SynthesisCells2022
Systematic Review of the Common Pathophysiological Mechanisms in COVID-19 and Neurodegeneration: The Role of Bioactive Compounds and Natural Antioxidants.
Synthesis in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- Headaches and facial pain attributed to SARS-CoV-2 infection and vaccination: a systematic review.European journal of neurology · 2024Pooled it
- COVID-19 Is Airborne AIDS: Provocative Oversimplification, Emerging Science, or Something in Between?AJPM focus · 2026Review
- Factors associated with older adults' cognitive decline 6 months after gamma-variant SARS-CoV-2 infection.Frontiers in neurology · 2024Article
- Review
- Rapid progression of probable Creutzfeldt-Jakob disease with concomitant COVID-19 infection.BMJ case reports · 2023Article
- Oxidative stress and COVID-19-associated neuronal dysfunction: mechanisms and therapeutic implications.Acta biochimica et biophysica Sinica · 2023Review
- miRNAs as a Potential Biomarker in the COVID-19 Infection and Complications Course, Severity, and Outcome.Diagnostics (Basel, Switzerland) · 2023Review
- Endogenous miRNA-Based Innate-Immunity against SARS-CoV-2 Invasion of the Brain.International journal of molecular sciences · 2023Review
- Article
- Updates on the Role of Probiotics against Different Health Issues: Focus onInternational journal of molecular sciences · 2022Review
- CGRP Plasma Levels Correlate with the Clinical Evolution and Prognosis of Hospitalized Acute COVID-19 Patients.Viruses · 2022Observational
- SARS-CoV-2 Invasion and Pathological Links to Prion Disease.Biomolecules · 2022Article
- SARS-CoV-2, long COVID, prion disease and neurodegeneration.Frontiers in neuroscience · 2022Article
- Type I interferon signaling in SARS-CoV-2 associated neurocognitive disorder (SAND): Mapping host-virus interactions to an etiopathogenesis.Frontiers in neurology · 2022Review
- SARS-CoV-2 Neuroinvasion, Inflammatory Neurodegeneration and Alzheimer's Disease.Frontiers in cellular neuroscience · 2022Article
- microRNA, the Innate-Immune System and SARS-CoV-2.Frontiers in cellular and infection microbiology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The novel coronavirus (2019-nCoVCOVID-19) belongs to the Beta coronavirus family, which contains MERS-CoV (Middle East respiratory syndrome coronavirus) and SARS-CoV (severe acute respiratory syndrome coronavirus). SARS-CoV-2 activates the innate immune system, thereby activating the inflammatory mechanism, causing the release of inflammatory cytokines. Moreover, it has been suggested that COVID-19 may penetrate the central nervous system, and release inflammatory cytokines in the brains, inducing neuroinflammation and neurodegeneration. Several links connect COVID-19 with Alzheimer's disease (AD), such as elevated oxidative stress, uncontrolled release of the inflammatory cytokines, and mitochondrial apoptosis. There are severe concerns that excessive immune cell activation in COVID-19 may aggravate the neurodegeneration and amyloid-beta pathology of AD. Here, we have collected the evidence, showing the links between the two diseases. The focus has been made to collect the information on the activation of the inflammation, its contributors, and shared therapeutic targets. Furthermore, we have given future perspectives, research gaps, and overlapping pathological bases of the two diseases. Lastly, we have given the short touch to the drugs that have equally shown rescuing effects against both diseases. Although there is limited information available regarding the exact links between COVID-19 and neuroinflammation, we have insight into the pathological contributors of the diseases. Based on the shared pathological features and therapeutic targets, we hypothesize that the activation of the immune system may induce neurological disorders by triggering oxidative stress and neuroinflammation.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.