The DOI matches its Crossref record; 191 of the 191 references it cites were found in a registry or an index.
Neuropathobiology of COVID-19: The Role for Glia
Open accessAbstract
SARS-CoV-2, which causes the Coronavirus Disease 2019 (COVID-19) pandemic, has a brain neurotropism through binding to the receptor angiotensin-converting enzyme 2 expressed by neurones and glial cells, including astrocytes and microglia. Systemic infection which accompanies severe cases of COVID-19 also triggers substantial increase in circulating levels of chemokines and interleukins that compromise the blood-brain barrier, enter the brain parenchyma and affect its defensive systems, astrocytes and microglia. Brain areas devoid of a blood-brain barrier such as the circumventricular organs are particularly vulnerable to circulating inflammatory mediators. The performance of astrocytes and microglia, as well as of immune cells required for brain health, is considered critical in defining the neurological damage and neurological outcome of COVID-19. In this review, we discuss the neurotropism of SARS-CoV-2, the implication of neuroinflammation, adaptive and innate immunity, autoimmunity, as well as astrocytic and microglial immune and homeostatic functions in the neurological and psychiatric aspects of COVID-19. The consequences of SARS-CoV-2 infection during ageing, in the presence of systemic comorbidities, and for the exposed pregnant mother and foetus are also covered.
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“Once the virus enters the CNS, it affects neurons, microglia, oligodendrocytes, and especially astrocytes, undermining neurons viability [17, 179, 180].”
From Cognitive decline following acute viral infections: literature review and projections for post-COVID-19 (2022) · cites this paper as [179]
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“In SARS-CoV-2, trans-nasal and trans-synaptic mechanisms might allow the virus to invade the olfactory bulb and brainstem, with both being the possible initial site for CNS invasion [179].”
From Cognitive decline following acute viral infections: literature review and projections for post-COVID-19 (2022) · cites this paper as [179]
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Cites
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“Indeed, many epidemiological studies suggest that early-life adversity can be associated with an increased occurrence of neurodevelopmental, neurological or neuropsychiatric disorders later in life (Halligan et al., 2007; Lupien et al., 2009; Knuesel et al., 2014).”
BackgroundResting microglial cells are highly dynamic surveillants of brain parenchyma in vivo
Nimmerjahn, A., Kirchhoff, F., & Helmchen, F. (2005) · Science · doi:10.1126/science.1110647 · Cited by 5,827 · cited 1×
“These microglia have an amoeboid instead of a surveilling (derived from to “surveil,” which means to keep a place or a person under surveillance) morphology (Davalos et al., 2005; Nimmerjahn et al., 2005) and express markers that suggest they are ready to cope with invading agents using phagocytosis and the release of…”
BackgroundIliff, J. J., Wang, M., Liao, Y., Plogg, B. A., Peng, W., Gundersen, G. A., Benveniste, H., Vates, G. E., Deane, R., Goldman, S. A., et al. (2012) · Science Translational Medicine · doi:10.1126/scitranslmed.3003748 · Cited by 5,824 · cited 1×
“Furthermore, the astroglia-based glymphatic waste collection system (Iliff et al., 2012) declines with age, which affects clearance of numerous by-products and toxic substances (Kress et al., 2014).”
BackgroundAstrocyte-endothelial interactions at the blood-brain barrier
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BackgroundCryan, J. F., O'Riordan, K. J., Cowan, C. S. M., Sandhu, K. V., Bastiaanssen, T. F. S., Boehme, M., Codagnone, M. G., Cussotto, S., Fulling, C., Golubeva, A. V., et al. (2019) · Physiological Reviews · doi:10.1152/physrev.00018.2018 · Cited by 5,286
Cited by
Sorted by citations
Microglia states and nomenclature: A field at its crossroads
Paolicelli, R. C., Sierra, A., Stevens, B., Tremblay, M.-E., Aguzzi, A., Ajami, B., Amit, I., Audinat, E., Bechmann, I., Bennett, M., et al. (2022) · Neuron · doi:10.1016/j.neuron.2022.10.020 · Cited by 1,973
Self-citationAstrocytes in human central nervous system diseases: a frontier for new therapies
Verkhratsky, A., Butt, A., Li, B., Illes, P., Zorec, R., Semyanov, A., Tang, Y., & Sofroniew, M. V. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01628-9 · Cited by 428
Self-citationPost-COVID-19 Depressive Symptoms: Epidemiology, Pathophysiology, and Pharmacological Treatment
Mazza, M. G., Palladini, M., Poletti, S., & Benedetti, F. (2022) · CNS Drugs · doi:10.1007/s40263-022-00931-3 · Cited by 248
“Accordingly, increased microglial activation in association with high levels of IL-6 and TNF-α have been observed in MDD episodes [82], whereas microglia activation has been implicated in both acute and chronic neurological complications of COVID-19 [83], and increased microglial activation has been demonstrated in po…”
BackgroundS1-Leitlinie Post-COVID/Long-COVID
Koczulla, A. R., Ankermann, T., Behrends, U., Berlit, P., Böing, S., Brinkmann, F., Franke, C., Glöckl, R., Gogoll, C., Hummel, T. R., et al. (2021) · Pneumologie · doi:10.1055/a-1551-9734 · Cited by 164
“[150] Tremblay ME, Madore C, Bordeleau M et al.”
BackgroundCould SARS-CoV-2 Spike Protein Be Responsible for Long-COVID Syndrome?
Theoharides, T. C. (2022) · Molecular Neurobiology · doi:10.1007/s12035-021-02696-0 · Cited by 156
“Increasing evidence indicates the involvement of neuroinflammation [71, 88, 89] that may damage brain blood vessels [90, 91], as well as brain cells [88, 92, 93], possibly via activation of microglia [94, 95] and mast cells [96].”
Background
Metadata
- Authors
- Tremblay, M.-E., Madore, C., Bordeleau, M., Tian, L., & Verkhratsky, A.
- Affiliations
- Institut National de Recherche pour l'Agriculture, l'Alimentation et l'Environnement (FR)
- Université Laval (CA)
- Peking University (CN)
- Ikerbasque (ES)
- Venue
- Frontiers in Cellular Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2020-11-11
- Volume
- 14
- Pages
- 592214-592214
- ISSN
- 1662-5102 (ISSN-L)
- PMC
- PMC7693550
- OpenAlex
- W3101561456
- Cited by
- 159
- References
- 188
- Citations by year
- 2026: 7 · 2025: 10 · 2024: 20 · 2023: 25 · 2022: 60 · 2021: 36 · 2020: 1
- FWCI
- 3.42
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Cellular Neuroscience (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- HAL (submittedVersion, cc-by)
- HAL (submittedVersion)
- cIRcle (University of British Columbia) (submittedVersion, cc-by-nc-nd)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- eScholarship@McGill (McGill) (submittedVersion)
- Oskar-Bordeaux (Universite de Bordeaux) (submittedVersion, cc-by)
- Research Explorer (The University of Manchester) (submittedVersion, other-oa)
- Open Collections
- Funders
- European Commission
- Eesti Teadusagentuur (MOBTT77)
- Fondation pour la Recherche Médicale
- Canadian Institutes of Health Research (Tier 2)
- Topics
- Health Sciences › Medicine › Clinical Neurology › Long-Term Effects of COVID-19
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Infectious Diseases › SARS-CoV-2 and COVID-19 Research
- Keywords
- COVID-19 pandemic, SARS-CoV-2, glial cells, astrocytes, microglia, neurotropism, ACE2 receptor, blood-brain barrier, neuroinflammation, chemokines, interleukins, circumventricular organs, autoimmunity, innate immunity, adaptive immunity, neurological complications, psychiatric aspects, aging, comorbidities, pregnancy, fetus
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