Evidence map›Paper›PMID 19679070›Full record

ReviewNeuron2009

The role of apolipoprotein E in Alzheimer's disease.

Jungsu Kim, Jacob M Basak, David M Holtzman

Registry-linked trialOpen access · bronzeAbstract readReview
In one paragraph

Review in Neuron, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03901261 (Cohort Study of Adult Patients With Down Syndrome at Risk of Developing Alzheimer's Disease), which is not on this map. Cited by 826 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
826citing papers in PubMed, 2 pooled it
54.3field-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.

NCT03901261 naunknown statusnot on this mapstarted 2019, after this paper: background citation

Cohort Study of Adult Patients With Down Syndrome at Risk of Developing Alzheimer's Disease

TypeinterventionalSponsorInstitut Jerome LejeuneRan2019 to 2023Enrolled200ConditionsDown Syndrome, Alzheimer DiseaseArmsNeuro-imaging, Lumbar puncture
3 · Its place in the literature

Who cites it

826 citing papers in PubMed, 2 syntheses or guidelines pooled it, 1,622 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
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  17. Spatially and temporally progressive hypoperfusion in Alzheimer's disease revealed by normative modeling.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  18. Dissecting Alzheimer's disease heritability across populations.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  19. Review
  20. Article

766 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 1 institution in 1 country.

Jungsu KimDepartment of Neurology, Developmental Biology, Hope Center for Neurological Disorders, Alzheimer's Disease Research Center, Washington University School of Medicine, St. Louis, MO 63110, USA.
Jacob M Basak
David M Holtzman
Hope Center for Neurological Disorders · US

Funding

Washington University Institute of Clinical and Translational Sciences (UL1)UL1RR024992 · NCRR · WASHINGTON UNIVERSITY · PI EVANOFF, BRADLEY A · 2007 to 2011
$45.4M
ZINC AND ISCHEMIC BRAIN INJURYP01NS032636 · NINDS · WASHINGTON UNIVERSITY · PI SANDS, MARK S · 1995 to 2010
$13.2M
Washington University Center for Translational NeuroscienceP30NS057105 · NINDS · WASHINGTON UNIVERSITY · PI HOLTZMAN, DAVID M. · 2006 to 2011
$8.7M
Effect of apoE on CNS neurons: Role of LRPR37AG013956 · NIA · WASHINGTON UNIVERSITY · PI HOLTZMAN, DAVID M. · 2004 to 2013
$3.8M
APOE EFFECT ON CNS NEURONS--ROLE OF LRPR01AG013956 · NIA · WASHINGTON UNIVERSITY · PI HOLTZMAN, DAVID M · 1996 to 2003
$1.2M
Effect of Human AD Brain-Derived Abeta Species on Synaptic FunctionK01AG029524 · NIA · WASHINGTON UNIVERSITY · PI CIRRITO, JOHN R · 2007 to 2011
$470k
NCRR NIH HHS UL1 RR024992NIA NIH HHS AG13956NIA NIH HHS K01 AG029524NIA NIH HHS R01 AG013956NIA NIH HHS R37 AG013956NINDS NIH HHS P01 NS032636NINDS NIH HHS P30 NS057105
6 · The paper itself

Abstract

The epsilon4 allele of apolipoprotein E (APOE) is the major genetic risk factor for Alzheimer's disease (AD). Although there have been numerous studies attempting to elucidate the underlying mechanism for this increased risk, how apoE4 influences AD onset and progression has yet to be proven. However, prevailing evidence suggests that the differential effects of apoE isoforms on Abeta aggregation and clearance play the major role in AD pathogenesis. Other potential mechanisms, such as the differential modulation of neurotoxicity and tau phosphorylation by apoE isoforms as well as its role in synaptic plasticity and neuroinflammation, have not been ruled out. Inconsistent results among studies have made it difficult to define whether the APOE epsilon4 allele represents a gain of toxic function, a loss of neuroprotective function, or both. Therapeutic strategies based on apoE propose to reduce the toxic effects of apoE4 or to restore the physiological, protective functions of apoE.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsApolipoproteins EBrainHumansMiceModels, BiologicalMutationAmyloid beta-PeptidesApolipoproteins E

Identifiers

PMID19679070
PMCPMC3044446
OpenAlexW2069121057

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.