Evidence map›Paper›PMID 28057414›Full record

ReviewTrends in endocrinology and metabolism: TEM2017

ApoE, ApoE Receptors, and the Synapse in Alzheimer's Disease.

Courtney Lane-Donovan, Joachim Herz

Open access · greenAbstract readReview
In one paragraph

Review in Trends in endocrinology and metabolism: TEM, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed, 1 pooled it
7.8field-weighted citation impact, top 2% 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

102 citing papers in PubMed, 1 synthesis or guideline pooled it, 159 citations in OpenAlex.

  1. Pooled it
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  11. Deletion of neuronal Idol ameliorates Alzheimer's disease-related pathologies via APOE receptors.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
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42 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

2 authors at 1 institution in 1 country.

Courtney Lane-DonovanDepartment of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Department of Neuroscience, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Center for Translational Neurodegeneration Research, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. Electronic address: Courtney.Lane@utsouthwestern.edu.
Joachim HerzDepartment of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Department of Neuroscience, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Center for Translational Neurodegeneration Research, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Department of Neurology and Neurotherapeutics, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Center for Neuroscience, Department of Neuroanatomy, Albert Ludwig University, Freiburg, Germany. Electronic address: Joachim.Herz@utsouthwestern.edu.
The University of Texas Southwestern Medical Center · US

Funding

Metabolism of the VLDL receptor and ApoE receptor 2R37HL063762 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI HERZ, JOACHIM J · 2010 to 2019
$4.0M
Physiology and Pathophysiology of Apolipoprotein E receptor-2 splicing in Alzheimer's diseaseRF1AG053391 · NIA · UT SOUTHWESTERN MEDICAL CENTER · PI HERZ, JOACHIM J · 2016 to 2020
$2.4M
Molecular Basis of Synaptic Suppression by ApoER01NS093382 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI HERZ, JOACHIM J · 2016 to 2020
$2.0M
The Role of Reelin in Adult Neuronal Function and Alzheimer's DiseaseF30AG047799 · NIA · UT SOUTHWESTERN MEDICAL CENTER · PI LANE-DONOVAN, COURTNEY E · 2014 to 2015
$58k
NHLBI NIH HHS R37 HL063762NIA NIH HHS F30 AG047799NIA NIH HHS RF1 AG053391NINDS NIH HHS R01 NS093382
6 · The paper itself

Abstract

As the population ages, neurodegenerative diseases such as Alzheimer's disease (AD) are becoming a significant burden on patients, their families, and health-care systems. Neurodegenerative processes may start up to 15 years before outward signs and symptoms of AD, as evidenced by data from AD patients and mouse models. A major genetic risk factor for late-onset AD is the ɛ4 isoform of apolipoprotein E (ApoE4), which is present in almost 20% of the population. In this review we discuss the contribution of ApoE receptor signaling to the function of each component of the tripartite synapse - the axon terminal, the postsynaptic dendritic spine, and the astrocyte - and examine how these systems fail in the context of ApoE4 and AD.

Indexed as

Alzheimer DiseaseAnimalsApolipoproteins EDisease Models, AnimalFemaleHumansLow Density Lipoprotein Receptor-Related Protein-1MaleReelin ProteinSynapsesApolipoproteins ELow Density Lipoprotein Receptor-Related Protein-1Reelin ProteinRELN protein, humanReln protein, mousecalcium homeostasisdendriteendosomeLRPNMDA receptorReelin.synaptic dysfunction

Identifiers

PMID28057414
PMCPMC5366078
OpenAlexW2568317134

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.