Evidence map›Paper›PMID 25918154›Full record

ArticleThe Journal of biological chemistry2015

Role of Apolipoprotein E in β-Amyloidogenesis: ISOFORM-SPECIFIC EFFECTS ON PROTOFIBRIL TO FIBRIL CONVERSION OF Aβ IN VITRO AND BRAIN Aβ DEPOSITION IN VIVO.

Yukiko Hori, Tadafumi Hashimoto, Hidetoshi Nomoto, Bradley T Hyman, Takeshi Iwatsubo

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

31 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Apolipoprotein E and Alzheimer's disease pathology in a diverse autopsy study.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  5. Review
  6. Article
  7. APOE ε4 is associated with decreased synaptic density in cognitively impaired participants.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Effect ofNature aging · 2021
    Article
  16. Review
  17. Some Candidate Drugs for Pharmacotherapy of Alzheimer's Disease.Pharmaceuticals (Basel, Switzerland) · 2021
    Review
  18. Review
  19. Remodeling Alzheimer-amyloidosis models by seeding.Molecular neurodegeneration · 2021
    Review
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 2 countries.

Yukiko HoriFrom the Department of Neuropathology and Neuroscience, Graduate School of Pharmaceutical Sciences and.
Tadafumi HashimotoFrom the Department of Neuropathology and Neuroscience, Graduate School of Pharmaceutical Sciences and the Department of Neuropathology, Graduate School of Medicine, University of Tokyo, Tokyo, 113-0033 Japan and the Department of Neurology/Alzheimer's Disease Research Unit, Massachusetts General Hospital, Charlestown, Massachusetts 02129.
Hidetoshi NomotoFrom the Department of Neuropathology and Neuroscience, Graduate School of Pharmaceutical Sciences and.
Bradley T Hymanthe Department of Neurology/Alzheimer's Disease Research Unit, Massachusetts General Hospital, Charlestown, Massachusetts 02129.
Takeshi IwatsuboFrom the Department of Neuropathology and Neuroscience, Graduate School of Pharmaceutical Sciences and the Department of Neuropathology, Graduate School of Medicine, University of Tokyo, Tokyo, 113-0033 Japan and iwatsubo@m.u-tokyo.ac.jp.
Harvard University · USHarvard University Press · USThe University of Tokyo · JP

Funding

THE ROLE OF ADVANCED CAA IN ALZHEIMER'S DEMENTIAP50AG005134 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI HYMAN, BRADLEY T. · 1985 to 2018
$42.1M
Research Education ComponentP30AG062421 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI Christine S Ritchie · 2019 to 2026
$36.5M
NIA NIH HHS P30 AG062421NIA NIH HHS P50 AG005134
6 · The paper itself

Abstract

Human APOE ϵ4 allele is a strong genetic risk factor of Alzheimer disease. Neuropathological and genetic studies suggested that apolipoprotein E4 (apoE4) protein facilitates deposition of amyloid β peptide (Aβ) in the brain, although the mechanism whereby apoE4 increases amyloid aggregates remains elusive. Here we show that injection of Aβ protofibrils induced Aβ deposition in the brain of APP transgenic mice, suggesting that Aβ protofibrils acted as a seed for aggregation and deposition of Aβ in vivo. Injection of Aβ protofibrils together with apoE3 significantly attenuated Aβ deposition, whereas apoE4 did not have this effect. In vitro assays revealed that the conversion of Aβ protofibrils to fibrils progressed more slowly upon coincubation with apoE2 or apoE3 compared with that with apoE4. Aβ protofibrils complexed with apoE4 were less stable than those with apoE2 or apoE3. These data suggest that the suppression effect of apoE2 or apoE3 on the structural conversion of Aβ protofibrils to fibrils is stronger than those of apoE4, thereby impeding β-amyloid deposition.

Indexed as

AmyloidAnimalsApolipoproteins EBrainEnzyme-Linked Immunosorbent AssayIn Vitro TechniquesMiceMice, TransgenicProtein IsoformsAmyloidApolipoproteins EProtein IsoformsAlzheimer diseaseamyloidamyloid-βapolipoprotein Eprotein stability

Identifiers

PMID25918154
PMCPMC4463458
OpenAlexW1993676790

What OpenQuestion holds

Textmetadata
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.