The circuit mechanisms of working memory: Key roles of the dorsolateral prefrontal cortex DOI
Amy F.T. Arnsten, Julio Martinez‐Trujillo

Elsevier eBooks, Journal Year: 2024, Volume and Issue: unknown

Published: Jan. 1, 2024

Language: Английский

Effects of COVID-19 on cognition and brain health DOI Creative Commons
Sijia Zhao, Sofia Toniolo, Adam Hampshire

et al.

Trends 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

38

Severe COVID-19 and long COVID are associated with high expression of STING, cGAS and IFN-α DOI Creative Commons
Maria Alice Freitas Queiroz,

Wandrey Roberto dos Santos Brito,

Keise Adrielle Santos Pereira

et al.

Scientific Reports, Journal Year: 2024, Volume and Issue: 14(1)

Published: Feb. 29, 2024

Abstract The cGAS-STING pathway appears to contribute dysregulated inflammation during coronavirus disease 2019 (COVID-19); however, inflammatory factors related long COVID are still being investigated. In the present study, we evaluated association of cGAS and STING gene expression levels plasma IFN-α, TNF-α IL-6 with COVID-19 severity in acute infection COVID, based on analysis blood samples from 148 individuals, 87 61 post-COVID-19 period. Quantification was performed by real-time PCR, cytokine were quantified ELISA flow cytometry. COVID-19, , TNF-α, higher patients severe than those nonsevere manifestations ( p < 0.05). Long associated elevated IFN-α Activation may an intense systemic state and, after resolution, induce autoinflammatory some tissues, resulting COVID.

Language: Английский

Citations

15

Improvement of immune dysregulation in individuals with long COVID at 24-months following SARS-CoV-2 infection DOI Creative Commons
Chansavath Phetsouphanh, Brendan Jacka, Sara Ballouz

et al.

Nature Communications, Journal Year: 2024, Volume and Issue: 15(1)

Published: April 17, 2024

Abstract This study investigates the humoral and cellular immune responses health-related quality of life measures in individuals with mild to moderate long COVID (LC) compared age gender matched recovered COVID-19 controls (MC) over 24 months. LC participants show elevated nucleocapsid IgG levels at 3 months, higher neutralizing capacity up 8 months post-infection. Increased spike-specific nucleocapsid-specific CD4 + T cells, PD-1, TIM-3 expression on CD8 cells were observed but these differences do not persist Some had detectable IFN-γ IFN-β, that was attributed reinfection antigen re-exposure. Single-cell RNA sequencing month timepoint shows similar cell proportions reconstitution naïve B subsets MC. No significant exhaustion scores or antigen-specific clones are observed. These findings suggest resolution activation return comparable between MC time. Improvement self-reported also evident majority (62%). PTX3, CRP platelet count associated improvements life.

Language: Английский

Citations

15

Unraveling Links between Chronic Inflammation and Long COVID: Workshop Report DOI Open Access
Pushpa Tandon, Natalie Abrams, Leela Rani Avula

et al.

The Journal of Immunology, Journal Year: 2024, Volume and Issue: 212(4), P. 505 - 512

Published: Feb. 5, 2024

As COVID-19 continues, an increasing number of patients develop long COVID symptoms varying in severity that last for weeks, months, or longer. Symptoms commonly include lingering loss smell and taste, hearing loss, extreme fatigue, "brain fog." Still, persistent cardiovascular respiratory problems, muscle weakness, neurologic issues have also been documented. A major problem is the lack clear guidelines diagnosing COVID. Although some studies suggest due to prolonged inflammation after SARS-CoV-2 infection, underlying mechanisms remain unclear. The broad range COVID-19's bodily effects responses initial viral infection are poorly understood. This workshop brought together multidisciplinary experts showcase discuss latest research on chronic might be associated with sequelae following infection.

Language: Английский

Citations

11

Stress and Inflammation Target Dorsolateral Prefrontal Cortex Function: Neural Mechanisms Underlying Weakened Cognitive Control DOI Creative Commons
Mary Kate P. Joyce, Stacy Uchendu,

Amy Arnsten

et al.

Biological Psychiatry, Journal Year: 2024, Volume and Issue: unknown

Published: June 1, 2024

Language: Английский

Citations

10

The kynurenine pathway of tryptophan metabolism: a neglected therapeutic target of COVID-19 pathophysiology and immunotherapy DOI Open Access
Abdulla A.‐B. Badawy

Bioscience Reports, Journal Year: 2023, Volume and Issue: 43(8)

Published: July 24, 2023

Abstract SARS-CoV-2 (COVID-19) exerts profound changes in the kynurenine (Kyn) pathway (KP) of tryptophan (Trp) metabolism that may underpin its pathophysiology. The KP is main source vital cellular effector NAD+ and intermediate metabolites modulate immune neuronal functions. Trp top influenced by COVID-19. Sixteen studies established virus-induced activation mediated mainly induction indoleamine 2,3-dioxygenase (IDO1) most affected tissues IDO2 lung increased release proinflammatory cytokines but could additionally involve flux plasma free (TDO) cortisol. major Kyn metabolite targeted COVID-19 kynurenic acid (KA), with greatest affinity for aryl hydrocarbon receptor (AhR), which also activated AhR initiates two important series events: a vicious circle involving IDO1 induction, KA accumulation further activation, poly (ADP-ribose) polymerase (PARP) leading to depletion cell death. virus deprives host inhibiting biosynthetic from quinolinic acid, while simultaneously acquiring promoting synthesis nicotinamide salvage pathway. Additionally, protective effects sirtuin 1 are minimised PARP activation. dysfunction mood neurological disorders acutely during ‘long COVID’. More potential vaccination therapy on required exploration therapeutic strategies modulation proposed.

Language: Английский

Citations

19

Blood brain barrier disruption and glutamatergic excitotoxicity in post-acute sequelae of SARS COV-2 infection cognitive impairment: potential biomarkers and a window into pathogenesis DOI Creative Commons
Joga Chaganti, Govinda Poudel, Lucette A. Cysique

et al.

Frontiers in Neurology, Journal Year: 2024, Volume and Issue: 15

Published: May 2, 2024

Objective To investigate the association between blood–brain barrier permeability, brain metabolites, microstructural integrity of white matter, and cognitive impairment (CI) in post-acute sequelae SARS-COV-2 infection (PASC). Methods In this multimodal longitudinal MRI study 14 PASC participants with CI 10 healthy controls were enrolled. All completed investigations at 3 months following acute (3 ± 2 weeks SD), 12 2.22 SD weeks. The assessments included a standard neurological assessment, screen using brief CogState battery multi-modal derived metrics from Dynamic contrast enhanced (DCE) perfusion Imaging, Diffusion Tensor Imaging (DTI), single voxel proton Magnetic Resonance Spectroscopy. These measures compared patients correlated scores. Results At baseline, relative to controls, had higher K-Trans Myo-inositol, lower levels Glutamate/Glutamine frontal matter (FWM) ( p &lt; 0.01) as well stem 0.05), FA MD FWM 0.05). participants, decreased baseline metabolite concentrations did not change significantly over time. Neurocognitive scores correlation increased permeability (K trans). Interpretation is associated BBB impairment, loss WM integrity, inflammation which but uniformly improved months. possibly mediated by glutamatergic excitotoxicity.

Language: Английский

Citations

7

The roles of the kynurenine pathway in COVID-19 neuropathogenesis DOI Creative Commons
Mona Dehhaghi,

Mostafa Heydari,

Hamed Kazemi Shariat Panahi

et al.

Infection, Journal Year: 2024, Volume and Issue: 52(5), P. 2043 - 2059

Published: May 27, 2024

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative agent of highly contagious disease Corona Virus Disease 2019 (COVID-19) that may lead to various neurological and psychological disorders can be acute, lasting days weeks or months possibly longer. latter known as long-COVID more recently post-acute sequelae COVID (PASC). During COVID-19 infection, a strong inflammatory response, cytokine storm, occurs in some patients. levels interferon-γ (IFN-γ), interferon-β (IFN-β), interleukin-6 (IL-6) tumour necrosis factor-alpha (TNF-α) are particularly increased. These cytokines activate enzyme indoleamine 2,3-dioxygenase 1 (IDO-1), catalysing first step tryptophan (Trp) catabolism through kynurenine pathway (KP) leading production several neurotoxic immunosuppressive metabolites. There already data showing elevation KP metabolites both acutely PASC, especially regarding cognitive impairment. Thus, it likely involvement significant SARS-CoV-2 pathogenesis neurologically.

Language: Английский

Citations

7

Navigating the Spectrum of Two Pediatric COVID-19 Complications: Multi-System Inflammatory Syndrome in Children and Post-Acute Sequelae of SARS-CoV-2 Infection DOI Open Access
Simon Parzen-Johnson, Ben Z. Katz

Journal of Clinical Medicine, Journal Year: 2024, Volume and Issue: 13(4), P. 1147 - 1147

Published: Feb. 18, 2024

This review summarizes the current scope of understanding associated with two common post-infectious complications COVID-19 infection: Multi-System Inflammatory Syndrome in Children (MIS-C) and Post-Acute Sequelae SARS-CoV-2 infection (PASC). It identifies gaps knowledge issues that may limit ability to fill these gaps. provides a framework drive continued research. A comprehensive literature was performed, identifying seminal articles describing emergence MIS-C PASC, works from focused on clinical implications pathophysiologic disorders. Although pediatric patients experienced few severe cases acute infection, burden disease sequelae is substantial. Mortality low, but morbidity significant. There are still numerous unknowns about pathophysiology both PASC; however, widespread immunity developing after increased vaccination prior it be difficult perform adequate prospective studies answer questions. Long-term sequalae seem minimal whereas, by definition, PASC an ongoing problem severe. The rapid sharing information regarding novel conditions such as key interventions related future outside those stemming COVID-19. seems unlikely return condition substantial numbers, there significant learning can gleaned existing general aspects epidemiology, equity, pathophysiology. additional resources need dedicated determining appropriate effective therapies moving forward.

Language: Английский

Citations

6

Resistance training's impact on blood biomarkers and cognitive function in older adults with low and high risk of mild cognitive impairment: a randomized controlled trial DOI Creative Commons
Wouter A.J. Vints, Evrim Gökçe,

Julija Šeikinaitė

et al.

European Review of Aging and Physical Activity, Journal Year: 2024, Volume and Issue: 21(1)

Published: April 10, 2024

Abstract Background The aging brain exhibits a neuroinflammatory state, driven partly by peripheral pro-inflammatory stimuli, that accelerates cognitive deterioration. A growing body of evidence clearly indicates physical exercise alleviates neuroinflammation and positively affects the process cognition. In this randomized controlled trial, we aimed to observe effect 12 weeks resistance training (RT) on biomarker levels, function changes their interrelationship, explore differences in those exercise-induced older adults with high risk mild impairment (MCI) compared low MCI. Methods Fifty-two participants (aged 60–85 years old, 28 female) were randomly allocated week lower limb RT program consisting two sessions per or waiting list control group. Montreal Cognitive Assessment (MoCA) was used stratify screened as (< 26/30) (≥ We assessed serum Interleukin 6 (IL-6), Insulin-like Growth Factor-1 (IGF-1), Kynurenine (KYN) levels. measurement consisted four subtests Automated Neuropsychological Metrics (ANAM), two-choice reaction time, go/no-go, mathematical processing, memory search test. Results Twelve improved Go/No-go test results MCI risk. did not significantly affect blood biomarkers. However, IGF-1 level increases associated improvements response time processing group, IL-6 total group participants. Finally, KYN levels differed between but no significant associations performance found. Conclusion Our study suggest different inhibitory may play role mechanism behind benefit be surrogate for neurodegeneration decline.

Language: Английский

Citations

6