Mid and long-term neurological and neuropsychiatric manifestations of post-COVID-19 syndrome: A meta-analysis

Journal of the Neurological Sciences, Journal Year: 2022, Volume and Issue: 434, P. 120162 - 120162

Published: Jan. 28, 2022

Language: Английский

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Pathophysiology and mechanism of long COVID: a comprehensive review

Annals of Medicine, Journal Year: 2022, Volume and Issue: 54(1), P. 1473 - 1487

Published: May 20, 2022

After almost 2 years of fighting against SARS-CoV-2 pandemic, the number patients enduring persistent symptoms long after acute infection is a matter concern. This set was referred to as "long COVID", and it defined more recently "Post COVID-19 condition" by World health Organization (WHO). Although studies have revealed that COVID can manifest whatever severity inaugural illness, underlying pathophysiology still enigmatic.To conduct comprehensive review address putative persisting COVID.We searched 11 bibliographic databases (Cochrane Library, JBI EBP Database, Medline, Embase, PsycInfo, CINHAL, Ovid Nursing Journals@Ovid, SciLit, EuropePMC, CoronaCentral). We selected put forward hypotheses on pathophysiology, well those encompassed in their research investigation.A total 98 articles were included systematic review, 54 which exclusively addressed while 44 involved patients. Studies displayed heterogeneity with respect initial timing analysis, or presence control group. likely results from long-term organ damage due acute-phase infection, specific mechanisms following illness could contribute later possibly affecting many organs. As such, autonomic nervous system account for without clear evidence damage. Immune dysregulation, auto-immunity, endothelial dysfunction, occult viral persistence, coagulation activation are main pathophysiological so far.Evidence why occur limited, available heterogeneous. Apart damage, hints suggest be symptoms. KEY MESSAGESLong-COVID multisystem disease develops regardless severity. Its clinical spectrum comprises wide range symptoms.The its unclear. phase accounts symptoms, long-lasting inflammatory been proposed, well.Existing involving Long-COVID highly heterogeneous, they include various levels different time frame well.

Language: Английский

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Peripheral inflammation and blood–brain barrier disruption: effects and mechanisms

CNS Neuroscience & Therapeutics, Journal Year: 2020, Volume and Issue: 27(1), P. 36 - 47

Published: Dec. 30, 2020

Abstract The blood–brain barrier (BBB) is an important physiological that separates the central nervous system (CNS) from peripheral circulation, which contains inflammatory mediators and immune cells. BBB regulates cellular molecular exchange between blood vessels brain parenchyma. Normal functioning of crucial for homeostasis proper function brain. It has been demonstrated inflammation can disrupt by various pathways, resulting in different CNS diseases. Recently, clinical research also showed complications following SARS‐CoV‐2 infection chimeric antigen receptor (CAR)‐T cell therapy, both lead to a cytokine storm circulation. Therefore, elucidation mechanisms underlying disruption induced will provide basis protecting context exacerbated In present review, we first summarize properties makes immune‐privileged organ. We then discuss relevance inflammation‐induced Finally, elaborate factors BBB.

Language: Английский

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Long‐COVID syndrome‐associated brain fog and chemofog: Luteolin to the rescue

BioFactors, Journal Year: 2021, Volume and Issue: 47(2), P. 232 - 241

Published: March 1, 2021

Abstract COVID‐19 leads to severe respiratory problems, but also long‐COVID syndrome associated primarily with cognitive dysfunction and fatigue. Long‐COVID symptoms, especially brain fog, are similar those experienced by patients undertaking or following chemotherapy for cancer (chemofog chemobrain), as well in myalgic encephalomyelitis/chronic fatigue (ME/CFS) mast cell activation (MCAS). The pathogenesis of fog these illnesses is presently unknown may involve neuroinflammation via cells stimulated pathogenic stress stimuli release mediators that activate microglia lead inflammation the hypothalamus. These processes could be mitigated phytosomal formulation (in olive pomace oil) natural flavonoid luteolin.

Language: Английский

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The structural basis of accelerated host cell entry by SARS‐CoV‐2†

FEBS Journal, Journal Year: 2020, Volume and Issue: 288(17), P. 5010 - 5020

Published: Dec. 2, 2020

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative agent of pandemic disease 2019 (COVID-19) that exhibits an overwhelming contagious capacity over other human coronaviruses (HCoVs). This structural snapshot describes bases underlying SARS-CoV-2 and explains its fast motion epithelia allow rapid cellular entry. Based on notable viral spike (S) protein features, we propose flat sialic acid-binding domain at N-terminal (NTD) S1 subunit leads to more effective first contact interaction with acid layer epithelium, this, in turn, allows faster 'surfing' epithelium receptor scanning by SARS-CoV-2. Angiotensin-converting enzyme (ACE-2) epithelial surface primary entry for SARS-CoV-2, protein-protein assays demonstrate high-affinity binding (S protein) ACE-2. To date, no high-frequency mutations were detected C-terminal S protein, where receptor-binding (RBD) located. Tight ACE-2 a conserved RBD suggests ACE2-RBD likely optimal. Moreover, contains cleavage site furin proteases, which accelerates cell The model proposed here basis accelerated host relative HCoVs also discusses emerging hypotheses are contribute development antiviral strategies combat

Language: Английский

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Post-COVID 19 Neurological Syndrome (PCNS); a novel syndrome with challenges for the global neurology community

Journal of the Neurological Sciences, Journal Year: 2020, Volume and Issue: 419, P. 117179 - 117179

Published: Oct. 13, 2020

Language: Английский

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SARS-CoV-2 drives NLRP3 inflammasome activation in human microglia through spike protein

Molecular Psychiatry, Journal Year: 2022, Volume and Issue: 28(7), P. 2878 - 2893

Published: Nov. 1, 2022

Coronavirus disease-2019 (COVID-19) is primarily a respiratory disease, however, an increasing number of reports indicate that SARS-CoV-2 infection can also cause severe neurological manifestations, including precipitating cases probable Parkinson's disease. As microglial NLRP3 inflammasome activation major driver neurodegeneration, here we interrogated whether promote activation. Using transgenic mice expressing human angiotensin-converting enzyme 2 (hACE2) as COVID-19 pre-clinical model, established the presence virus in brain together with and upregulation comparison to uninfected mice. Next, utilising model monocyte-derived microglia, identified isolates bind enter microglia absence viral replication. This interaction directly induced robust activation, even another priming signal. Mechanistically, demonstrated purified spike glycoprotein activated LPS-primed ACE2-dependent manner. Spike protein could prime through NF-κB signalling, allowing for either ATP, nigericin or α-synuclein. Notably, protein-mediated was significantly enhanced α-synuclein fibrils entirely ablated by NLRP3-inhibition. Finally, demonstrate infected hACE2 treated orally post-infection inhibitory drug MCC950, have reduced increased survival untreated These results support possible mechanism innate immune SARS-CoV-2, which explain vulnerability developing symptoms akin disease individuals, potential therapeutic avenue intervention.

Language: Английский

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Could SARS-CoV-2 Spike Protein Be Responsible for Long-COVID Syndrome?

Molecular Neurobiology, Journal Year: 2022, Volume and Issue: 59(3), P. 1850 - 1861

Published: Jan. 13, 2022

Language: Английский

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Neuroinvasion and Neurotropism by SARS-CoV-2 Variants in the K18-hACE2 Mouse

Viruses, Journal Year: 2022, Volume and Issue: 14(5), P. 1020 - 1020

Published: May 11, 2022

Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) not only affects the respiratory tract but also causes neurological symptoms such as loss of smell and taste, headache, fatigue or severe cerebrovascular complications. Using transgenic mice expressing human angiotensin-converting enzyme (hACE2), we investigated spatiotemporal distribution pathomorphological features in CNS following intranasal infection with SARS-CoV-2 variants, well after prior influenza A virus infection. Apart from Omicron, found all variants to frequently spread within CNS. Infection was restricted neurons appeared olfactory bulb mainly basally oriented regions brain into spinal cord, independent ACE2 expression without evidence neuronal cell death, axonal damage demyelination. However, microglial activation, microgliosis a mild macrophage T dominated inflammatory response consistently observed, accompanied by apoptotic death endothelial, immune cells, their apparent Microgliosis apoptosis indicate potential role microglia for pathogenesis viral effect COVID-19 possible impairment functions, especially long COVID. These data may be informative selection therapeutic candidates broadly support investigation agents adequate penetration relevant

Language: Английский

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Long COVID and neuropsychiatric manifestations (Review)

Experimental and Therapeutic Medicine, Journal Year: 2022, Volume and Issue: 23(5)

Published: April 1, 2022

There is accumulating evidence in the literature indicating that a number of patients with coronavirus disease 2019 (COVID‑19) may experience range neuropsychiatric symptoms, persisting or even presenting following resolution acute COVID‑19. Among manifestations more frequently associated 'long COVID' are depression, anxiety, post‑traumatic stress disorder, sleep disturbances, fatigue and cognitive deficits, can potentially be debilitating negatively affect patients' wellbeing, albeit majority cases symptoms tend to improve over time. Despite variations results obtained from studies using different methodological approaches define syndrome, most widely accepted factors higher risk developing include severity foregoing COVID‑19, female sex, presence comorbidities, history mental health an elevation levels inflammatory markers, further research required establish causal associations. To date, pathophysiological mechanisms implicated remain only partially elucidated, while role indirect effects COVID‑19 pandemic, such as social isolation uncertainty concerning social, financial recovery post‑COVID, have also been highlighted. Given alarming 'long‑COVID', interdisciplinary cooperation for early identification who at high persistent presentations, beyond recovery, crucial ensure appropriate integrated physical support provided, aim mitigating risks long‑term disability societal individual level.

Language: Английский

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