Evidence map›Paper›PMID 34589750›Full record

ReviewBrain, behavior, & immunity - health2021

The role of oxidative stress in HIV-associated neurocognitive disorders.

Sarah Buckley, Sarah Byrnes, Catherine Cochrane, Michael Roche, Jacob D Estes, Stavros Selemidis, Thomas A Angelovich, Melissa J Churchill

Open access · goldAbstract readReview
In one paragraph

Review in Brain, behavior, & immunity - health, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

44 citing papers in PubMed, 53 citations in OpenAlex.

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  20. Single-cell analysis of CD14Frontiers in immunology · 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

8 authors at 4 institutions in 2 countries.

Sarah BuckleyChronic Infectious and Inflammatory Diseases Program, School of Health and Biomedical Sciences, RMIT University, Melbourne, Australia.
Sarah ByrnesChronic Infectious and Inflammatory Diseases Program, School of Health and Biomedical Sciences, RMIT University, Melbourne, Australia.
Catherine CochraneChronic Infectious and Inflammatory Diseases Program, School of Health and Biomedical Sciences, RMIT University, Melbourne, Australia.
Michael RocheChronic Infectious and Inflammatory Diseases Program, School of Health and Biomedical Sciences, RMIT University, Melbourne, Australia.
Jacob D EstesChronic Infectious and Inflammatory Diseases Program, School of Health and Biomedical Sciences, RMIT University, Melbourne, Australia.
Stavros SelemidisChronic Infectious and Inflammatory Diseases Program, School of Health and Biomedical Sciences, RMIT University, Melbourne, Australia.
Thomas A AngelovichChronic Infectious and Inflammatory Diseases Program, School of Health and Biomedical Sciences, RMIT University, Melbourne, Australia.
Melissa J ChurchillChronic Infectious and Inflammatory Diseases Program, School of Health and Biomedical Sciences, RMIT University, Melbourne, Australia.
RMIT University · AUBurnet Institute · AUOregon National Primate Research Center · USThe Royal Melbourne Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

HIV-associated neurocognitive disorders (HAND) are a leading cause of morbidity in up to 50% of individuals living with HIV, despite effective treatment with antiretroviral therapy (ART). Current evidence suggests that chronic inflammation associated with HIV is especially attributed to the dysregulated production of reactive oxygen species (ROS) that contribute to neurodegeneration and poor clinical outcomes. While ROS have beneficial effects in eliciting immune responses to infection, chronic ROS production causes damage to macromolecules such as DNA and lipids that has been linked to altered redox homeostasis associated with antioxidant dysregulation. As a result, this disruption in the balance between antioxidant-dependent mechanisms of ROS inactivation and ROS production by enzymes such as the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase family, as well as from the electron transport chain of the mitochondria can result in oxidative stress. This is particularly relevant to the brain, which is exquisitely susceptible to oxidative stress due to its inherently high lipid concentration and ROS levels that have been linked to many neurodegenerative diseases that have similar stages of pathogenesis to HAND. In this review, we discuss the possible role and mechanisms of ROS production leading to oxidative stress that underpin HAND pathogenesis even when HIV is suppressed by current gold-standard antiretroviral therapies. Furthermore, we highlight that pathological ROS can serve as biomarkers for HIV-dependent HAND, and how manipulation of oxidative stress and antioxidant-dependent pathways may facilitate novel strategies for HIV cure.

Indexed as

ARTHANDHIVNeurodegenerationOxidative stressROS

Identifiers

PMID34589750
PMCPMC8474476
OpenAlexW3133541806

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.