Evidence map›Paper›PMID 30760557›Full record

ArticleLife science alliance2019

Opposing Roles of apolipoprotein E in aging and neurodegeneration.

Eloise Hudry, Jacob Klickstein, Claudia Cannavo, Rosemary Jackson, Alona Muzikansky, Sheetal Gandhi, David Urick, Taylie Sargent, Lauren Wrobleski, Allyson D Roe and 5 more

Open access · goldAbstract read
In one paragraph

Article in Life science alliance, 2019. 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
2.1field-weighted citation impact, top 13% 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, 29 citations in OpenAlex.

  1. Review
  2. International journal of molecular sciences · 2025
    Article
  3. Article
  4. Multifaceted roles of APOE in Alzheimer disease.Nature reviews. Neurology · 2024
    Review
  5. Review
  6. Article
  7. Potential Modifying Effect of theInternational journal of molecular sciences · 2023
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. APOE-amyloid interaction: Therapeutic targets.Neurobiology of disease · 2020
    Review
  18. Review
  19. Article
  20. Article
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

15 authors at 3 institutions in 2 countries.

Eloise HudryAlzheimer Research Unit, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA ehudry@mgh.harvard.edu.ORCID 0000-0003-3654-9663
Jacob KlicksteinAlzheimer Research Unit, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
Claudia CannavoCentre for Discovery Brain Sciences, UK Dementia Research Institute, and Edinburgh Neuroscience, The University of Edinburgh, Edinburgh, UK.
Rosemary JacksonCentre for Discovery Brain Sciences, UK Dementia Research Institute, and Edinburgh Neuroscience, The University of Edinburgh, Edinburgh, UK.
Alona MuzikanskyDepartment of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
Sheetal GandhiAlzheimer Research Unit, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
David UrickAlzheimer Research Unit, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
Taylie SargentAlzheimer Research Unit, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.ORCID 0000-0003-3473-7812
Lauren WrobleskiAlzheimer Research Unit, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
Allyson D RoeAlzheimer Research Unit, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
Steven S HouAlzheimer Research Unit, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
Kishore V KuchibhotlaJohns Hopkins University, Baltimore, MD, USA.
Rebecca A BetenskyDepartment of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
Tara Spires-JonesCentre for Discovery Brain Sciences, UK Dementia Research Institute, and Edinburgh Neuroscience, The University of Edinburgh, Edinburgh, UK.
Bradley T HymanAlzheimer Research Unit, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
Harvard University · USUK Dementia Research Institute · GBJohns Hopkins University · US

Funding

Research Education ComponentP30AG066507 · NIA · JOHNS HOPKINS UNIVERSITY · PI MARILYN S. ALBERT · 2020 to 2026
$29.3M
Novel Strategies and Mechanisms to Target APOE and Alzheimer's DiseaseR01AG047644 · NIA · WASHINGTON UNIVERSITY · PI HOLTZMAN, DAVID M. · 2014 to 2018
$2.8M
Role of apolipoprotein E in age and amyloid beta related neuronal dysfunctionR00AG047336 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI HUDRY, ELOISE · 2017 to 2019
$747k
Role of apolipoprotein E in age and amyloid beta related neuronal dysfunctionK99AG047336 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI HUDRY, ELOISE · 2015 to 2016
$273k
NIA NIH HHS K99 AG047336NIA NIH HHS P30 AG066507NIA NIH HHS R00 AG047336NIA NIH HHS R01 AG047644Wellcome Trust
6 · The paper itself

Abstract

Apolipoprotein E (APOE) effects on brain function remain controversial. Removal of APOE not only impairs cognitive functions but also reduces neuritic amyloid plaques in mouse models of Alzheimer's disease (AD). Can APOE simultaneously protect and impair neural circuits? Here, we dissociated the role of APOE in AD versus aging to determine its effects on neuronal function and synaptic integrity. Using two-photon calcium imaging in awake mice to record visually evoked responses, we found that genetic removal of APOE improved neuronal responses in adult APP/PSEN1 mice (8-10 mo). These animals also exhibited fewer neuritic plaques with less surrounding synapse loss, fewer neuritic dystrophies, and reactive glia. Surprisingly, the lack of APOE in aged mice (18-20 mo), even in the absence of amyloid, disrupted visually evoked responses. These results suggest a dissociation in APOE's role in AD versus aging: APOE may be neurotoxic during early stages of amyloid deposition, although being neuroprotective in latter stages of aging.

Indexed as

AgingAlzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAmyloidosisAnimalsApolipoproteins EDisease Models, AnimalEvoked Potentials, VisualHumansLoss of Function MutationMiceMice, Inbred C57BLMice, TransgenicNeurogliaNeuronsAmyloid beta-PeptidesAmyloid beta-Protein Precursorapolipoprotein E (Arg61), mouseApolipoproteins EAPP protein, humanPresenilin-1PSEN1 protein, human

Identifiers

PMID30760557
PMCPMC6374993
OpenAlexW2914866847

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.