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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]
In the citing paper
“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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Cited by
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Self-citationPost-COVID-19 Depressive Symptoms: Epidemiology, Pathophysiology, and Pharmacological Treatment
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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
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Theoharides, T. C. (2022) · Molecular Neurobiology · doi:10.1007/s12035-021-02696-0 · Cited by 156
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Neuroinvasion and Neurotropism by SARS-CoV-2 Variants in the K18-hACE2 Mouse
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BackgroundLong COVID and neuropsychiatric manifestations (Review)
Efstathiou, V., Stefanou, M., Demetriou, M., Siafakas, N., Makris, M. P., Tsivgoulis, G. K., Zoumpourlis, V., Kympouropoulos, S. P., Tsoporis, J. N., Spandidos, D. A., et al. (2022) · Experimental and Therapeutic Medicine · doi:10.3892/etm.2022.11290 · Cited by 118
“Patients affected by ‘long COVID’ include also those who initially had mild or asymptomatic disease, pointing to residual effects that involve multiple organ systems, including the peripheral and central nervous system (CNS) (23,31,32).”
InfluentialDamiano, R. F., Guedes, B. F., de Rocca, C. C., de Pádua Serafim, A., Castro, L. H. M., Munhoz, C. D., Nitrini, R., Filho, G. B., Miguel, E. C., Lucchetti, G., et al. (2022) · European Archives of Psychiatry and Clinical Neuroscience · doi:10.1007/s00406-021-01286-4 · Cited by 98
“Once the virus enters the CNS, it affects neurons, microglia, oligodendrocytes, and especially astrocytes, undermining neurons viability [17, 179, 180].”
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Petersen, M., Nägele, F. L., Mayer, C., Schell, M., Petersen, E. L., Kühn, S., Gallinat, J., Fiehler, J., Pasternak, O., Matschke, J., et al. (2023) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2217232120 · Cited by 83
“Evidence of neuroinflammation was reported in histopathological and clinical studies of COVID-19 patients: virus invasion (24, 25), activation of glial cells (9, 26, 27), and a cytokine response in the cerebrospinal fluid accompanying neurological and psychiatric COVID-19 symptoms (10).”
Can COVID-19 pandemic boost the epidemic of neurodegenerative diseases?
Verkhratsky, A., Li, Q., Melino, S., Melino, G., & Shi, Y. (2020) · Biology Direct · doi:10.1186/s13062-020-00282-3 · Cited by 81
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“We advance the premise that brain perivascular inflammation is a critical pathogenetic factor in long COVID mostly due to SARS-CoV-2 activating brain mast cells and microglia resulting in the release of inflammatory, neurotoxic, and vasoactive mediators [60,61].”
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Pacheco‐Herrero, M., Soto-Rojas, L. O., Harrington, C. R., Flores-Martinez, Y. M., Villegas-Rojas, M. M., León-Aguilar, A. M., Martínez-Gómez, P. A., Campa-Córdoba, B. B., Apátiga-Pérez, R., Corniel-Taveras, C. N., et al. (2021) · Frontiers in Neurology · doi:10.3389/fneur.2021.660087 · Cited by 71
Neurotropic Viruses, Astrocytes, and COVID-19
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“This phenomenon is typical for severe COVID-19 pathogenesis, which eventually leads to BBB alterations and neuroinflammation (Najjar et al., 2020; Tremblay et al., 2020).”
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“Despite their CNS homeostasis and neuronal cell functions, microglia and astrocytes are mainly involved in the protective immune responses during neuroinflammation (Facci et al., 2018; Jha et al., 2019; Tremblay et al., 2020).”
BackgroundSelf-citationDid the COVID-19 Pandemic Increase the Incidence of Acute Macular Neuroretinopathy?
Azar, G., Bonnin, S., Vasseur, V., Faure, C., Salviat, F., Vignal‐Clermont, C., Titah, C., Farès, S., Boulanger-Scemama, É., Derrien, S., et al. (2021) · Journal of Clinical Medicine · doi:10.3390/jcm10215038 · Cited by 58
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SARS-CoV-2 involvement in central nervous system tissue damage
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“Given the presence of ACE2 receptors in microglia and astrocytes, it may be possible to relate SARS-CoV-2 with glial activation (Tremblay et al. 2020).”
BackgroundBrain microstructural changes and fatigue after COVID-19
Bispo, D. D. D. C., Brandão, P. R. D. P., Pereira, D. A., Maluf, F. B., Dias, B. A., Paranhos, H. R., von Glehn, F., de Oliveira, A. C. P., Regattieri, N. A. T., Silva, L. S., et al. (2022) · Frontiers in Neurology · doi:10.3389/fneur.2022.1029302 · Cited by 56
“Neurons, oligodendrocytes, and other glial cells may have impaired physiological functions during SARS-CoV-2 inflammatory insult, leading to a disturbance of brain homeostasis (62).”
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Mehrabani, M. M., Karvandi, M. S., Maafi, P., & Doroudian, M. (2022) · Reviews in Medical Virology · doi:10.1002/rmv.2334 · Cited by 53
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“The brain’s defensive system and systemic inflammation can influence the CNS through both innate and adaptive immune systems through their cellular elements [64,97].”
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“Besides, reactive microglia generally adopt different morphologies, for example, shifting to amoeboid shapes with bigger somas and less ramified processes, as opposed to the steady-state, highly branched “surveilling” phenotype (Figure 1; Savage et al., 2019; Tremblay et al., 2020).”
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“Furthermore, microglia modulate the CNS micro-milieu, thereby reduce the severity of demyelination, and influence neuronal repair in cerebral cortex (Lavi and Cong 2020; Tremblay et al. 2020).”
BackgroundNeurological sequela and disruption of neuron-glia homeostasis in SARS-CoV-2 infection
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“The virus also triggers a pro-inflammatory response, which can render the BBB susceptible to damage, leading to immune cell infiltration into the brain along with viral penetration (Tremblay et al., 2020; Solomon, 2021).”
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BackgroundTREM2, microglial and ischemic stroke
Wang, H., Li, X., Wang, Q., Ma, J., Gao, X., & Wang, M. (2023) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2023.578108 · Cited by 32
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Self-citationWhat can neuroimmunology teach us about the symptoms of long-COVID?
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“All these routes were proposed based on current evidences (Satarker and Nampoothiri 2020; Tremblay et al. 2020; Lima et al. 2020; Jakhmola et al. 2020).”
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“Once inside the brain, SARS-CoV2 invades tissues with ACE-2 receptors including the frontotemporal cortex, circumventricular organs, thalamus, and brainstem involving the rostral ventrolateral medulla among others.(28,29) ACE-2 expression has also been reported in the hypothalamus and pituitary gland.”
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“Given that the large number of functions performed by glial cells in the neuroinflammatory response, it could be expected that activation of astrocytes has a major impact on the CNS during SARSCoV-2 infection [23, 24].”
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Pazdro-Zastawny, K., Dorobisz, K., Misiak, P., Kruk-Krzemień, A., & Zatoński, T. (2022) · Frontiers in Neurology · doi:10.3389/fneur.2022.956515 · Cited by 33
Plasmalogens and platelet‐activating factor roles in chronic inflammatory diseases
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“Genetic variants and environmental risk factors altering these microglial functions are further associated with most if not all CNS disorders, including neurodevelopmental, neuropsychiatric, and neurodegenerative.(99,100) These findings highlight the importance of evaluating the outcomes of decreased, but also restore…”
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“Increasing evidence indicates the involvement of neuro-inflammation [64–66] that may damage brain blood vessels [67, 68] and brain cells [64, 69, 70] possibly via activation of microglia [71, 72].”
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Roczkowsky, A., Limonta, D., Fernandes, J. P., Branton, W. G., Clarke, M., Hlavay, B. A., Noyce, R. S., Joseph, J. T., Ogando, N. S., Das, S., et al. (2023) · Annals of Neurology · doi:10.1002/ana.26679 · Cited by 29
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“These conditions include neurotrauma (Burda et al. 2016; Faulkner et al. 2004), systemic inflammation and sepsis (Shulyatnikova and Verkhratsky 2019; Tremblay et al. 2020), microbial or viral neuroinfection (Soung and Klein 2018; Zorec et al. 2019), toxic encephalopathies (Li et al. 2021;…”
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“This cascade of events can dysregulate neurogenesis and disrupt the normal functioning of neurons, oligodendrocytes, and neuroglial cells [100].”
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Acute and long-term effects of COVID-19 on brain and mental health: A narrative review
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“Glia-induced neuroinflammation is a common pathological observation in neurological cases of COVID-19 (Tremblay et al., 2020; Vargas et al., 2020), as microglia and astrocytes are key pathogen-combating players in the brain during SARS-CoV-2 infection (McMahon et al.”
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“24 In addition, studies of single-nucleus transcriptomes of frontal cortex and the choroid plexus in 30 SARS-CoV-2 patients reveal cellular changes in COVID-19-associated microglia and astrocytes that share features with pathological cell states in neurodegenerative disorders, such as Alzheimer…”
Fetal brain vulnerability to SARS-CoV-2 infection
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Alterations in microbiota of patients with COVID‐19: implications for therapeutic interventions
Qiu, Y., Mo, C., Chen, L., Ye, W., Chen, G., & Zhu, T. (2024) · MedComm · doi:10.1002/mco2.513 · Cited by 18
“119 Glial activation and neuroinflammation may play an important role in cognitive impairment caused by COVID-19.”
BackgroundHayden, M. R. (2021) · Neuroglia · doi:10.3390/neuroglia2010004 · Cited by 19
“Furthermore, the major histocompatibility complex (MHC)positive antigen presenting cells will present these viral antigens to the acquired immune system’s auto-reactive T-cells that will form the antibody which will then develop the antigen–antibody complex [94,99].”
BackgroundImmunological Interfaces: The COVID-19 Pandemic and Depression
Perlmutter, A. (2021) · Frontiers in Neurology · doi:10.3389/fneur.2021.657004 · Cited by 18
Genetics of COVID ‐19 and myalgic encephalomyelitis/chronic fatigue syndrome: a systematic review
Tziastoudi, M., Cholevas, C., Stefanidis, I., & Theoharides, T. C. (2022) · Annals of Clinical and Translational Neurology · doi:10.1002/acn3.51631 · Cited by 19
“Microglia have been implicated in COVID-19(228) and were also associated with neuroinflammation.(229) Microglia have important functions both in health and disease of the central nervous system (CNS), especially with respect to neuroinflammation 232 and neurodegenerative diseases.”
BackgroundAstrocytes in the pathophysiology of neuroinfection
Zorec, R., & Verkhratsky, A. (2022) · Essays in Biochemistry · doi:10.1042/ebc20220082 · Cited by 16
Self-citationSARS-CoV-2 Infection: Paving Way for Sleep Disorders in Long Term!
Gupta, R. M., & Pandi-Perumal, S. R. (2021) · Sleep and Vigilance · doi:10.1007/s41782-021-00145-5 · Cited by 16
“, brainstem, circumventricular organ, subfornical area, paraventricular nucleus, and rostroventrolateral medulla [10].”
BackgroundPost‐COVID‐19 neuropsychiatric syndrome: Is maladaptive glial recovery to blame?
Steardo, L., Steardo, L., Verkhratsky, A., & Scuderi, C. (2021) · Acta Physiologica · doi:10.1111/apha.13717 · Cited by 15
Self-citationVolk, P., Manesh, M. R., Warren, M. E., Besko, K., de Andrade, E. G., Wicki‐Stordeur, L. E., & Swayne, L. A. (2023) · Journal of Neurochemistry · doi:10.1111/jnc.16016 · Cited by 14
Microglia as potential key regulators in viral-induced neuroinflammation
Ismail, F. S., Faustmann, T. J., Faustmann, P. M., & Corvace, F. (2024) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2024.1426079 · Cited by 13
Nelson, B. K., Farah, L. N., Grier, A., Su, W., Chen, J., Sossi, V., Sekhon, M. S., Stoessl, A. J., Wellington, C. L., Honer, W. G., et al. (2024) · NeuroImage · doi:10.1016/j.neuroimage.2024.120859 · Cited by 16
“We found lower MD in the long COVID group, but no differences in other DTI metrics or cognitive performance.”
Backgroundda Cunha, L. N. O. L., Tizziani, T., Souza, G. B., Moreira, M. A., Neto, J. S. S., Santos, C. V. D. D., de Carvalho, M. G., Dalmarco, E. M., Turqueti, L. B., Scotti, L., et al. (2021) · Current Medicinal Chemistry · doi:10.2174/0929867328666210726094955 · Cited by 12
Neuroinvasion and neurotropism by SARS-CoV-2 variants in the K18-hACE2 mousePreprint
Seehusen, F., Clark, J. J., Sharma, P., Bentley, E. G., Kirby, A., Subramaniam, K. S., Wunderlin, S., Hughes, G. L., Patterson, E. I., Michael, B. D., et al. (2021) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2021.04.16.440173 · Cited by 12
DiNicolantonio, J. J., McCarty, M. F., Barroso-Aranda, J., Assanga, S. B. I., Luján, L. M. L., & O’Keefe, J. H. (2021) · Open Heart · doi:10.1136/openhrt-2021-001663 · Cited by 11
Valenza, M., Steardo, L., Steardo, L., Verkhratsky, A., & Scuderi, C. (2021) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2021.748136 · Cited by 12
Self-citationGonçalves, C., Sesterheim, P., Wartchow, K. M., Bobermin, L. D., Leipnitz, G., & Quincozes‐Santos, A. (2022) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2022.905218 · Cited by 11
“Another very important aspect of COVID-19 is the greater vulnerability of elderly patients; possibly the aging of astrocytes makes these individuals more susceptible to Sars-CoV-2-induced dysfunction (Tremblay et al., 2020).”
BackgroundKhullar, S., & Wang, D. (2023) · Human Molecular Genetics · doi:10.1093/hmg/ddad009 · Cited by 12
Autopsy findings of pediatric COVID-19: a systematic review
Octavius, G. S., Wijaya, J. H., Tan, A. O., Muljono, M. P., Chandra, S., & Juliansen, A. (2022) · Egyptian Journal of Forensic Sciences · doi:10.1186/s41935-022-00288-0 · Cited by 11
SARS-CoV-2 infection is associated with increased odds of insomnia, RLS and dream enactment behavior
Kumar, N., Goyal, A., Hussain, A., Saini, L. K., Chawla, O., Arora, P. K., Daga, R., Tikka, S. K., Goyal, S., Kanchan, S., et al. (2022) · Indian Journal of Psychiatry · doi:10.4103/indianjpsychiatry.indianjpsychiatry_586_21 · Cited by 10
“[17] Thus, the present study was planned to study the effect of SARS-CoV-2 infection to the occurrence of insomnia, RLS and DEB.”
Peripheral nervous system involvement associated with COVID-19. A systematic review of literature
Hanganu, A. R., Constantin, A. M., Moise, E.-S., Niculae, C., Olaru, I. D., Băicuş, C., & Hristea, A. (2023) · PLoS ONE · doi:10.1371/journal.pone.0283827 · Cited by 10
SARS-CoV-2 hampers dopamine production in iPSC-derived dopaminergic neurons
Cappelletti, G., Carsana, E. V., Lunghi, G., Breviario, S., Vanetti, C., Fonzo, A. D., Frattini, E., Magni, M., Zecchini, S., Clerici, M., et al. (2023) · Experimental and Molecular Pathology · doi:10.1016/j.yexmp.2023.104874 · Cited by 10
Dialogue between Neuroinflammation and Neurodegenerative Diseases in COVID-19
Chowdhury, B., Sharma, A., Satarker, S., Mudgal, J., & Nampoothiri, M. (2021) · Journal of Environmental Pathology Toxicology and Oncology · doi:10.1615/jenvironpatholtoxicoloncol.2021038365 · Cited by 10
SARS-CoV-2-Induced Amyloidgenesis: Not One, but Three Hypotheses for Cerebral COVID-19 Outcomes
Gonçalves, C., Bobermin, L. D., Sesterheim, P., & Netto, C. A. (2022) · Metabolites · doi:10.3390/metabo12111099 · Cited by 10
“Note that the brain endothelium is closely surrounded by the feet of astrocytes, forming the BBB [19].”
BackgroundInfluentialEvidence of Microglial Immune Response Following Coronavirus PHEV Infection of CNS
Zhang, J., Li, Z., Lu, H., Shi, J., Gao, R., Ma, Y., Lan, Y., Guan, J., Zhao, K., Gao, F., et al. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2021.804625 · Cited by 10
COVID‐19 and cognitive impairment: From evidence to SARS‐CoV‐2 mechanism
Pan, H., Niu, J., Feng, L., Yin, Y. L., Dang, C., Lu, Y., Li, L., Ji, J., Yang, K., Wang, L., et al. (2024) · Brain‐X · doi:10.1002/brx2.58 · Cited by 9
Crosstalk between SARS-CoV-2 Infection and Neurological Disorders: A Review
Azhar, A., Wali, M. A., Rashid, Q., Khan, W. H., Alhosaini, K. A., Owais, M., & Kamal, M. A. (2022) · CNS & Neurological Disorders - Drug Targets · doi:10.2174/1871527321666220418114009 · Cited by 8
Post-Acute Sequelae of SARS-CoV-2 Infection: A Descriptive Clinical Study
Gutiérrez-Martínez, L., Karten, J., Kritzer, M. D., Josephy‐Hernandez, S. E., Kim, D. D., Newhouse, A. L., Pasinski, M., Praschan, N. C., Razafsha, M., Rubin, D. B., et al. (2022) · Journal of Neuropsychiatry · doi:10.1176/appi.neuropsych.21070193 · Cited by 8
Human Brain In Vitro Model for Pathogen Infection-Related Neurodegeneration Study
Yan, Y., & Cho, A. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25126522 · Cited by 7
“During severe COVID-19, the increase in circulating chemokines and interleukins can compromise the BBB, allowing these inflammatory mediators to affect glial cells [174].”
BackgroundRole Of Retroelements In The Development Of COVID-19 Neurological Consequences
Mustafin, R. N., Kazantseva, A. V., Kovas, Y. V., & Хуснутдинова, Э. К. (2022) · Russian Open Medical Journal · doi:10.15275/rusomj.2022.0313 · Cited by 7
“The key factor in CNS inflammation caused by SARS-CoV-2 is the activation of astrocytes and microglia [95], which are the main sources of cytokines in the inflamed CNS, including interferon and interleukins involved in the development of a cytokine storm in the brain [96].”
BackgroundChoi, S. S. A., Chan, H. H., Chan, C. M., Wang, X., Webb, S., Leung, K. W., Tsim, K. W. K., & Miller, A. L. (2022) · Journal of Virology · doi:10.1128/jvi.01418-22 · Cited by 7
“It has been proposed that such entry pathways might contribute to the long-term effects of COVID-19 (long-COVID) infection (75, 115, 116, 150), which at present are not well understood and might have the potential to be targeted by antiviral agents (53, 114, 151).”
BackgroundDeveloping brain under renewed attack: viral infection during pregnancy
Recaioglu, H., & Kolk, S. M. (2023) · Frontiers in Neuroscience · doi:10.3389/fnins.2023.1119943 · Cited by 6
“Exceptionally, yolk sac-derived microglial cells appearing and migrating to the developing brain (GW4-24; Menassa and Gomez-Nicola, 2018) not only participate in brain development in critical stages but also are the resident macrophages of the brain acting as first-line defenders against pathogens (Tremblay et al., 20…”
BackgroundOneyear longitudinal study on biomarkers of blood–brain barrier permeability in COVID-19 patients
Wallensten, J., Havervall, S., Power, Y., Åsberg, M., Borg, K., Nager, A., Thålin, C., & Mobarrez, F. (2024) · Scientific Reports · doi:10.1038/s41598-024-73321-y · Cited by 7
“One hypothesis is that SARS-CoV-2 activates microglia and astrocytes, inducing an inflammatory response and increasing cytokine production, which results in a feedback loop that affects glia cells in the brain 9 and subsequently the BBB integrity 3 .”
BackgroundGoldstein, M. R., & Cheslock, M. (2021) · Medical Hypotheses · doi:10.1016/j.mehy.2021.110645 · Cited by 8
Neurotropic SARS-CoV-2: Causalities and Realities
Pardasani, M., & Abraham, N. M. (2022) · IntechOpen eBooks · doi:10.5772/intechopen.108573 · Cited by 5
Impact of COVID-19 on Anxiety and Depression - Biopsychosocial Factors
Bertollo, A. G., Galvan, A. C. L., Mingoti, M. E. D., Dallagnol, C., & Ignácio, Z. M. (2023) · CNS & Neurological Disorders - Drug Targets · doi:10.2174/1871527322666230210100048 · Cited by 6
Groppa, S. A., Ciolac, D., Duarte, C. L., Garcia, C., Gasnaș, D., Leahu, P., Efremova, D., Alexandru, G., Bălănuță, T., Mîrzac, D., et al. (2021) · Advances in experimental medicine and biology · doi:10.1007/5584_2021_675 · Cited by 6
SARS-CoV-2 Attacks in the Brain: Focus on the Sialome
Wielgat, P., Narejko, K., & Car, H. (2022) · Cells · doi:10.3390/cells11091458 · Cited by 6
Mora, V. P., Kalergis, A. M., & Böhmwald, K. (2024) · Microorganisms · doi:10.3390/microorganisms12081713 · Cited by 6
“The potential disruption of the BBB, a protective barrier against foreign molecules, facilitates the virus’s ability to infect the brain [22,69].”
BackgroundInfluentialCappelletti, G., Brambilla, L., Strizzi, S., Limanaqi, F., Melzi, V., Rizzuti, M., Nizzardo, M., Saulle, I., Trabattoni, D., Corti, S. P., et al. (2025) · The FASEB Journal · doi:10.1096/fj.202401604rrr · Cited by 5
“59,116,117 The initiation of an inflammatory reaction in SARS- CoV- 2-infected HCOs was further substantiated by the increased expression of genes associated with the inflammasome pathway, particularly NLRP3 and IL-18.”
Lipid metabolism, microglia, and stroke
Chen, L., Zhang, M., Wei, W., Li, Q., Wang, L., Zhao, M., He, L., Xu, H., Yang, P., & Zhang, P. (2025) · Neural Regeneration Research · doi:10.4103/nrr.nrr-d-24-01523 · Cited by 7
“Microglia are extremely dynamic and constantly responding to episodes of health or disease by adapting diverse states and fulfilling different functions (Vay et al., 2018; Tremblay et al., 2020).”
SARS-CoV-2 and Brain Health: New Challenges in the Era of the Pandemic
Ahmed, W., Jia, F., Zhang, Y., & Chen, L. (2023) · Microorganisms · doi:10.3390/microorganisms11102511 · Cited by 5
Kato, Y., Tago, K., Fukatsu, S., Okabe, M., Shirai, R., Oizumi, H., Ohbuchi, K., Yamamoto, M., Mizoguchi, K., Miyamoto, Y., et al. (2022) · Non-Coding RNA · doi:10.3390/ncrna8030042 · Cited by 5
“As a result, the cell composition in the CNS collapses and neuronal cells can also be seriously damaged [11,13,14].”
BackgroundMild chronic hypoxia and the brain: an ambiguous relationship
Wszędybył-Winklewska, M., Czuba, E., Malinowski, K. S., Waśkow, M., Michalak, K., & Winklewski, P. J. (2026) · Journal of Neuroinflammation · doi:10.1186/s12974-025-03652-8 · Cited by 5
“Hypoxia serves as both a direct trigger of CNS inflammation through HIF-1α-mediated immune cell activation and an indirect facilitator through BBB compromise and peripheral immune cell infiltration [112, 133].”
Microglia and putative macrophages of the subfornical organ: structural and functional features
Гусельникова, В. В., Razenkova, V. A., Суфиева, Д. А., & Korzhevsky, D. E. (2022) · Bulletin of Russian State Medical University · doi:10.24075/brsmu.2022.020 · Cited by 4
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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