Evidence map›Paper›PMID 30958347›Full record

ArticleJournal of Alzheimer's disease : JAD2019

Neuroprotective Effects of the Amylin Analog, Pramlintide, on Alzheimer's Disease Are Associated with Oxidative Stress Regulation Mechanisms.

Sarah Patrick, Rachel Corrigan, John Grizzanti, Megan Mey, Jeff Blair, Merce Pallas, Antonio Camins, Hyoung-Gon Lee, Gemma Casadesus

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 22% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Mechanism of Metal Complexes in Alzheimer's Disease.International journal of molecular sciences · 2024
    Review
  4. Review
  5. Exploring the Role of Metabolic Hormones in Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2024
    Article
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  7. Article
  8. Review
  9. Review
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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

9 authors at 3 institutions in 2 countries.

Sarah PatrickSchool of Biomedical Sciences, Kent State University, Kent, OH, USA.
Rachel CorriganSchool of Biomedical Sciences, Kent State University, Kent, OH, USA.
John GrizzantiSchool of Biomedical Sciences, Kent State University, Kent, OH, USA.
Megan MeySchool of Biomedical Sciences, Kent State University, Kent, OH, USA.
Jeff BlairSchool of Biomedical Sciences, Kent State University, Kent, OH, USA.
Merce PallasFacultat de Farmacia, Universitat de Barcelona, Barcelona, Spain.
Antonio CaminsFacultat de Farmacia, Universitat de Barcelona, Barcelona, Spain.
Hyoung-Gon LeeDepartment of Biology, The University of Texas San Antonio, San Antonio, TX, USA.
Gemma CasadesusSchool of Biomedical Sciences, Kent State University, Kent, OH, USA.
Kent State University · USUniversitat de Barcelona · ESThe University of Texas at San Antonio · US

Funding

Mechanisms of Metabolic Hormone Amylin Action on Alzheimer's Disease PathogenesisR15AG050292 · NIA · KENT STATE UNIVERSITY · PI CASADESUS, GEMMA · 2016 to 2016
$444k
NIA NIH HHS R15 AG050292
6 · The paper itself

Abstract

Administration of the recombinant analog of the pancreatic amyloid amylin, Pramlintide, has shown therapeutic benefits in aging and Alzheimer's disease (AD) models, both on cognition and amyloid-β (Aβ) pathology. However, the neuroprotective mechanisms underlying the benefits of Pramlintide remain unclear. Given the early and critical role of oxidative stress in AD pathogenesis and the known reactive oxygen species (ROS) modulating function of amyloids, we sought to determine whether Pramlintide's neuroprotective effects involve regulation of oxidative stress mechanisms. To address this, we treated APP/PS1 transgenic mice with Pramlintide for 3 months, starting at 5.5 months prior to widespread AD pathology onset, and measured cognition (Morris Water Maze), AD pathology, and oxidative stress-related markers and enzymes in vivo. In vitro, we determined the ability of Pramlintide to modulate H2O2-induced oxidative stress levels. Our data show that Pramlintide improved cognitive function, altered amyloid-processing enzymes, reduced plaque burden in the hippocampus, and regulated endogenous antioxidant enzymes (MnSOD and GPx1) and the stress marker HO-1 in a location specific manner. In vitro, Pramlintide treatment in neuronal models reduced H2O2-induced endogenous ROS production and lipid peroxidation in a dose-dependent manner. Together, these results indicate that Pramlintide's benefits on cognitive function and pathology may involve antioxidant-like properties of this compound.

Indexed as

Alzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsDisease Models, AnimalIslet Amyloid PolypeptideMaleMaze LearningMiceMice, TransgenicNeuronsNeuroprotective AgentsOxidative StressPresenilin-1Ubiquitin-Protein LigasesAmyloid beta-Protein PrecursorIslet Amyloid PolypeptideNeuroprotective AgentspramlintidePresenilin-1Rbck1 protein, mouseUbiquitin-Protein LigasesAlzheimer’s diseaseamylinmetabolismneuroprotectionoxidative stresspramlintide

Identifiers

PMID30958347
PMCPMC6584632
OpenAlexW2927733829

What OpenQuestion holds

Textmetadata
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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.