Evidence map›Paper›PMID 30334443›Full record

ReviewMinerva medica2019

Evaluating the link between Paraoxonase-1 levels and Alzheimer's disease development.

Carlo Cervellati, Giuseppe Valacchi, Veronica Tisato, Giovanni Zuliani, Judit Marsillach

Open access · greenAbstract readReview
In one paragraph

Review in Minerva medica, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.8field-weighted citation impact, top 11% 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

29 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Homocysteine Thiolactone Detoxifying Enzymes and Alzheimer's Disease.International journal of molecular sciences · 2024
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Frontier on Alzheimer's Disease.International journal of molecular sciences · 2023
    Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Review
  20. Article
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 at 2 institutions in 2 countries.

Carlo CervellatiDepartment of Biomedical and Specialist Surgical Sciences, University of Ferrara, Ferrara, Italy - crvcrl@unife.it.
Giuseppe ValacchiPlants for Human Health Institute, Department of Animal Sciences, NC Research Campus, North Carolina State University, Kannapolis, NC, USA.
Veronica TisatoDepartment of Morphology, Surgery and Experimental Medicine and LTTA Center, University of Ferrara, Ferrara, Italy.
Giovanni ZulianiDepartment of Morphology, Surgery and Experimental Medicine and LTTA Center, University of Ferrara, Ferrara, Italy.
Judit MarsillachDivision of Medical Genetics, Department of Medicine, University of Washington, Seattle, WA, USA.
University of Ferrara · ITUniversity of Washington Medical Center · US

Funding

Transform Dissemination and Implementation Science in CTSA ProgramsUL1TR002319 · NCATS · UNIVERSITY OF WASHINGTON · PI John K. Amory · 2017 to 2026
$100.0M
NCATS NIH HHS UL1 TR002319
6 · The paper itself

Abstract

At present, the etiopathogenesis of Alzheimer's disease (AD), the most common form of dementia, remains far to be fully deciphered. In the recent years, also the centrality of amyloid-β peptide in the pathogenesis of the neurodegenerative disease has been questioned and other hypotheses have been advanced. Notably, a common denominator of many of these theoretical models is represented by oxidative stress, which is widely proposed to play a role in the disease initiation and/or progression. Paraoxonase 1 (PON1) is a high-density lipoprotein (HDL)-associated enzyme that endows its carrier with multiple biological functions, including the ability to contrast oxidative damage to lipid components of lipoproteins and cells and protect from toxicity of specific organophosphorus pesticides. The peculiar multi-functionality nature of PON1 might be the key for explaining the vast epidemiological data showing a close association between low serum PON1 activity and risk of several diseases, including cardiovascular and neurodegenerative diseases, in particular AD. In this review, we discuss the possible link between PON1 with AD pathogenesis and we hypothesize eventual mechanistic pathways that could account from epidemiological observations. We also highlight the methodological issue limitation in PON1 studies that still impede to give a definitive and certain picture of its effective biological impact on human health including AD.

Indexed as

Alzheimer DiseaseAryldialkylphosphataseHumansAryldialkylphosphatase

Identifiers

PMID30334443
PMCPMC7451062
OpenAlexW2938719029

What OpenQuestion holds

Textmetadata
LicenceTDM
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.