Evidence map›Paper›PMID 28522792›Full record

ArticleAging2017

Transgenic autoinhibition of p21-activated kinase exacerbates synaptic impairments and fronto-dependent behavioral deficits in an animal model of Alzheimer's disease.

Cyril Bories, Dany Arsenault, Myriam Lemire, Cyntia Tremblay, Yves De Koninck, Frédéric Calon

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

Article in Aging, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. PAK1 inhibitor NVS-PAK1-1 preserves dendritic spines in amyloid/tau exposed neurons and 5xFAD mice.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
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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

6 authors at 3 institutions in 1 country.

Cyril BoriesResearch Center of Institut Universitaire en Santé Mentale de Québec, Quebec City, QC, Canada.
Dany ArsenaultFaculty of Pharmacy Laval University, Quebec City, QC, Canada.
Myriam LemireResearch Center of Institut Universitaire en Santé Mentale de Québec, Quebec City, QC, Canada.
Cyntia TremblayFaculty of Pharmacy Laval University, Quebec City, QC, Canada.
Yves De KoninckResearch Center of Institut Universitaire en Santé Mentale de Québec, Quebec City, QC, Canada.
Frédéric CalonFaculty of Pharmacy Laval University, Quebec City, QC, Canada.
Institut Universitaire en Santé Mentale de Québec · CACentre hospitalier de l'Université Laval · CAUniversité Laval · CA

Funding

CIHR MOP102532
6 · The paper itself

Abstract

Defects in p21-activated kinase (PAK) lead to dendritic spine abnormalities and are sufficient to cause cognition impairment. The decrease in PAK in the brain of Alzheimer's disease (AD) patients is suspected to underlie synaptic and dendritic disturbances associated with its clinical expression, particularly with symptoms related to frontal cortex dysfunction. To investigate the role of PAK combined with Aβ and tau pathologies (3xTg-AD mice) in the frontal cortex, we generated a transgenic model of AD with a deficit in PAK activity (3xTg-AD-dnPAK mice). PAK inactivation had no effect on Aβ40 and Aβ42 levels, but increased the phosphorylation ratio of tau in detergent-insoluble protein fractions in the frontal cortex of 18-month-old heterozygous 3xTg-AD mice. Morphometric analyses of layer II/III pyramidal neurons in the frontal cortex showed that 3xTg-AD-dnPAK neurons exhibited significant dendritic attrition, lower spine density and longer spines compared to NonTg and 3xTg-AD mice. Finally, behavioral assessments revealed that 3xTg-AD-dnPAK mice exhibited pronounced anxious traits and disturbances in social behaviors, reminiscent of fronto-dependent symptoms observed in AD. Our results substantiate a critical role for PAK in the genesis of neuronal abnormalities in the frontal cortex underlying the emergence of psychiatric-like symptoms in AD.

Indexed as

Behavior, AnimalAlzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsAnxietyCalcium-Calmodulin-Dependent Protein Kinase Type 2Disease Models, AnimalExploratory BehaviorFrontal LobeGenetic Predisposition to DiseaseInterpersonal RelationsLocomotionMice, 129 StrainMice, Inbred C57BLMice, TransgenicAmyloid beta-Peptidesamyloid beta-protein (1-40)amyloid beta-protein (1-42)Amyloid beta-Protein PrecursorCalcium-Calmodulin-Dependent Protein Kinase Type 2Camk2a protein, mousep21-Activated KinasesPeptide FragmentsPresenilin-1tau Proteins3xTg-AD miceAlzheimerelectrophysiologyfrontal cortexmorphologyp21-activated kinase

Identifiers

PMID28522792
PMCPMC5472739
OpenAlexW2616592117

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.