting timing extent play process any repair damage treatment strategies. This review evaluates summarises some latest research on during disease infection with focus effects BBB. BBB's crucial protecting also bottleneck central nervous system drug development. Therefore, innovative strategies carry therapeutics across novel models screen drugs, study complex, overlapping mechanisms urgently needed.

Language: Английский

Citations

35
The neurobiology of SARS-CoV-2 infection DOI
Jenny Meinhardt,

Simon Streit,

Carsten Dittmayer

et al.

Nature reviews. Neuroscience, Journal Year: 2023, Volume and Issue: 25(1), P. 30 - 42

Published: Dec. 4, 2023

Language: Английский

Citations

35
SARS-CoV-2 Spike Protein Accumulation in the Skull-Meninges-Brain Axis: Potential Implications for Long-Term Neurological Complications in post-COVID-19 DOI Creative Commons
Zhouyi Rong, Hongcheng Mai,

Saketh Kapoor

et al.

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2023, Volume and Issue: unknown

Published: April 5, 2023

ABSTRACT Coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2), has been associated mainly with a range of neurological symptoms, including brain fog and tissue loss, raising concerns about virus’s potential chronic impact on central nervous system. In this study, we utilized mouse models human post-mortem tissues to investigate presence distribution SARS-CoV-2 spike protein in skull-meninges-brain axis. Our results revealed accumulation skull marrow, meninges, parenchyma. The injection alone cell death brain, highlighting direct effect tissue. Furthermore, observed deceased long after their COVID-19 infection, suggesting that spike’s persistence may contribute long-term symptoms. was neutrophil-related pathways dysregulation proteins involved PI3K-AKT as well complement coagulation pathway. Overall, our findings suggest trafficking from CNS borders into parenchyma identified differentially regulated present insights mechanisms underlying immediate consequences diagnostic therapeutic opportunities. Graphical Summary Short axis presents molecular targets for complications long-COVID-19 patients .

Language: Английский

Citations

25
Engineered Wnt7a ligands rescue blood–brain barrier and cognitive deficits in a COVID-19 mouse model DOI Creative Commons
Troy N. Trevino, A Fogel,

Guliz Otkiran

et al.

Brain, Journal Year: 2024, Volume and Issue: 147(5), P. 1636 - 1643

Published: Feb. 2, 2024

Abstract Respiratory infection with SARS-CoV-2 causes systemic vascular inflammation and cognitive impairment. We sought to identify the underlying mechanisms mediating cerebrovascular dysfunction following mild respiratory infection. To this end, we performed unbiased transcriptional analysis brain endothelial cell signalling pathways dysregulated by mouse adapted MA10 in aged immunocompetent C57Bl/6 mice vivo. This revealed significant suppression of Wnt/β-catenin signalling, a critical regulator blood–brain barrier (BBB) integrity. therefore hypothesized that enhancing activity would offer protection against BBB permeability, neuroinflammation, neurological signs acute Indeed, found delivery cerebrovascular-targeted, engineered Wnt7a ligands protected integrity, reduced T-cell infiltration brain, microglial activation Importantly, strategy also mitigated induced deficits novel object recognition assay for learning memory pole descent task bradykinesia. These observations suggest enhancement or its downstream effectors could be potential interventional strategies restoring health viral infections.

Language: Английский

Citations

11
Blood-brain barrier biomarkers DOI

Juan F. Zapata-Acevedo,

Alejandra Mantilla-Galindo,

Karina Vargas-Sánchez

et al.

Advances in clinical chemistry, Journal Year: 2024, Volume and Issue: unknown, P. 1 - 88

Published: Jan. 1, 2024

Language: Английский

Citations

10
Persistence of spike protein at the skull-meninges-brain axis may contribute to the neurological sequelae of COVID-19 DOI Creative Commons
Zhouyi Rong, Hongcheng Mai, Gregor Ebert

et al.

Cell Host & Microbe, Journal Year: 2024, Volume and Issue: 32(12), P. 2112 - 2130.e10

Published: Nov. 29, 2024

SARS-CoV-2 infection is associated with long-lasting neurological symptoms, although the underlying mechanisms remain unclear. Using optical clearing and imaging, we observed accumulation of spike protein in skull-meninges-brain axis human COVID-19 patients, persisting long after viral clearance. Further, biomarkers neurodegeneration were elevated cerebrospinal fluid from COVID proteomic analysis skull, meninges, brain samples revealed dysregulated inflammatory pathways neurodegeneration-associated changes. Similar distribution patterns SARS-CoV-2-infected mice. Injection alone was sufficient to induce neuroinflammation, proteome changes axis, anxiety-like behavior, exacerbated outcomes mouse models stroke traumatic injury. Vaccination reduced but did not eliminate Our findings suggest persistent at borders may contribute lasting sequelae COVID-19.

Language: Английский

Citations

10