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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COVID-19 and cognitive impairment: neuroinvasive and blood‒brain barrier dysfunction

Journal of Neuroinflammation, Journal Year: 2022, Volume and Issue: 19(1)

Published: Sept. 7, 2022

Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has led to a global pandemic. Although COVID-19 was initially described as disease, there is growing evidence that SARS-CoV-2 able invade the brains of patients and cause cognitive impairment. It been reported may have invasive effects on variety cranial nerves, including olfactory, trigeminal, optic, vagus spread other brain regions via infected nerve endings, retrograde transport, transsynaptic transmission. In addition, blood-brain barrier (BBB), composed neurovascular units (NVUs) lining microvasculature, acts physical between cells circulating immune system regulate transfer substances blood parenchyma. Therefore, BBB be an important structure for direct indirect interaction with circulation. this review, we assessed potential involvement neuroinvasion under infection, impact disorder infection

Language: Английский

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Long COVID, the Brain, Nerves, and Cognitive Function

Neurology International, Journal Year: 2023, Volume and Issue: 15(3), P. 821 - 841

Published: July 6, 2023

SARS-CoV-2, a single-stranded RNA coronavirus, causes an illness known as coronavirus disease 2019 (COVID-19). Long-term complications are increasing issue in patients who have been infected with COVID-19 and may be result of viral-associated systemic central nervous system inflammation or arise from virus-induced hypercoagulable state. incite changes brain function wide range lingering symptoms. Patients often experience fatigue note fog, sensorimotor symptoms, sleep disturbances. Prolonged neurological neuropsychiatric symptoms prevalent can interfere substantially everyday life, leading to massive public health concern. The mechanistic pathways by which SARS-CoV-2 infection sequelae important subject ongoing research. Inflammation- induced blood-brain barrier permeability viral neuro-invasion direct nerve damage involved. Though the mechanisms uncertain, resulting documented numerous patient reports studies. This review examines constellation spectrum seen long COVID incorporates information on prevalence these contributing factors, typical course. Although treatment options generally lacking, potential therapeutic approaches for alleviating improving quality life explored.

Language: Английский

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Stellate ganglion block reduces symptoms of Long COVID: A case series

Journal of Neuroimmunology, Journal Year: 2021, Volume and Issue: 362, P. 577784 - 577784

Published: Dec. 8, 2021

After recovering from COVID-19, a significant proportion of symptomatic and asymptomatic individuals develop Long COVID. Fatigue, orthostatic intolerance, brain fog, anosmia, ageusia/dysgeusia in COVID resemble "sickness behavior," the autonomic nervous system response to pro-inflammatory cytokines (Dantzer et al., 2008). Aberrant network adaptation sympathetic/parasympathetic imbalance is expected produce long-standing dysautonomia. Cervical sympathetic chain activity can be blocked with local anesthetic, allowing regional "reboot." In this case series, we successfully treated two patients using stellate ganglion block, implicating dysautonomia pathophysiology suggesting novel treatment.

Language: Английский

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Neuroinflammation and Its Impact on the Pathogenesis of COVID-19

Frontiers in Medicine, Journal Year: 2021, Volume and Issue: 8

Published: Nov. 24, 2021

Coronavirus disease 2019 (COVID-19) is an infectious caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The clinical manifestations of COVID-19 include dry cough, difficult breathing, fever, fatigue, and may lead to pneumonia failure. There are significant gaps in the current understanding whether SARS-CoV-2 attacks CNS directly or through activation peripheral immune system cell infiltration. Although modality neurological impairments associated with has not been thoroughly investigated, latest studies have observed that induces neuroinflammation long-term consequences. Here we review literature on possible cellular molecular mechanisms induced-neuroinflammation. Activation innate increased cytokine levels, chemokines, free radicals SARS-CoV-2-induced pathogenic response at blood-brain barrier (BBB). BBB disruption allows immune/inflammatory infiltration into activating resident cells (such as microglia astrocytes). This highlights involved COVID-19-induced neuroinflammation, which neuronal death. A better these will help gain substantial knowledge about potential role changes plan therapeutic intervention strategies.

Language: Английский

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Neurological complications associated with Covid‐19; molecular mechanisms and therapeutic approaches

Reviews in Medical Virology, Journal Year: 2022, Volume and Issue: 32(6)

Published: Feb. 9, 2022

Abstract With the progression of investigations on pathogenesis severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2), neurological complications have emerged as a critical aspect ongoing disease 2019 (Covid‐19) pandemic. Besides well‐known symptoms, many manifestations such anosmia/ageusia, headaches, dizziness, seizures, and strokes been documented in hospitalised patients. The neurotropism background coronaviruses has led to speculation that are caused by direct invasion SARS‐CoV‐2 into nervous system. This is proposed occur through infection peripheral nerves or via systemic blood circulation, termed neuronal haematogenous routes invasion, respectively. On other hand, aberrant immune responses insufficiency associated with Covid‐19 suggested affect system indirectly. Deleterious roles cytokine storm hypoxic conditions blood‐brain barrier disruption, coagulation abnormalities, autoimmune neuropathies well investigated infections, Covid‐19. Here, we review latest discoveries focussing possible molecular mechanisms indirect impacts try elucidate link between some potential therapeutic strategies pathways.

Language: Английский

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SARS‐COV‐2 infection and Parkinson's disease: Possible links and perspectives

Journal of Neuroscience Research, Journal Year: 2023, Volume and Issue: 101(6), P. 952 - 975

Published: Jan. 30, 2023

Parkinson's disease (PD) is a neurodegenerative disorder characterized by the progressive loss of dopaminergic neurons in substantia nigra. The hallmarks are presence Lewy bodies composed mainly aggregated α-synuclein and immune activation inflammation brain. neurotropism SARS-CoV-2 with induction cytokine storm neuroinflammation can contribute to development PD. Interestingly, overexpression PD patients may limit neuroinvasion degeneration neurons; however, on other hand, this virus speed up aggregation. review aims discuss potential link between COVID-19 risk PD, highlighting need for further studies authenticate association. We have also overviewed influence infection course management. In context, we presented prospects controlling pandemic related cases that, beyond global vaccination novel anti-SARS-CoV-2 agents, include graphene-based nanoscale platforms offering antiviral anti-amyloid strategies against

Language: Английский

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Long COVID and its association with neurodegenerative diseases: pathogenesis, neuroimaging, and treatment

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

Published: April 4, 2024

Corona Virus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), has presented unprecedented challenges to world. Changes after COVID-19 have had a significant impact on patients with neurodegenerative diseases. This study aims explore mechanism of diseases examining main pathways central nervous system infection SARS-CoV-2. Research indicated that chronic inflammation and abnormal immune response are primary factors leading neuronal damage long-term consequences COVID-19. In some patients, concurrent inflammatory leads increased release pro-inflammatory cytokines, which may significantly prognosis. Molecular imaging can accurately assess severity in phase. Furthermore, use FDG-PET is advocated quantify relationship between neuroinflammation psychiatric cognitive symptoms who recovered from Future development should focus aggressive post-infection control targeted therapies target ACE2 receptors, ERK1/2, Ca 2+ .

Language: Английский

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Quantitative susceptibility mapping at 7 T in COVID-19: brainstem effects and outcome associations

Brain, Journal Year: 2024, Volume and Issue: 147(12), P. 4121 - 4130

Published: June 27, 2024

Abstract Post-mortem studies have shown that patients dying from severe acute respiratory syndrome coronavirus (SARS-CoV-2) infection frequently pathological changes in their CNS, particularly the brainstem. Many of these are proposed to result para-infectious and/or post-infection immune responses. Clinical symptoms such as fatigue, breathlessness, and chest pain reported post-hospitalized disease 2019 (COVID-19) patients. We propose part due damage key neuromodulatory brainstem nuclei. While involvement has been demonstrated phase illness, evidence long-term change on MRI is inconclusive. therefore used ultra-high field (7 T) quantitative susceptibility mapping (QSM) test hypothesis abnormalities persist post-COVID associated with persistence symptoms. 7 T QSM data 30 patients, scanned 93–548 days after hospital admission for COVID-19 compared them 51 age-matched controls without prior history infection. correlated patients’ signals severity (duration scale), inflammatory response during illness (C-reactive protein, D-dimer platelet levels), functional recovery (modified Rankin depression (Patient Health Questionnaire-9) anxiety (Generalized Anxiety Disorder-7). In survivors, MR increased medulla, pons midbrain regions Specifically, there was inferior medullary reticular formation raphe pallidus obscurus. regions, higher tissue had worse severity, markers, significantly recovery. This study contributes understanding effects Using non-invasive MRI, we show pathophysiological processes survivors.

Language: Английский

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Deconstructing the functional neuroanatomy of the choroid plexus: an ontogenetic perspective for studying neurodevelopmental and neuropsychiatric disorders

Molecular Psychiatry, Journal Year: 2022, Volume and Issue: 27(9), P. 3573 - 3582

Published: May 26, 2022

Abstract The choroid plexus (CP) is a delicate and highly vascularized structure in the brain comprised of dense network fenestrated capillary loops that help synthesis, secretion circulation cerebrospinal fluid (CSF). This unique neuroanatomical arachnoid villi stemming from frond-like surface projections—that protrude into lumen four cerebral ventricles—providing key source nutrients to parenchyma addition serving as ‘sink’ for central nervous system metabolic waste. In fact, functions CP are often described being analogous those liver kidney. Beyond forming barrier/interface between blood CSF compartments, has been identified modulator leukocyte trafficking, inflammation, cognition, circadian rhythm gut brain-axis. recent years, advances molecular biology techniques neuroimaging along with use sophisticated animal models have played an integral role shaping our understanding how CP–CSF changes relation maturation neural circuits during critical periods development. this article we provide ontogenetic perspective review experimental evidence implicating pathophysiology neurodevelopmental neuropsychiatric disorders.

Language: Английский

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