Evidence map›Paper›PMID 25358504›Full record

ReviewMolecules and cells2014

Apolipoprotein E in synaptic plasticity and Alzheimer's disease: potential cellular and molecular mechanisms.

Jaekwang Kim, Hyejin Yoon, Jacob Basak, Jungsu Kim

Open access · diamondAbstract readReview
In one paragraph

Review in Molecules and cells, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
85citing 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

85 citing papers in PubMed, 1 synthesis or guideline pooled it, 135 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Age at menopause,Research square · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
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  14. Pathways to Alzheimer's Disease: The Intersecting Roles of Clusterin and Apolipoprotein E in Amyloid-β Regulation and Neuronal Health.Pathophysiology : the official journal of the International Society for Pathophysiology · 2024
    Review
  15. Article
  16. Insights gained over 60 years on factors shaping post-stroke aphasia recovery: A commentary on Vignolo (1964).Cortex; a journal devoted to the study of the nervous system and behavior · 2024
    Article
  17. Review
  18. Article
  19. Article
  20. Review

25 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

4 authors at 3 institutions in 1 country.

Jaekwang KimDepartment of Neuroscience, Mayo Clinic College of Medicine, Jacksonville, FL 32224, USA.
Hyejin YoonDepartment of Neuroscience, Mayo Clinic College of Medicine, Jacksonville, FL 32224, USA ; Neurobiology of Disease Graduate Program, Mayo Graduate School, Jacksonville, FL 32224, USA.
Jacob BasakDepartment of Neurology, Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, MO 63110, USA.
Jungsu KimDepartment of Neuroscience, Mayo Clinic College of Medicine, Jacksonville, FL 32224, USA ; Neurobiology of Disease Graduate Program, Mayo Graduate School, Jacksonville, FL 32224, USA.
Jacksonville College · USMayo Clinic in Florida · USWashington University in St. Louis · US

Funding

THE PGRN/TDP-43 AXIS IN ALZHEIMER?S DISEASE AND NEURODEGENERATIONP50AG016574 · NIA · MAYO CLINIC ROCHESTER · PI BU, GUOJUN · 1999 to 2018
$36.9M
NIA NIH HHS NIH AG016574NIA NIH HHS P50 AG016574
6 · The paper itself

Abstract

Alzheimer's disease (AD) is clinically characterized with progressive memory loss and cognitive decline. Synaptic dysfunction is an early pathological feature that occurs prior to neurodegeneration and memory dysfunction. Mounting evidence suggests that aggregation of amyloid-β (Aβ) and hyperphosphorylated tau leads to synaptic deficits and neurodegeneration, thereby to memory loss. Among the established genetic risk factors for AD, the ɛ4 allele of apolipoprotein E (APOE) is the strongest genetic risk factor. We and others previously demonstrated that apoE regulates Aβ aggregation and clearance in an isoform-dependent manner. While the effect of apoE on Aβ may explain how apoE isoforms differentially affect AD pathogenesis, there are also other underexplored pathogenic mechanisms. They include differential effects of apoE on cerebral energy metabolism, neuroinflammation, neurovascular function, neurogenesis, and synaptic plasticity. ApoE is a major carrier of cholesterols that are required for neuronal activity and injury repair in the brain. Although there are a few conflicting findings and the underlying mechanism is still unclear, several lines of studies demonstrated that apoE4 leads to synaptic deficits and impairment in long-term potentiation, memory and cognition. In this review, we summarize current understanding of apoE function in the brain, with a particular emphasis on its role in synaptic plasticity and the underlying cellular and molecular mechanisms, involving low-density lipoprotein receptor-related protein 1 (LRP1), syndecan, and LRP8/ApoER2.

Indexed as

Neuronal PlasticityAlzheimer DiseaseAmyloid beta-PeptidesAnimalsApolipoproteins EBrainHumansSynapsesAmyloid beta-PeptidesApolipoproteins EAlzheimer’s diseaseApoER2Apolipoprotein EHSPGLRP1synaptic plasticity

Identifiers

PMID25358504
PMCPMC4255096
OpenAlexW2040546047

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.