Parkinson's Disease in the Era of a Novel Respiratory Virus Pandemic

Otero‐Losada, Matilde; Kobiec, Tamara; Udovin, Lucas; Chevalier, Guenson; Quarracino, Cecilia; Maissonave, Camila Menéndez; Bordet, Sofía; Capani, Francisco; Pérez-Lloret, Santiago

doi:10.3389/fneur.2020.00995

Cited by 5 publications

(3 citation statements)

References 21 publications

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“…Infection with SARS-CoV-2 and other viruses can cause movement disorders[37,38] and may increase the risk of Parkinson’s Disease. [39] Hence further research on a potential association between Parkinsonian symptoms and ChAdOx1 is warranted.…”

Section: Discussionmentioning

confidence: 99%

Disproportionality analysis of adverse neurological and psychiatric reactions with the ChAdOx1 (Oxford-AstraZeneca) and BNT162b2 (Pfizer-BioNTech) COVID-19 vaccines in the United Kingdom

Pérez-Lloret

Petrovsky

Alami

et al. 2021

Preprint

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Objective: The information on neurologic or psychiatric adverse reactions to the COVID-19 vaccines is limited. Our objective was to examine the odds of neurological and psychiatric adverse reactions to BNT162b2 (Pfizer-BioNTech) and ChAdOx1 (Oxford-AstraZeneca) COVID-19 vaccines. Methods: We analyzed all Adverse Vaccine Reaction reports to the United Kingdom Medicines and Healthcare products Regulatory Agency between December 9, 2020 and June 30, 2021 that mentioned the BNT162b2 or ChAdOx1 vaccines. We compared the rates of adverse neurological and psychiatric reactions with ChAdOx1 to those with BNT162b2. P-values were obtained by a Bonferroni-adjusted Z-test for proportions. Results: As of June 30, 2021, 53.2 M doses of ChAdOx1 and 46.1 M doses of BNT162b2 had been administered. We extracted information from 300,518 distinct reports. The number of individual adverse neurologic or psychiatric reaction reports were less than 200/M doses administered, except headache which was reported in 1,550 and 395 cases/M doses of ChAdOx1 and BNT162b2, respectively. Compared to BNT162b2, cerebral hemorrhagic or thrombotic events, headaches and migraines, Guillain-Barre syndrome and paresthesias, tremor and freezing, delirium, hallucinations, nervousness, poor sleep quality, and postural dizziness were more frequently reported with ChAdOx1. Reactions more frequently reported with BNT162b2 than ChAdOx1 were Bell's palsy, facial paralysis, dysgeusia, anxiety, and presyncope or syncope. Conclusion: Significant differences in the neurologic and psychiatric adverse event profiles of the ChAdOx1 and BNT162b2 vaccines may exist, emphasizing the need for additional research. The beneficial and protective effects of the COVID-19 vaccines far outweigh the low potential risk of neurologic and psychiatric reactions.

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Section: Discussionmentioning

confidence: 99%

Disproportionality analysis of adverse neurological and psychiatric reactions with the ChAdOx1 (Oxford-AstraZeneca) and BNT162b2 (Pfizer-BioNTech) COVID-19 vaccines in the United Kingdom

Pérez-Lloret

Petrovsky

Alami

et al. 2021

Preprint

Self Cite

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“…Also, 148 of 694 (vs. 4,074 of 74,065 in non-PD patients) in a cohort from the United States ( Zhang et al, 2020c ), as well as 23 of 117 PD patients followed in Spain, the United Kingdom, Iran and Italy across 21 health centers, died of COVID-19 complications ( Fasano et al, 2020 ). Consequently, an area of future concern is whether SARS-CoV-2 infection would expand the exploding cases of PD worldwide ( Otero-Losada et al, 2020 ). In the past, the incidence of parkinsonism was observed to increase after the Spanish flu pandemic in 1918 with people born during the pandemic having 2–3-fold risk to develop parkinsonism compared to people born before to 1888 or after 1924 ( Jang et al, 2009 ; Eldeeb et al, 2020 ).…”

Section: Perspectives: Implications Of Microglial Reactivity In Sars-mentioning

confidence: 99%

Microglial Implications in SARS-CoV-2 Infection and COVID-19: Lessons From Viral RNA Neurotropism and Possible Relevance to Parkinson’s Disease

Awogbindin

Ben-Azu

Olusola

et al. 2021

Front. Cell. Neurosci.

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Since December 2019, humankind has been experiencing a ravaging severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) outbreak, the second coronavirus pandemic in a decade after the Middle East respiratory syndrome coronavirus (MERS-CoV) disease in 2012. Infection with SARS-CoV-2 results in Coronavirus disease 2019 (COVID-19), which is responsible for over 3.1 million deaths worldwide. With the emergence of a second and a third wave of infection across the globe, and the rising record of multiple reinfections and relapses, SARS-CoV-2 infection shows no sign of abating. In addition, it is now evident that SARS-CoV-2 infection presents with neurological symptoms that include early hyposmia, ischemic stroke, meningitis, delirium and falls, even after viral clearance. This may suggest chronic or permanent changes to the neurons, glial cells, and/or brain vasculature in response to SARS-CoV-2 infection or COVID-19. Within the central nervous system (CNS), microglia act as the central housekeepers against altered homeostatic states, including during viral neurotropic infections. In this review, we highlight microglial responses to viral neuroinfections, especially those with a similar genetic composition and route of entry as SARS-CoV-2. As the primary sensor of viral infection in the CNS, we describe the pathogenic and neuroinvasive mechanisms of RNA viruses and SARS-CoV-2 vis-à-vis the microglial means of viral recognition. Responses of microglia which may culminate in viral clearance or immunopathology are also covered. Lastly, we further discuss the implication of SARS-CoV-2 CNS invasion on microglial plasticity and associated long-term neurodegeneration. As such, this review provides insight into some of the mechanisms by which microglia could contribute to the pathophysiology of post-COVID-19 neurological sequelae and disorders, including Parkinson’s disease, which could be pervasive in the coming years given the growing numbers of infected and re-infected individuals globally.

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“…Neurodegenerative diseases and particularly Alzheimer disease and Parkinson disease share some common clinical manifestations with COVID-19: 1) dysosmias at early stages of Alzheimer disease (see literature meta-analysis in ( Silva et al., 2018 )) or both anosmia and dysgeusia in Parkinson disease ( Tarakad and Jankovic, 2017 ; Poewe et al., 2017 ; Otero-Losada et al., 2020 ); 2) histopathological alterations of the olfactory mucosa early on ( Talamo et al., 1989 ) ( Perry et al., 2003 ) and subsequent degeneration of the olfactory bulb ( Murphy et al., 1990 ) in the course of both diseases, the latter progressing in parallel with the evolution from mild cognitive impairment to full dementia ( Bathini et al., 2019 ). Pathophysiological findings of aggregated α-synuclein have been tentatively associated with hyposmia in Parkinson disease ( Poewe et al., 2017 ).…”

Section: Evolution Of the Covid-19 Clinical And Neurological Picturementioning

confidence: 99%

The unfolding palette of COVID-19 multisystemic syndrome and its neurological manifestations

Barrantes

2021

Brain, Behavior, & Immunity - Health

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Although our current knowledge of the pathophysiology of COVID-19 is still fragmentary, the information so far accrued on the tropism and life cycle of its etiological agent SARS-CoV-2, together with the emerging clinical data, suffice to indicate that the severe acute pulmonary syndrome is the main, but not the only manifestation of COVID-19. Necropsy studies are increasingly revealing underlying endothelial vasculopathies in the form of micro-haemorrhages and micro-thrombi. Intertwined with defective antiviral responses, dysregulated coagulation mechanisms, abnormal hyper-inflammatory reactions and responses, COVID-19 is disclosing a wide pathophysiological palette. An additional property in categorising the disease is the combination of tissue (e.g. neuro- and vasculo-tropism) with organ tropism, whereby the virus preferentially attacks certain organs with highly developed capillary beds, such as the lungs, gastrointestinal tract, kidney and brain. These multiple clinical presentations confirm that the acute respiratory syndrome as described initially is increasingly unfolding as a more complex nosological entity, a multiorgan syndrome of systemic breadth. The neurological manifestations of COVID-19, the focus of this review, reflect this manifold nature of the disease.

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Parkinson's Disease in the Era of a Novel Respiratory Virus Pandemic

Cited by 5 publications

References 21 publications

Disproportionality analysis of adverse neurological and psychiatric reactions with the ChAdOx1 (Oxford-AstraZeneca) and BNT162b2 (Pfizer-BioNTech) COVID-19 vaccines in the United Kingdom

Disproportionality analysis of adverse neurological and psychiatric reactions with the ChAdOx1 (Oxford-AstraZeneca) and BNT162b2 (Pfizer-BioNTech) COVID-19 vaccines in the United Kingdom

Microglial Implications in SARS-CoV-2 Infection and COVID-19: Lessons From Viral RNA Neurotropism and Possible Relevance to Parkinson’s Disease

The unfolding palette of COVID-19 multisystemic syndrome and its neurological manifestations

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