Evidence map›Paper›PMID 33142819›Full record

ArticleBrain sciences2020

COVID-19 and Parkinson's Disease: Shared Inflammatory Pathways Under Oxidative Stress.

Zahara L Chaudhry, Donika Klenja, Najma Janjua, Gerta Cami-Kobeci, Bushra Y Ahmed

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Brain sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.3field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 35 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 2 countries.

Zahara L ChaudhryInstitute of Biomedical & Environmental Science and Technology, School of Life Sciences, Faculty of Creative Arts, Technologies & Science, University Square, University of Bedfordshire, Luton LU1 3JU, UK.
Donika KlenjaSchool of Cellular and Molecular Medicine, University of Bristol, University Walk, Bristol BS8 1TD, UK.
Najma JanjuaFaculty of Medicine, Kawasaki Medical School, 577 Matsushima, Kurashiki, Okayama 701-0192, Japan.
Gerta Cami-KobeciInstitute of Biomedical & Environmental Science and Technology, School of Life Sciences, Faculty of Creative Arts, Technologies & Science, University Square, University of Bedfordshire, Luton LU1 3JU, UK.
Bushra Y AhmedInstitute of Biomedical & Environmental Science and Technology, School of Life Sciences, Faculty of Creative Arts, Technologies & Science, University Square, University of Bedfordshire, Luton LU1 3JU, UK.
University of Bedfordshire · GBKawasaki Medical School · JPUniversity of Bristol · GB

Funding

University of Bedfordshire RES 07339 (The work was partially supported by Research-informed teaching grant to the corresponding author.
6 · The paper itself

Abstract

The current coronavirus pandemic caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has resulted in a serious global health crisis. It is a major concern for individuals living with chronic disorders such as Parkinson's disease (PD). Increasing evidence suggests an involvement of oxidative stress and contribution of NFκB in the development of both COVID-19 and PD. Although, it is early to identify if SARS-CoV-2 led infection enhances PD complications, it is likely that oxidative stress may exacerbate PD progression in COVID-19 affected individuals and/or vice versa. In the current study, we sought to investigate whether NFκB-associated inflammatory pathways following oxidative stress in SARS-CoV-2 and PD patients are correlated. Toward this goal, we have integrated bioinformatics analysis obtained from Basic Local Alignment Search Tool of Protein Database (BLASTP) search for similarities of SARS-CoV-2 proteins against human proteome, literature review, and laboratory data obtained in a human cell model of PD. A Parkinson's like state was created in 6-hydroxydopamine (6OHDA)-induced differentiated dopamine-containing neurons (dDCNs) obtained from an immortalized human neural progenitor cell line derived from the ventral mesencephalon region of the brain (ReNVM). The results indicated that SARS-CoV-2 infection and 6OHDA-induced toxicity triggered stimulation of caspases-2, -3 and -8 via the NFκB pathway resulting in the death of dDCNs. Furthermore, specific inhibitors for NFκB and studied caspases reduced the death of stressed dDCNs. The findings suggest that knowledge of the selective inhibition of caspases and NFκB activation may contribute to the development of potential therapeutic approaches for the treatment of COVID-19 and PD.

Indexed as

6OHDAapoptosiscaspaseinhibitorsnuclear factor kappa B (NFκB)oxidative stressParkinson’s diseaseSARS-CoV-2

Identifiers

PMID33142819
PMCPMC7693814
OpenAlexW3096355925

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.