Evidence map›Paper›PMID 26759481›Full record

ArticleCerebral cortex (New York, N.Y. : 1991)2017

Intraneuronal Amyloid Beta Accumulation Disrupts Hippocampal CRTC1-Dependent Gene Expression and Cognitive Function in a Rat Model of Alzheimer Disease.

Edward N Wilson, Andrew R Abela, Sonia Do Carmo, Simon Allard, Adam R Marks, Lindsay A Welikovitch, Adriana Ducatenzeiler, Yogita Chudasama, A Claudio Cuello

Open access · bronzeAbstract read
In one paragraph

Article in Cerebral cortex (New York, N.Y. : 1991), 2017. 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
4.9field-weighted citation impact, top 5% 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, 55 citations in OpenAlex.

  1. Review
  2. Article
  3. S-Nitrosylation of CRTC1 in Alzheimer's disease impairs CREB-dependent gene expression induced by neuronal activity.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  9. Review
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  11. Aminothioneine, a product derived from golden oyster mushrooms (Biochemistry and biophysics reports · 2021
    Article
  12. Frontiers in pharmacology · 2021
    Article
  13. Article
  14. Article
  15. Article
  16. Early intraneuronal amyloid triggers neuron-derived inflammatory signaling in APP transgenic rats and human brain.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  17. Article
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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 1 institution in 2 countries.

Edward N WilsonDepartment of Pharmacology and Therapeutics, McGill University, Montreal, QCCanadaH3G 1Y6.
Andrew R AbelaDepartment of Psychology, McGill University, Montreal, QCCanadaH3A 1B1.
Sonia Do CarmoDepartment of Pharmacology and Therapeutics, McGill University, Montreal, QCCanadaH3G 1Y6.
Simon AllardDepartment of Pharmacology and Therapeutics, McGill University, Montreal, QCCanadaH3G 1Y6.
Adam R MarksDepartment of Pharmacology and Therapeutics, McGill University, Montreal, QCCanadaH3G 1Y6.
Lindsay A WelikovitchDepartment of Pharmacology and Therapeutics, McGill University, Montreal, QCCanadaH3G 1Y6.
Adriana DucatenzeilerDepartment of Pharmacology and Therapeutics, McGill University, Montreal, QCCanadaH3G 1Y6.
Yogita ChudasamaDepartment of Psychology, McGill University, Montreal, QC Canada H3A 1B1.
A Claudio CuelloDepartment of Pharmacology and Therapeutics, McGill University, Montreal, QC Canada H3G 1Y6.
McGill University · CA

Funding

Neural Circuits Underlying the Control of Executive and Emotional BehaviorZIAMH002951 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI CHUDASAMA, YOGITA · 2016 to 2025
$17.5M
CIHR 102507-1
6 · The paper itself

Abstract

In Alzheimer disease (AD), the accumulation of amyloid beta (Aβ) begins decades before cognitive symptoms and progresses from intraneuronal material to extracellular plaques. To date, however, the precise mechanism by which the early buildup of Aβ peptides leads to cognitive dysfunction remains unknown. Here, we investigate the impact of the early Aβ accumulation on temporal and frontal lobe dysfunction. We compared the performance of McGill-R-Thy1-APP transgenic AD rats with wild-type littermate controls on a visual discrimination task using a touchscreen operant platform. Subsequently, we conducted studies to establish the biochemical and molecular basis for the behavioral alterations. It was found that the presence of intraneuronal Aβ caused a severe associative learning deficit in the AD rats. This coincided with reduced nuclear translocation and genomic occupancy of the CREB co-activator, CRTC1, and decreased production of synaptic plasticity-associated transcripts Arc, c-fos, Egr1, and Bdnf. Thus, blockade of CRTC1-dependent gene expression in the early, preplaque phase of AD-like pathology provides a molecular basis for the cognitive deficits that figure so prominently in early AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsCognitionDisease Models, AnimalFemaleHippocampusInterneuronsMaleNeuronal PlasticityNeuronsRats, TransgenicTranscription FactorsAmyloid beta-PeptidesAmyloid beta-Protein PrecursorCrtc1 protein, ratTranscription FactorsAlzheimer diseaseamyloid betaCRTC1learning and memorytouchscreen operant platform

Identifiers

PMID26759481
PMCPMC5378482
OpenAlexW2310987806

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.