Dialogue between Neuroinflammation and Neurodegenerative Diseases in COVID-19

Chowdhury, Bisruta; Sharma, Anita; Satarker, Sairaj; Mudgal, Jayesh; Nampoothiri, Madhavan

doi:10.1615/jenvironpatholtoxicoloncol.2021038365

Cited by 8 publications

(5 citation statements)

References 104 publications

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“…Central cytokines and chemokines play a role in inducing hyperalgesia and allodynia, while a sustained increase leads to chronic widespread pain at several body locations, suggesting that neuroinflammation drives widespread chronic pain through central sensitisation [ 47 ]. Therefore, neuroinflammation is expected to play a role in persisting symptoms after COVID-19 infection as well [ 48 , 49 ].…”

Section: Discussionmentioning

confidence: 99%

Is Central Sensitisation the Missing Link of Persisting Symptoms after COVID-19 Infection?

Goudman

Smedt

Noppen

et al. 2021

JCM

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Patients recovered from a COVID-19 infection often report vague symptoms of fatigue or dyspnoea, comparable to the manifestations in patients with central sensitisation. The hypothesis was that central sensitisation could be the underlying common aetiology in both patient populations. This study explored the presence of symptoms of central sensitisation, and the association with functional status and health-related quality of life, in patients post COVID-19 infection. Patients who were previously infected with COVID-19 filled out the Central Sensitisation Inventory (CSI), the Post-COVID-19 Functional Status (PCFS) Scale and the EuroQol with five dimensions, through an online survey. Eventually, 567 persons completed the survey. In total, 29.73% of the persons had a score of <40/100 on the CSI and 70.26% had a score of ≥40/100. Regarding functional status, 7.34% had no functional limitations, 9.13% had negligible functional limitations, 37.30% reported slight functional limitations, 42.86% indicated moderate functional limitations and 3.37% reported severe functional limitations. Based on a one-way ANOVA test, there was a significant effect of PCFS Scale group level on the total CSI score (F(4,486) = 46.17, p < 0.001). This survey indicated the presence of symptoms of central sensitisation in more than 70% of patients post COVID-19 infection, suggesting towards the need for patient education and multimodal rehabilitation, to target nociplastic pain.

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Section: Discussionmentioning

confidence: 99%

Is Central Sensitisation the Missing Link of Persisting Symptoms after COVID-19 Infection?

Goudman

Smedt

Noppen

et al. 2021

JCM

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“…SARS-CoV-2 attaches to ACE2 receptors ( 29 ), and enters vascular endothelial cells through endocytosis and exocytosis, allowing for cell-to-cell transmission of the virus ( 28 ). Studies have shown that SARS-CoV-2 can interact with macrophages, microglia, and astrocytes in the CNS, triggering the release of cytokines and causing high inflammation ( 30 ). This inflammatory state can result in increased permeability of the BBB, dysfunction of cerebrovascular endothelial cells, and disruption of BBB integrity.…”

Section: Possible Mechanisms Of Long-term Effects On the Nervous Systemmentioning

confidence: 99%

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

Zhao,

Xia,

Jiao

et al. 2024

Front. Neurol.

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Corona Virus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), has presented unprecedented challenges to the world. Changes after acute COVID-19 have had a significant impact on patients with neurodegenerative diseases. This study aims to explore the mechanism of neurodegenerative diseases by examining the main pathways of central nervous system infection of SARS-CoV-2. Research has indicated that chronic inflammation and abnormal immune response are the primary factors leading to neuronal damage and long-term consequences of COVID-19. In some COVID-19 patients, the concurrent inflammatory response leads to increased release of pro-inflammatory cytokines, which may significantly impact the prognosis. Molecular imaging can accurately assess the severity of neurodegenerative diseases in patients with COVID-19 after the acute phase. Furthermore, the use of FDG-PET is advocated to quantify the relationship between neuroinflammation and psychiatric and cognitive symptoms in patients who have recovered from COVID-19. Future development should focus on aggressive post-infection control of inflammation and the development of targeted therapies that target ACE2 receptors, ERK1/2, and Ca2+.

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“…Based on the pertinent studies, SARS-CoV-2 can bring about a hyper-inflammatory condition through its interaction with macrophages, microglia, and astrocytes in the CNS and the subsequent release of cytokines [44]. Such status can give rise to increased BBB permeability, cerebrovascular endothelial dysfunction, and BBB destruction, which eventuates to the entrance Physiology International 109 (2022) 2, 135-162 of more inflammatory factors into the CNS, leading to neurological disorders and neurodegenerative diseases [32,33,[45][46][47][48][49][50][51][52][53][54][55][56][57][58][59][60].…”

Section: Coronavirus-mediated Neuropathogenesismentioning

confidence: 99%

Molecular mechanisms highlighting the potential role of COVID-19 in the development of neurodegenerative diseases

Rahmani

Ghashghayi

Zendehdel

et al. 2022

PhysInt

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Coronavirus disease 2019 (COVID-19) is a contagious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). In addition to the pulmonary manifestations, COVID-19 patients may present a wide range of neurological disorders as extrapulmonary presentations. In this view, several studies have recently documented the worsening of neurological symptoms within COVID-19 morbidity in patients previously diagnosed with neurodegenerative diseases (NDs). Moreover, several cases have also been reported in which the patients presented parkinsonian features after initial COVID-19 symptoms. These data raise a major concern about the possibility of communication between SARS-CoV-2 infection and the initiation and/or worsening of NDs. In this review, we have collected compelling evidence suggesting SARS-CoV-2, as an environmental factor, may be capable of developing NDs. In this respect, the possible links between SARS-CoV-2 infection and molecular pathways related to most NDs and the pathophysiological mechanisms of the NDs such as Alzheimer's disease, vascular dementia, frontotemporal dementia, Parkinson's disease, and amyotrophic lateral sclerosis will be explained.

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Dialogue between Neuroinflammation and Neurodegenerative Diseases in COVID-19

Cited by 8 publications

References 104 publications

Is Central Sensitisation the Missing Link of Persisting Symptoms after COVID-19 Infection?

Is Central Sensitisation the Missing Link of Persisting Symptoms after COVID-19 Infection?

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

Molecular mechanisms highlighting the potential role of COVID-19 in the development of neurodegenerative diseases

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