Future Virology, Journal Year: 2025, Volume and Issue: unknown, P. 1 - 15
Published: March 21, 2025
Language: Английский
Future Virology, Journal Year: 2025, Volume and Issue: unknown, P. 1 - 15
Published: March 21, 2025
Language: Английский
Nature reviews. Immunology, Journal Year: 2023, Volume and Issue: 23(10), P. 618 - 634
Published: July 11, 2023
Language: Английский
Citations
261EClinicalMedicine, Journal Year: 2023, Volume and Issue: 62, P. 102086 - 102086
Published: July 21, 2023
Cognitive impairment has been reported after many types of infection, including SARS-CoV-2. Whether deficits following SARS-CoV-2 improve over time is unclear. Studies to date have focused on hospitalised individuals with up a year follow-up. The presence, magnitude, persistence and correlations effects in community-based cases remain relatively unexplored.
Language: Английский
Citations
63Frontiers in Immunology, Journal Year: 2022, Volume and Issue: 13
Published: Dec. 15, 2022
Background Coronavirus disease 2019 (COVID-19) caused by SARS-CoV-2 infection is associated with disorders affecting the peripheral and central nervous system. A high number of patients develop post-COVID-19 syndrome persistence a large spectrum symptoms, including neurological, beyond 4 weeks after infection. Several potential mechanisms in acute phase have been hypothesized, damage blood-brain-barrier (BBB). We tested weather markers BBB association brain injury systemic inflammation may help identifying blood signature for severity neurological complications. Methods Blood biomarkers disruption (MMP-9, GFAP), neuronal (NFL) (PPIA, IL-10, TNFα) were measured two COVID-19 patient cohorts (ICUCovid; n=79) complications (NeuroCovid; n=78), control groups free from history, healthy subjects (n=20) amyotrophic lateral sclerosis (ALS; n=51). Samples collected during first second wave pandemic Lombardy, Italy. Evaluations done at chronic phases Results are levels similar to or higher than ALS. NeuroCovid display lower cytokine storm inducer PPIA but MMP-9 ICUCovid patients. There was evidence different temporal dynamics compared IL-10 showing highest phase. On contrary, patients, dependency long-term. also found clear NFL GFAP levels, deceased levels. Discussion The overall picture points an increased risk disruption. Our observations provide hints therapeutic approaches mitigating reduce dysfunction
Language: Английский
Citations
59Trends in Cognitive Sciences, Journal Year: 2023, Volume and Issue: 27(11), P. 1053 - 1067
Published: Aug. 30, 2023
COVID-19 is associated with a range of neurological, cognitive, and mental health symptoms both acutely chronically that can persist for many months after infection in people long-COVID syndrome. Investigations cognitive function neuroimaging have begun to elucidate the nature some these symptoms. They reveal that, although deficits may be related brain imaging abnormalities people, also occur absence objective or changes. Furthermore, impairment detected even asymptomatic individuals. We consider evidence regarding symptoms, deficits, neuroimaging, as well their possible underlying mechanisms.
Language: Английский
Citations
38Journal of Neurology, Journal Year: 2023, Volume and Issue: 270(7), P. 3315 - 3328
Published: May 15, 2023
Language: Английский
Citations
24BMJ, Journal Year: 2023, Volume and Issue: unknown, P. e073923 - e073923
Published: Aug. 18, 2023
Abstract Although neurological complications of SARS-CoV-2 infection are relatively rare, their potential long term morbidity and mortality have a significant impact, given the large numbers infected patients. Covid-19 is now in differential diagnosis number common syndromes including encephalopathy, encephalitis, acute demyelinating encephalomyelitis, stroke, Guillain-Barré syndrome. Physicians should be aware pathophysiology underlying these presentations to diagnose treat patients rapidly appropriately. good evidence has been found for neurovirulence, neuroinvasive neurotropic limited. The most immune mediated vascular, or both. A proportion developed covid, which can include neuropsychiatric presentations. mechanisms covid remain unclear. longer consequences with covid-19 on brain, particularly terms neurodegeneration, will only become apparent time follow-up.
Language: Английский
Citations
23Nature Communications, Journal Year: 2023, Volume and Issue: 14(1)
Published: Dec. 22, 2023
To understand neurological complications of COVID-19 better both acutely and for recovery, we measured markers brain injury, inflammatory mediators, autoantibodies in 203 hospitalised participants; 111 with acute sera (1-11 days post-admission) 92 convalescent (56 COVID-19-associated diagnoses). Here show that compared to 60 uninfected controls, tTau, GFAP, NfL, UCH-L1 are increased infection at timepoints NfL GFAP significantly higher participants complications. Inflammatory mediators (IL-6, IL-12p40, HGF, M-CSF, CCL2, IL-1RA) associated altered consciousness injury. Autoantibodies more common than controls some (including against MYL7, UCH-L1, GRIN3B) frequent consciousness. Additionally, elevated unrelated attenuated systemic autoantibody responses. Overall, evidence neuroglial injury late disease these correlate dysregulated innate adaptive immune responses acutely.
Language: Английский
Citations
23bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2024, Volume and Issue: unknown
Published: May 31, 2024
Abstract SARS-CoV-2 infections worldwide led to a surge in cases of Long COVID, post-infectious syndrome. It has been hypothesized that autoantibodies play crucial role the development COVID and other syndromes, such as fibromyalgia myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). In this study, we tested hypothesis by passively transferring total IgG from patients mice. Using Glial Fibrillary Acidic Protein (GFAP) type-I interferon expression, stratified into three subgroups, each with unique plasma proteome signatures. Remarkably, transfer two which are characterized higher levels neuronal proteins leukocyte activation markers, induced pronounced persistent sensory hypersensitivity distinct kinetics. Conversely, third subgroup, enriched skeletal cardiac muscle profiles, reduced locomotor activity mice without affecting their motor coordination. These findings demonstrate replicates disease symptoms, underscoring IgG’s causative pathogenesis. This work proposes murine model mirrors COVID’s pathophysiological mechanisms, may be used tool for screening developing targeted therapeutics.
Language: Английский
Citations
15Brain, 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
11Scientific Reports, Journal Year: 2024, Volume and Issue: 14(1)
Published: June 11, 2024
Abstract Post-COVID Syndrome has emerged as a significant public health concern worldwide with increasing evidence to suggest that individuals who have had an acute COVID-19 infection report lingering memory and attention difficulties, even in fully recovered no longer experiencing symptoms of COVID-19. The present study sought investigate the profile objective subjective cognitive difficulties people Syndrome, from COVID never We further explore extent which self-reported fatigue stress are related difficulties. 162 participants including 50 living 59 but 53 experienced tested positive for were recruited Academic Prolific complete series online questionnaires neurocognitive tasks. Subjective function was measured using Cognitive Failures Questionnaire Cognitron test battery. found measures not significantly related, suggesting self-reports “brain fog” reflecting objectively dysfunction. A MANOVA revealed deficits driven by heightened perceived status. Objective function, however, status whereby we observed been exposed regardless whether they or recovered, compared This suggests can long term effects on without persistent symptoms. Encouragingly, associated time since initial showing improved over However, did observe same improvement dysfunction number neurological presently experienced. These results add accumulating literature is following infection, appear improve those yet persist Syndrome.
Language: Английский
Citations
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