Evidence map›Paper›PMID 20594620›Full record

ArticleNeurobiology of aging2012

Amyloid β1-42 oligomer inhibits myelin sheet formation in vitro.

Makoto Horiuchi, Izumi Maezawa, Aki Itoh, Kouji Wakayama, Lee-Way Jin, Takayuki Itoh, Charles Decarli

Abstract read
In one paragraph

Article in Neurobiology of aging, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

49 citing papers in PubMed, 81 citations in OpenAlex.

  1. Article
  2. Article
  3. Entwined processes in Alzheimer's disease: Brain cellular senescence and Alzheimer's disease pathology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Astrocyte and oligodendrocyte pathology in Alzheimer's disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  9. Review
  10. Article
  11. Article
  12. Neuroprotective Effect ofPharmaceuticals (Basel, Switzerland) · 2024
    Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Myelin in Alzheimer's disease: culprit or bystander?Acta neuropathologica communications · 2023
    Review
  19. Article
  20. Review
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

7 authors at 2 institutions in 1 country.

Makoto HoriuchiDepartment of Neurology, University of California Davis, School of Medicine, Sacramento, CA 95817, United States.
Izumi Maezawa
Aki Itoh
Kouji Wakayama
Lee-Way Jin
Takayuki Itoh
Charles Decarli
University of California, Davis · USShriners Hospitals for Children - Northern California · US

Funding

UC Davis Alzheimer's Disease Core CenterP30AG010129 · NIA · UNIVERSITY OF CALIFORNIA DAVIS · PI DECARLI, CHARLES · 1991 to 2020
$28.3M
Inhibition of Alzheimer's Beta-Amyloid Fibril FormationR01AG025500 · NIA · KANSAS STATE UNIVERSITY · PI HUA, DUY H · 2006 to 2009
$1.1M
Identify Abeta Oligomer Inhibitors By Combinatorial ChemistryR21AG031362 · NIA · UNIVERSITY OF CALIFORNIA AT DAVIS · PI JIN, LEE-WAY · 2008 to 2009
$355k
NIA NIH HHS P30 AG010129NIA NIH HHS P30 AG10129NIA NIH HHS R01 AG025500NIA NIH HHS R21 AG031362
6 · The paper itself

Abstract

Accumulating evidence indicates that white matter degeneration contributes to the neural disconnections that underlie Alzheimer's disease pathophysiology. Although this white matter degeneration is partly attributable to axonopathy associated with neuronal degeneration, amyloid β (Aβ) protein-mediated damage to oligodendrocytes could be another mechanism. To test this hypothesis, we studied effects of soluble Aβ in oligomeric form on survival and differentiation of cells of the oligodendroglial lineage using highly purified oligodendroglial cultures from rats at different developmental stages. Aβ oligomer at 10 μM or higher reduced survival of mature oligodendrocytes, whereas oligodendroglial progenitor cells (OPCs) were relatively resistant to the Aβ oligomer-mediated cytotoxicity. Further study revealed that Aβ oligomer even at 1 μM accelerated 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) formazan exocytosis in mature oligodendrocytes, and, more significantly, inhibited myelin sheet formation after induction of in vitro differentiation of OPCs. These results imply a novel pathogenetic mechanism underlying Aβ oligomer-mediated white matter degeneration, which could impair myelin maintenance and remyelination by adult OPCs, resulting in accumulating damage to myelinating axons thereby contributing to neural disconnections.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsAnimals, NewbornMyelin SheathNerve Fibers, MyelinatedOligodendrogliaPeptide FragmentsPrimary Cell CultureRatsRats, Inbred LewStem CellsTumor Cells, CulturedWallerian DegenerationAmyloid beta-Peptidesamyloid beta-protein (1-42)Peptide Fragments

Identifiers

PMID20594620
PMCPMC3013291
OpenAlexW2018767861

What OpenQuestion holds

Textmetadata
LicenceTDM
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.