Evidence map›Paper›PMID 27922847›Full record

ReviewCurrent opinion in lipidology2017

Apolipoprotein E metabolism and functions in brain and its role in Alzheimer's disease.

Fan Liao, Hyejin Yoon, Jungsu Kim

Open access · hybridAbstract readReview
In one paragraph

Review in Current opinion in lipidology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.

0numbers the graph read from it
0cells of the map it votes in
107citing papers in PubMed
7.4field-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

107 citing papers in PubMed, 194 citations in OpenAlex.

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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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  17. ApoE3 Christchurch and tau interaction as a protective mechanism against Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
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  19. Review
  20. Review

47 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 3 institutions in 1 country.

Fan LiaoaDepartment of Neurology, Washington University School of Medicine, St. Louis, Missouri bNeurobiology of Disease Graduate Program, Mayo Graduate School cDepartment of Neuroscience, Mayo Clinic, Jacksonville, Florida, USA.
Hyejin Yoon
Jungsu Kim
Mayo Clinic in Florida · USSt. Luke's Hospital · USWashington University in St. Louis · US

Funding

Role of microRNA-33 in Alzheimer's diseaseR01AG053500 · NIA · MAYO CLINIC JACKSONVILLE · PI KIM, JUNGSU · 2016 to 2020
$2.0M
Role of LDLR in regulating metabolism of Apolipoprotein E and Amyloid-betaR01AG053242 · NIA · MAYO CLINIC JACKSONVILLE · PI KIM, JUNGSU · 2016 to 2020
$2.0M
The role of aging-associated microRNAs in Alzheimer's diseaseR01AG054102 · NIA · MAYO CLINIC JACKSONVILLE · PI KIM, JUNGSU · 2016 to 2020
$2.0M
microRNA-758-3p in cognition and Alzheimer's DiseaseR21AG050804 · NIA · MAYO CLINIC JACKSONVILLE · PI KIM, JUNGSU · 2016 to 2017
$430k
NIA NIH HHS R01 AG053242NIA NIH HHS R01 AG053500NIA NIH HHS R01 AG054102NIA NIH HHS R21 AG050804
6 · The paper itself

Abstract

purpose of reviewAPOE4 genotype is the strongest genetic risk factor for Alzheimer's disease. Prevailing evidence suggests that amyloid β plays a critical role in Alzheimer's disease. The objective of this article is to review the recent findings about the metabolism of apolipoprotein E (ApoE) and amyloid β and other possible mechanisms by which ApoE contributes to the pathogenesis of Alzheimer's disease. RECENT

findingsApoE isoforms have differential effects on amyloid β metabolism. Recent studies demonstrated that ApoE-interacting proteins, such as ATP-binding cassette A1 (ABCA1) and LDL receptor, may be promising therapeutic targets for Alzheimer's disease treatment. Activation of liver X receptor and retinoid X receptor pathway induces ABCA1 and other genes, leading to amyloid β clearance. Inhibition of the negative regulators of ABCA1, such as microRNA-33, also induces ABCA1 and decreases the levels of ApoE and amyloid β. In addition, genetic inactivation of an E3 ubiquitin ligase, myosin regulatory light chain interacting protein, increases LDL receptor levels and inhibits amyloid accumulation. Although amyloid β-dependent pathways have been extensively investigated, there have been several recent studies linking ApoE with vascular function, neuroinflammation, metabolism, synaptic plasticity, and transcriptional regulation. For example, ApoE was identified as a ligand for a microglial receptor, TREM2, and studies suggested that ApoE may affect the TREM2-mediated microglial phagocytosis. SUMMARY: Emerging data suggest that ApoE affects several amyloid β-independent pathways. These underexplored pathways may provide new insights into Alzheimer's disease pathogenesis. However, it will be important to determine to what extent each mechanism contributes to the pathogenesis of Alzheimer's disease.

Indexed as

Alzheimer DiseaseAnimalsApolipoproteins EBrainGene Expression RegulationHumansNeuronal PlasticityTranscription, GeneticApolipoproteins E

Identifiers

PMID27922847
PMCPMC5213812
OpenAlexW2559764604

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.