Evidence map›Paper›PMID 24559670›Full record

ReviewNeuron2014

ApoE and Aβ in Alzheimer's disease: accidental encounters or partners?

Takahisa Kanekiyo, Huaxi Xu, Guojun Bu

Open access · bronzeAbstract readReview
In one paragraph

Review in Neuron, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 361 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
361citing papers in PubMed, 4 pooled it
27.4field-weighted citation impact, top 1% 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

361 citing papers in PubMed, 4 syntheses or guidelines pooled it, 620 citations in OpenAlex.

  1. Pooled it
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  3. A haptoglobin (HP) structural variant alters the effect of APOE alleles on Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023
    Pooled it
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301 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

3 authors at 2 institutions in 2 countries.

Takahisa KanekiyoDepartment of Neuroscience, Mayo Clinic, Jacksonville, FL 32224, USA.
Huaxi XuFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, College of Medicine, Xiamen University, Xiamen 361005, China.
Guojun BuDepartment of Neuroscience, Mayo Clinic, Jacksonville, FL 32224, USA; Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, College of Medicine, Xiamen University, Xiamen 361005, China. Electronic address: bu.guojun@mayo.edu.
Xiamen University · CNMayo Clinic in Florida · US

Funding

Viral Vectors CoreP01NS074969 · NINDS · WASHINGTON UNIVERSITY · PI SNIDER, BARBARA JOY · 2012 to 2021
$13.0M
TRANSGENIC MOUSE COREP01AG030128 · NIA · UNIVERSITY OF ILLINOIS AT CHICAGO · PI WEEBER, EDWIN JOHN · 2009 to 2013
$9.4M
Regulation of Protein Trafficking in NeurodegenerationR01NS046673 · NINDS · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI XU, HUAXI · 2003 to 2018
$5.8M
ApoE Receptor Pathways to Intraneuronal AbetaR01AG027924 · NIA · WASHINGTON UNIVERSITY · PI LI, YONGHE · 2006 to 2021
$3.7M
Identifying genes in Beta-Amyloid ProductionR01AG021173 · NIA · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI XU, HUAXI · 2004 to 2015
$3.3M
BRAIN LIPID METABOLISM, DENDRITES AND SYNAPSES IN AGING AND ALZHEIMER'S DISEASER01AG035355 · NIA · MAYO CLINIC JACKSONVILLE · PI BU, GUOJUN · 2010 to 2019
$3.1M
ApoE isoform-specific therapy for Alzheimer diseaseRF1AG046205 · NIA · MAYO CLINIC JACKSONVILLE · PI ZHAO, NA · 2019 to 2019
$3.1M
Roles of SN27 in regulating glutamate receptors during neurodegenerationR01AG044420 · NIA · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI XU, HUAXI · 2013 to 2017
$2.0M
ApoE isoform-specific therapy for Alzheimer diseaseR01AG046205 · NIA · MAYO CLINIC JACKSONVILLE · PI BU, GUOJUN · 2013 to 2017
$1.6M
LRP AND APP PROCESSING IN NEURODEGENERATIONR01AG031784 · NIA · WASHINGTON UNIVERSITY · PI BU, GUOJUN · 2008 to 2009
$398k
NIA NIH HHS P01 AG030128NIA NIH HHS P01AG030128NIA NIH HHS R01 AG021173NIA NIH HHS R01 AG027924NIA NIH HHS R01AG027924NIA NIH HHS R01 AG031784NIA NIH HHS R01 AG035355NIA NIH HHS R01AG035355NIA NIH HHS R01 AG044420NIA NIH HHS R01 AG046205NIA NIH HHS R01AG046205NIA NIH HHS RF1 AG046205NINDS NIH HHS P01 NS074969NINDS NIH HHS P01NS074969NINDS NIH HHS R01 NS046673
6 · The paper itself

Abstract

Among the three human apolipoprotein E (apoE) isoforms, apoE4 increases the risk of Alzheimer's disease (AD). While transporting cholesterol is a primary function, apoE also regulates amyloid-β (Aβ) metabolism, aggregation, and deposition. Although earlier work suggests that different affinities of apoE isoforms to Aβ might account for their effects on Aβ clearance, recent studies indicate that apoE also competes with Aβ for cellular uptake through apoE receptors. Thus, several factors probably determine the variable effects apoE has on Aβ. In this Review, we examine biochemical, structural, and functional studies and propose testable models that address the complex mechanisms underlying apoE-Aβ interaction and how apoE4 may increase AD risk and also serve as a target pathway for therapy.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsApolipoproteins EBrainHumansNeuronsRisk FactorsAmyloid beta-PeptidesApolipoproteins E

Identifiers

PMID24559670
PMCPMC3983361
OpenAlexW2051765035

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.