Evidence map›Paper›PMID 20696774›Full record

ArticleThe American journal of pathology2010

Early oligodendrocyte/myelin pathology in Alzheimer's disease mice constitutes a novel therapeutic target.

Maya K Desai, Michael A Mastrangelo, Deborah A Ryan, Kelly L Sudol, Wade C Narrow, William J Bowers

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers.

0numbers the graph read from it
0cells of the map it votes in
139citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

139 citing papers in PubMed, 225 citations in OpenAlex.

  1. Trial
  2. Diffusion MRI reveals amyloid plaque-associated cellular signatures through spatial transcriptomic integration.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  3. Review
  4. Article
  5. When myelin breaks, tau aggregates - a new perspective on Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Targeting neuroinflammation in neurodegenerative disorders: the emerging potential of semaglutide.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  13. Article
  14. Emerging Role of Oligodendrocytes Malfunction in the Progression of Alzheimer's Disease.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
    Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

79 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

6 authors at 1 institution in 1 country.

Maya K DesaiDepartment of Pharmacology and Physiology, University of Rochester Medical Center, Rochester, New York, USA.
Michael A Mastrangelo
Deborah A Ryan
Kelly L Sudol
Wade C Narrow
William J Bowers
University of Rochester Medical Center · US

Funding

Gene-based TNF-alpha activity modulation in 3xTg-AD miceR01AG026328 · NIA · UNIVERSITY OF ROCHESTER · PI BOWERS, WILLIAM J. · 2007 to 2011
$1.4M
Training in Neuroinflammation and Glial Cell BiologyT32NS051152 · NINDS · UNIVERSITY OF ROCHESTER · PI O'BANION, M. KERRY · 2005 to 2009
$870k
NIA NIH HHS R01 AG026328NIA NIH HHS R01-AG026328NINDS NIH HHS T32 NS051152NINDS NIH HHS T32-NS051152
6 · The paper itself

Abstract

The detection of myelin disruptions in Alzheimer's disease (AD)-affected brain raises the possibility that oligodendrocytes undergo pathophysiological assault over the protracted course of this neurodegenerative disease. Oligodendrocyte compromise arising from direct toxic effects imparted by pathological amyloid-beta peptides and/or through signals derived from degenerating neurons could play an important role in the disease process. We previously demonstrated that 3xTg-AD mice, which harbor the human amyloid precursor protein Swedish mutant transgene, presenilin knock-in mutation, and tau P301L mutant transgene, exhibit significant alterations in overall myelination patterns and oligodendrocyte status at time points preceding the appearance of amyloid and tau pathology. Herein, we demonstrate that Abeta(1-42) leads to increased caspase-3 expression and apoptotic cell death of both nondifferentiated and differentiated mouse oligodendrocyte precursor (mOP) cells in vitro. Through use of a recombinant adeno-associated virus serotype-2 (rAAV2) vector expressing an Abeta(1-42)-specific intracellular antibody (intrabody), oligodendrocyte and myelin marker expression, as well as myelin integrity, were restored in the vector-infused brain regions of 3xTg-AD mice. Overall, this work provides further insights into the impact of Abeta(1-42)-mediated toxicity on the temporal and spatial progression of subtle myelin disruption during the early presymptomatic stages of AD and may help to validate new therapeutic options designed to avert these early impairments.

Indexed as

Amyloid beta-Protein PrecursorAnalysis of VarianceAnimalsApoptosisBlotting, WesternCaspase 3Cell LineDisease Models, AnimalEntorhinal CortexHumansImmunohistochemistryMiceMice, TransgenicMicroscopy, ElectronMyelin SheathOligodendrogliaAmyloid beta-Protein PrecursorCaspase 3tau Proteins

Identifiers

PMID20696774
PMCPMC2928974
OpenAlexW2085359313

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.