Evidence map›Paper›PMID 35257690›Full record

ReviewNeuropharmacology2022

Inflammation at the crossroads of COVID-19, cognitive deficits and depression.

Natalia M Lyra E Silva, Fernanda G Q Barros-Aragão, Fernanda G De Felice, Sergio T Ferreira

Open access · greenAbstract readReview
In one paragraph

Review in Neuropharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
11.4field-weighted citation impact, top 1% 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

50 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Neurodegenerative and Cognitive Consequences of Long COVID.International journal of molecular sciences · 2026
    Review
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  12. Sex differences in the central and peripheral omega 3 oxylipin response to acute systemic inflammation.American journal of physiology. Regulatory, integrative and comparative physiology · 2025
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  14. 5-HTJournal of advanced research · 2025
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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

4 authors at 3 institutions in 3 countries.

Natalia M Lyra E SilvaCentre for Neuroscience Studies, Department of Biomedical and Molecular Sciences, Queen's University, Kingston, ON, Canada; Department of Psychiatry, Queen's University, Kingston, ON, Canada. Electronic address: ndml@queensu.ca.
Fernanda G Q Barros-AragãoD'OR Institute for Research & Education, RJ, Brazil; Institute of Medical Biochemistry Leopoldo de Meis, Federal University of Rio de Janeiro, RJ, Brazil. Electronic address: fernanda.aragao@idor.org.
Fernanda G De FeliceCentre for Neuroscience Studies, Department of Biomedical and Molecular Sciences, Queen's University, Kingston, ON, Canada; Department of Psychiatry, Queen's University, Kingston, ON, Canada; D'OR Institute for Research & Education, RJ, Brazil; Institute of Medical Biochemistry Leopoldo de Meis, Federal University of Rio de Janeiro, RJ, Brazil.
Sergio T FerreiraD'OR Institute for Research & Education, RJ, Brazil; Institute of Medical Biochemistry Leopoldo de Meis, Federal University of Rio de Janeiro, RJ, Brazil; Institute of Biophysics Carlos Chagas Filho, Federal University of Rio de Janeiro, RJ, Brazil.
Queen's University · CACzech Academy of Sciences, Institute of Biophysics · CZD’Or Institute for Research and Education · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute neurological alterations have been associated with SARS-CoV-2 infection. Additionally, it is becoming clear that coronavirus disease 2019 (COVID-19) survivors may experience long-term neurological abnormalities, including cognitive deficits and mood alterations. The mechanisms underlying acute and long-term impacts of COVID-19 in the brain are being actively investigated. Due to the heterogeneous manifestations of neurological outcomes, it is possible that different mechanisms operate following SARS-CoV-2 infection, which may include direct brain infection by SARS-CoV-2, mechanisms resulting from hyperinflammatory systemic disease, or a combination of both. Inflammation is a core feature of COVID-19, and both central and systemic inflammation are known to lead to acute and persistent neurological alterations in other diseases. Here, we review evidence indicating that COVID-19 is associated with neuroinflammation, along with blood-brain barrier dysfunction. Similar neuroinflammatory signatures have been associated with Alzheimer's disease and major depressive disorder. Current evidence demonstrates that patients with pre-existing cognitive and neuropsychiatric deficits show worse outcomes upon infection by SARS-CoV-2 and, conversely, COVID-19 survivors may be at increased risk of developing dementia and mood disorders. Considering the high prevalence of COVID-19 patients that recovered from infection in the world and the alarming projections for the prevalence of dementia and depression, investigation of possible molecular similarities between those diseases may shed light on mechanisms leading to long-term neurological abnormalities in COVID-19 survivors.

Indexed as

AffectBlood-Brain BarrierCognitive DysfunctionCOVID-19DepressionHumansInflammationNeuroinflammatory DiseasesSARS-CoV-2Virus DiseasesBlood-brain barrierCytokineMemoryMood disordersNeuro-infectious diseasesSARS-CoV-2

Identifiers

PMID35257690
PMCPMC8894741
OpenAlexW4214895349

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.