Evidence map›Paper›PMID 27911303›Full record

ArticleJournal of Alzheimer's disease : JAD2017

Amylin Treatment Reduces Neuroinflammation and Ameliorates Abnormal Patterns of Gene Expression in the Cerebral Cortex of an Alzheimer's Disease Mouse Model.

Erming Wang, Haihao Zhu, Xiaofan Wang, Adam C Gower, Max Wallack, Jan Krzysztof Blusztajn, Neil Kowall, Wei Qiao Qiu

Open access · greenAbstract read
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 10% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Amylin: From Mode of Action to Future Clinical Potential in Diabetes and Obesity.Diabetes therapy : research, treatment and education of diabetes and related disorders · 2025
    Review
  5. Exploring the Role of Metabolic Hormones in Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2024
    Article
  6. Review
  7. Genome-wide methylomic regulation of multiscale gene networks in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023
    Article
  8. Article
  9. Multiple Sclerosis: Inflammatory and Neuroglial Aspects.Current issues in molecular biology · 2023
    Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Review
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 1 institution in 1 country.

Erming WangDepartment of Pharmacology and Experimental Therapeutics, Boston University School of Medicine, Boston, MA, USA.
Haihao ZhuDepartment of Pharmacology and Experimental Therapeutics, Boston University School of Medicine, Boston, MA, USA.
Xiaofan WangDepartment of Pharmacology and Experimental Therapeutics, Boston University School of Medicine, Boston, MA, USA.
Adam C GowerClinical and Translational Science Institute, Boston University School of Medicine, Boston, MA, USA.
Max WallackDepartment of Pharmacology and Experimental Therapeutics, Boston University School of Medicine, Boston, MA, USA.
Jan Krzysztof BlusztajnDepartment of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, MA, USA.
Neil KowallDepartment of Neurology, Boston University School of Medicine, Boston, MA, USA.
Wei Qiao QiuDepartment of Pharmacology and Experimental Therapeutics, Boston University School of Medicine, Boston, MA, USA.
Boston University · US

Funding

Boston University Clinical and Translational Science Institute - U ProgramU54TR001012 · NCATS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI CENTER, DAVID M. · 2014 to 2014
$3.9M
Plasma Amylin Impact on Cognitive Function and Brain Morphology in the Framingham Heart StudyR01AG049899 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI AU, RHODA, QIU, WEI QIAO WENDY · 2015 to 2019
$2.3M
BMP9 as a juvenile protective factor in cognitive agingR01AG045031 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI BLUSZTAJN, JAN KRZYSZTOF · 2014 to 2018
$1.8M
Midcareer Investigator Award in Amylin, Cognition, and Alzheimer's DiseaseK24AG050842 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI QIU, WEI QIAO WENDY · 2015 to 2019
$850k
Amylin as a Diagnostic Test and Potential Treatment for Alzheimers DiseaseR21AG045757 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI QIU, WEI QIAO WENDY · 2014 to 2015
$444k
NCATS NIH HHS U54 TR001012NIA NIH HHS K24 AG050842NIA NIH HHS R01 AG045031NIA NIH HHS R01 AG049899NIA NIH HHS R21 AG045757
6 · The paper itself

Abstract

Our recent study has demonstrated that peripheral amylin treatment reduces the amyloid pathology in the brain of Alzheimer's disease (AD) mouse models, and improves their learning and memory. We hypothesized that the beneficial effects of amylin for AD was beyond reducing the amyloids in the brain, and have now directly tested the actions of amylin on other aspects of AD pathogenesis, especially neuroinflammation. A 10-week course of peripheral amylin treatment significantly reduced levels of cerebral inflammation markers, Cd68 and Iba1, in amyloid precursor protein (APP) transgenic mice. Mechanistic studies indicated the protective effect of amylin required interaction with its cognate receptor because silencing the amylin receptor expression blocked the amylin effect on Cd68 in microglia. Using weighted gene co-expression network analysis, we discovered that amylin treatment influenced two gene modules linked with amyloid pathology: 1) a module related to proinflammation and transport/vesicle process that included a hub gene of Cd68, and 2) a module related to mitochondria function that included a hub gene of Atp5b. Amylin treatment restored the expression of most genes in the APP cortex toward levels observed in the wild-type (WT) cortex in these two modules including Cd68 and Atp5b. Using a human dataset, we found that the expression levels of Cd68 and Atp5b were significantly correlated with the neurofibrillary tangle burden in the AD brain and with their cognition. These data suggest that amylin acts on the pathological cascade in animal models of AD, and further supports the therapeutic potential of amylin-type peptides for AD.

Indexed as

EncephalitisAlzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsAntigens, CDAntigens, Differentiation, MyelomonocyticAnti-Inflammatory AgentsCalcium-Binding ProteinsCD68 MoleculeCell Line, TransformedCerebral CortexDisease Models, AnimalGene Expression RegulationHumansIslet Amyloid PolypeptideLipopolysaccharidesAif1 protein, mouseAmyloid beta-Protein PrecursorAntigens, CDAntigens, Differentiation, MyelomonocyticAnti-Inflammatory AgentsATP5b protein, mouseCalcium-Binding ProteinsCD68 antigen, humanCD68 MoleculeIslet Amyloid PolypeptideLipopolysaccharidesMicrofilament ProteinsMitochondrial Proton-Translocating ATPasesReceptors, Islet Amyloid PolypeptideAlzheimer’s diseaseamylinhub genetranscriptomeWGCNA

Identifiers

PMID27911303
PMCPMC5331853
OpenAlexW2557437925

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.