Evidence map›Paper›PMID 24698766›Full record

ArticleNeurobiology of aging2014

Altered neurotransmission in the lateral amygdala in aged human apoE4 targeted replacement mice.

Rebecca C Klein, Shawn K Acheson, Brian E Mace, Patrick M Sullivan, Scott D Moore

Open access · greenAbstract read
In one paragraph

Article in Neurobiology of aging, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

20 citing papers in PubMed, 31 citations in OpenAlex.

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  4. Modeling neurodegenerative and neurodevelopmental disorders in theLearning & memory (Cold Spring Harbor, N.Y.) · 2024
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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

5 authors at 4 institutions in 1 country.

Rebecca C KleinDepartment of Psychiatry, Duke University Medical Center, Durham, NC, USA; MIRECC, Durham Veterans Affairs Medical Center, Durham, NC, USA.
Shawn K AchesonDepartment of Psychiatry, Duke University Medical Center, Durham, NC, USA; Neurobiology Research Lab, Durham Veterans Affairs Medical Center, Durham, NC, USA.
Brian E MaceGRECC, Durham Veterans Affairs Medical Center, Durham, NC, USA; Department of Medicine (Geriatrics), Duke University Medical Center, Durham, NC, USA.
Patrick M SullivanGRECC, Durham Veterans Affairs Medical Center, Durham, NC, USA; Department of Medicine (Geriatrics), Duke University Medical Center, Durham, NC, USA.
Scott D MooreDepartment of Psychiatry, Duke University Medical Center, Durham, NC, USA; MIRECC, Durham Veterans Affairs Medical Center, Durham, NC, USA. Electronic address: sdmoore@duke.edu.
Durham VA Medical Center · USDuke Medical Center · USGeriatric Research Education and Clinical Center · USMental Illness Research, Education and Clinical Centers · US

Funding

APOE4 and Loss of Synaptic IntegrityR01AG025975 · NIA · DUKE UNIVERSITY · PI SULLIVAN, PATRICK M · 2006 to 2009
$860k
Ethanol actions on ion channels in the extended amygdalaU01AA020938 · NIAAA · DUKE UNIVERSITY · PI MOORE, SCOTT D. · 2011 to 2015
$625k
Mechanisms underlying neuropeptide release in the extended amygdalaI01BX001271 · VA · DURHAM VA MEDICAL CENTER · PI MOORE, SCOTT D. · 2013 to 2020
–
Novel Prophylactic Pharmacotherapy in an Animal Model of Closed Head InjuryIK2BX001267 · VA · DURHAM VA MEDICAL CENTER · PI ACHESON, SHAWN · 2012 to 2016
–
BLRD VA I01 BX001271BLRD VA IK2 BX001267NIAAA NIH HHS U01 AA020938NIA NIH HHS R01 AG025975NIA NIH HHS R01 AG025975-01
6 · The paper itself

Abstract

The human APOE4 allele is associated with an early age of onset and increased risk of Alzheimer's disease (AD). Apolipoprotein E is secreted as part of a high-density lipoprotein-like particle by glial cells in the brain for the primary purpose of transport of lipophilic compounds involved in the maintenance of synapses. Previous studies examining synaptic integrity in the amygdala of human apoE targeted replacement (TR) mice showed a decrease in spontaneous excitatory synaptic activity, dendritic arbor, and spine density associated with apoE4 compared with apoE3 and apoE2 in adult male mice. In the present study, we assessed how APOE genotype affects synaptic integrity of amygdala neurons by comparing electrophysiological and morphometric properties in human apoE3, E4, and E2/4 TR mice at the age of 18-20 months. In contrast to adult mice, we found that aged apoE4 TR mice exhibited the highest level of excitatory synaptic activity compared with other cohorts. Additionally, apoE4 mice had significantly greater spontaneous inhibitory activity than all other cohorts. Taken together, there was a significant interaction between genotypes when comparing inhibition relative to excitation; there was a simple main effect of frequency type with an imbalance toward inhibition in apoE4 mice but not in apoE3 or apoE2/4 mice. These results suggest that apoE isoforms differentially influence synaptic transmission throughout the life span, where aging coupled with apoE4 expression, results in an imbalance in maintaining integrity of synaptic transmission.

Indexed as

AllelesGenotypeAlzheimer DiseaseAmygdalaAnimalsApolipoprotein E4Electrophysiological PhenomenaHumansMaleMice, TransgenicNeuronsRiskSynaptic TransmissionApolipoprotein E4Alzheimer's dementiaAmygdalaApolipoprotein ESynaptic

Identifiers

PMID24698766
PMCPMC4248786
OpenAlexW2012994438

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.