Evidence map›Paper›PMID 37843394›Full record

ReviewPhysiological reviews2024

Oxidative damage in neurodegeneration: roles in the pathogenesis and progression of Alzheimer disease.

Marzia Perluigi, Fabio Di Domenico, D Allan Butterfield

Open access · greenAbstract readReview
In one paragraph

Review in Physiological reviews, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 134 papers.

0numbers the graph read from it
0cells of the map it votes in
134citing papers in PubMed
56.8field-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

134 citing papers in PubMed, 196 citations in OpenAlex.

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  17. Is Ergothioneine an Important Source of Plasma TrimethylamineAntioxidants (Basel, Switzerland) · 2026
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74 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 2 countries.

Marzia PerluigiDepartment of Biochemical Sciences "A. Rossi Fanelli," Laboratory affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti, Sapienza University of Rome, Rome, Italy.
Fabio Di DomenicoDepartment of Biochemical Sciences "A. Rossi Fanelli," Laboratory affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti, Sapienza University of Rome, Rome, Italy.
D Allan ButterfieldDepartment of Chemistry and Sanders-Brown Center on Aging, University of Kentucky, Lexington, Kentucky, United States.ORCID 0000-0003-3254-5286
Istituto Pasteur · ITUniversity of Kentucky · US

Funding

APOE and the PPP: Glucose Metabolism and Oxidative Stress in Alzheimer's DiseaseR01AG060056 · NIA · UNIVERSITY OF KENTUCKY · PI JOHNSON, LANCE ALLEN · 2018 to 2022
$2.5M
NIA NIH HHS R01 AG060056
6 · The paper itself

Abstract

Alzheimer disease (AD) is associated with multiple etiologies and pathological mechanisms, among which oxidative stress (OS) appears as a major determinant. Intriguingly, OS arises in various pathways regulating brain functions, and it seems to link different hypotheses and mechanisms of AD neuropathology with high fidelity. The brain is particularly vulnerable to oxidative damage, mainly because of its unique lipid composition, resulting in an amplified cascade of redox reactions that target several cellular components/functions ultimately leading to neurodegeneration. The present review highlights the "OS hypothesis of AD," including amyloid beta-peptide-associated mechanisms, the role of lipid and protein oxidation unraveled by redox proteomics, and the antioxidant strategies that have been investigated to modulate the progression of AD. Collected studies from our groups and others have contributed to unraveling the close relationships between perturbation of redox homeostasis in the brain and AD neuropathology by elucidating redox-regulated events potentially involved in both the pathogenesis and progression of AD. However, the complexity of AD pathological mechanisms requires an in-depth understanding of several major intracellular pathways affecting redox homeostasis and relevant for brain functions. This understanding is crucial to developing pharmacological strategies targeting OS-mediated toxicity that may potentially contribute to slow AD progression as well as improve the quality of life of persons with this severe dementing disorder.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesHumansLipidsOxidation-ReductionOxidative StressQuality of LifeAmyloid beta-PeptidesLipidsAlzheimer disease and lipid peroxidation and protein oxidationAlzheimer disease and translational approachesAβ and oxidative damageDown syndrome and Alzheimer disease and oxidative stressoxidative stress and energy dysmetabolism

Identifiers

PMID37843394
PMCPMC11281823
OpenAlexW4387660906

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.