Evidence map›Paper›PMID 39456461›Full record

ReviewAntioxidants (Basel, Switzerland)2024

The Dual Role of Amyloid Beta-Peptide in Oxidative Stress and Inflammation: Unveiling Their Connections in Alzheimer's Disease Etiopathology.

Hugo Fanlo-Ucar, Pol Picón-Pagès, Víctor Herrera-Fernández, Gerard Ill-Raga, Francisco J Muñoz

Abstract readReview
In one paragraph

Review in Antioxidants (Basel, Switzerland), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

48 citing papers in PubMed, 1 synthesis or guideline pooled it.

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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.

Hugo Fanlo-UcarLaboratory of Molecular Physiology, Department of Medicine and Life Sciences, Faculty of Medicine and Life Sciences, Universitat Pompeu Fabra, 08003 Barcelona, Spain.ORCID 0000-0001-7420-6501
Pol Picón-PagèsLaboratory of Molecular Physiology, Department of Medicine and Life Sciences, Faculty of Medicine and Life Sciences, Universitat Pompeu Fabra, 08003 Barcelona, Spain.ORCID 0000-0002-6471-3072
Víctor Herrera-FernándezLaboratory of Molecular Physiology, Department of Medicine and Life Sciences, Faculty of Medicine and Life Sciences, Universitat Pompeu Fabra, 08003 Barcelona, Spain.ORCID 0000-0001-8895-5765
Gerard Ill-RagaLaboratory of Molecular Physiology, Department of Medicine and Life Sciences, Faculty of Medicine and Life Sciences, Universitat Pompeu Fabra, 08003 Barcelona, Spain.ORCID 0000-0002-0898-5356
Francisco J MuñozLaboratory of Molecular Physiology, Department of Medicine and Life Sciences, Faculty of Medicine and Life Sciences, Universitat Pompeu Fabra, 08003 Barcelona, Spain.ORCID 0000-0002-1343-3599

Funding

Ministerio de Ciencia, Innovación y Universidades (Spain) PID2020-117691RB-I00/AEI/10.13039/501100011033
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disease, and it is currently the seventh leading cause of death worldwide. It is characterized by the extracellular aggregation of the amyloid β-peptide (Aβ) into oligomers and fibrils that cause synaptotoxicity and neuronal death. Aβ exhibits a dual role in promoting oxidative stress and inflammation. This review aims to unravel the intricate connection between these processes and their contribution to AD progression. The review delves into oxidative stress in AD, focusing on the involvement of metals, mitochondrial dysfunction, and biomolecule oxidation. The distinct yet overlapping concept of nitro-oxidative stress is also discussed, detailing the roles of nitric oxide, mitochondrial perturbations, and their cumulative impact on Aβ production and neurotoxicity. Inflammation is examined through astroglia and microglia function, elucidating their response to Aβ and their contribution to oxidative stress within the AD brain. The blood-brain barrier and oligodendrocytes are also considered in the context of AD pathophysiology. We also review current diagnostic methodologies and emerging therapeutic strategies aimed at mitigating oxidative stress and inflammation, thereby offering potential treatments for halting or slowing AD progression. This comprehensive synthesis underscores the pivotal role of Aβ in bridging oxidative stress and inflammation, advancing our understanding of AD and informing future research and treatment paradigms.

Indexed as

Alzheimer’s diseaseamyloid β-peptideBACE1neurodegenerationnitro-oxidative stress

Identifiers

PMID39456461
PMCPMC11505517

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.