Evidence map›Paper›PMID 39543985›Full record

ArticleJournal of Alzheimer's disease : JAD2024

Sexual dimorphism, altered hippocampal glutamatergic neurotransmission, and cognitive impairment in APP knock-in mice.

Caleigh A Findley, Samuel A McFadden, Tiarra Hill, Mackenzie R Peck, Kathleen Quinn, Kevin N Hascup, Erin R Hascup

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Lifespan of male and female APP/PS1 and APPJournal of Alzheimer's disease : JAD · 2025
    Article
  3. Lifespan of male and female APP/PS1 and APPbioRxiv : the preprint server for biology · 2024
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors.

Caleigh A FindleyNeuroscience Institute, Dale and Deborah Smith Center for Alzheimer's Research and Treatment, Departments of Neurology, Southern Illinois University School of Medicine, Springfield, IL, USA.
Samuel A McFaddenNeuroscience Institute, Dale and Deborah Smith Center for Alzheimer's Research and Treatment, Departments of Neurology, Southern Illinois University School of Medicine, Springfield, IL, USA.
Tiarra HillNeuroscience Institute, Dale and Deborah Smith Center for Alzheimer's Research and Treatment, Departments of Neurology, Southern Illinois University School of Medicine, Springfield, IL, USA.
Mackenzie R PeckNeuroscience Institute, Dale and Deborah Smith Center for Alzheimer's Research and Treatment, Departments of Neurology, Southern Illinois University School of Medicine, Springfield, IL, USA.
Kathleen QuinnNeuroscience Institute, Dale and Deborah Smith Center for Alzheimer's Research and Treatment, Departments of Neurology, Southern Illinois University School of Medicine, Springfield, IL, USA.
Kevin N HascupNeuroscience Institute, Dale and Deborah Smith Center for Alzheimer's Research and Treatment, Departments of Neurology, Southern Illinois University School of Medicine, Springfield, IL, USA.
Erin R HascupNeuroscience Institute, Dale and Deborah Smith Center for Alzheimer's Research and Treatment, Departments of Neurology, Southern Illinois University School of Medicine, Springfield, IL, USA.ORCID 0000-0003-1037-0809

Funding

NIA NIH HHS R01 AG057767NIA NIH HHS R01 AG061937
6 · The paper itself

Abstract

backgroundIt is well established that glutamatergic neurotransmission plays an essential role in learning and memory. Previous studies indicate that glutamate dynamics shift with Alzheimer's disease (AD) progression, contributing to negative cognitive outcomes.

objectiveIn this study, we characterized hippocampal glutamatergic signaling with age and disease progression in a knock-in mouse model of AD (APP

methodsAt 2-4 and 18+ months old, male and female APP

resultsGlutamate recordings support elevated stimulus-evoked glutamate release in the DG and CA3 of young APP

conclusionsThese findings confirm a sex-dependent hyper-to-hypoactivation glutamatergic paradigm in APP

Indexed as

Amyloid beta-Protein PrecursorCognitive DysfunctionGene Knock-In TechniquesGlutamic AcidHippocampusMice, Inbred C57BLMice, TransgenicSex CharacteristicsSynaptic TransmissionAlzheimer DiseaseAnimalsDisease Models, AnimalFemaleMaleMaze LearningMiceAmyloid beta-Protein PrecursorGlutamic AcidAlzheimer's diseaseamyloid-βcognitionglutamatelearningmemorysex differences

Identifiers

PMID39543985
PMCPMC11639043

What Socratic 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 Socratic graph.