Evidence map›Paper›PMID 29804228›Full record

ArticleMolecular neurobiology2019

Impaired Wnt Signaling in the Prefrontal Cortex of Alzheimer's Disease.

Jonas Folke, Bente Pakkenberg, Tomasz Brudek

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
–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

81 citing papers in PubMed.

  1. Review
  2. Mapping cross-domain drivers of Alzheimer's disease risk through integrated network analysis.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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  15. Selection signatures detection in Nelore, Gir, and Red Sindhi cattle breeds.Mammalian genome : official journal of the International Mammalian Genome Society · 2025
    Article
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  17. Review
  18. Review
  19. Article
  20. Review

21 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.

Jonas FolkeResearch Laboratory for Stereology and Neuroscience, Bispebjerg-Frederiksberg Hospital, University Hospital of Copenhagen, Nielsine Nielsens Vej 6B, Building 11B, 2nd floor, DK-2400, Copenhagen, Denmark. Jonas.folke@regionh.dk.ORCID http://orcid.org/0000-0002-0940-3098
Bente PakkenbergResearch Laboratory for Stereology and Neuroscience, Bispebjerg-Frederiksberg Hospital, University Hospital of Copenhagen, Nielsine Nielsens Vej 6B, Building 11B, 2nd floor, DK-2400, Copenhagen, Denmark.
Tomasz BrudekResearch Laboratory for Stereology and Neuroscience, Bispebjerg-Frederiksberg Hospital, University Hospital of Copenhagen, Nielsine Nielsens Vej 6B, Building 11B, 2nd floor, DK-2400, Copenhagen, Denmark.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Wnt pathway is involved in synaptic plasticity and neuronal survival, and alterations in Wnt signaling have previously been reported both in aging and neurodegenerative diseases, including Alzheimer's disease (AD). This study sought to evaluate Wnt signaling pathway interplay integrity across prefrontal lobe structures in AD patients compared to normal aging. Using the open-access BrainCloud™ database, 84 gene expression profiles and clustering effect were analyzed in the dorsomedial prefrontal cortex (PFC) across a time span of 21-78 years of age. Next, expression levels of the selected genes were investigated in post-mortem brain tissue from 30 AD patients and 30 age-matched controls in three interdependent brain areas of the PFC. Results were assessed in relation to Braak stage and cognitive impairment of the patients. We found a general age-related factor in Wnt pathway genes with a group of genes being closely interrelated in their expression across the time span investigated in healthy individuals. This interrelation was altered in the AD brains studied, as several genes presented aberrant transcription, even though not always being altered at protein levels. Noteworthy, beta(β)-catenin and glycogen synthase kinase 3-beta (GSK3β) showed a dynamic switch in protein levels and activity, especially in the orbitofrontal cortex and the medial frontal gyrus. A significant decrease in β-catenin protein levels were inversely associated with increased GSK3β tyrosine activating phosphorylation, in addition to downstream effects associated with disease progression and cognitive decline. This study is the first that comprehensively evaluates Wnt signaling pathway in the prefrontal cortical lobe structures of AD brains, in relation to age-related coordinated Wnt signaling changes. Our findings further support that increased kinase activity of GSK3β is associated with AD pathology in the PFC.

Indexed as

AgedAged, 80 and overAlzheimer DiseaseAmyloid beta-Peptidesbeta CateninFemaleGlycogen Synthase Kinase 3 betaHumansMaleMiddle AgedNeuronal PlasticityPhosphorylationPrefrontal CortexProteolysisWnt Signaling PathwayAmyloid beta-Peptidesbeta CateninCTNNB1 protein, humanGlycogen Synthase Kinase 3 betaAlzheimer’s diseaseBeta-cateninBraak stagingBrainCloud™Glycogen synthase kinase 3-betaWnt signaling pathway

Identifiers

PMID29804228

What OpenQuestion holds

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Registered trials

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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.