Evidence map›Paper›PMID 20966549›Full record

ArticleJournal of Alzheimer's disease : JAD2011

Passive (amyloid-β) immunotherapy attenuates monoaminergic axonal degeneration in the AβPPswe/PS1dE9 mice.

Ying Liu, Michael K Lee, Maria M James, Donald L Price, David R Borchelt, Juan C Troncoso, Esther S Oh

Open access · bronzeAbstract read
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.5field-weighted citation impact, top 34% 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

12 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Mouse models of Anti-Aβ immunotherapies.Molecular neurodegeneration · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Inflammatory process in Alzheimer's Disease.Frontiers in integrative neuroscience · 2013
    Article
  12. 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.

Ying LiuDepartment of Pathology, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Michael K Lee
Maria M James
Donald L Price
David R Borchelt
Juan C Troncoso
Esther S Oh
Johns Hopkins University · USJohns Hopkins Medicine · US

Funding

'T V ASSESSMENT - MEMORY DISORDERED PATIENTS'P50AG005146 · NIA · JOHNS HOPKINS UNIVERSITY · PI HUGANIR, RICHARD L · 1985 to 2019
$37.6M
SYNUCLEINS--CELL BIOLOGY AND TRANSGENIC MICER01NS038065 · NINDS · UNIVERSITY OF MINNESOTA · PI LEE, MICHAEL K · 2000 to 2011
$3.3M
Abeta and Monoaminergic Neurodegeneration in Transgenic Mouse Models of ADR01AG029401 · NIA · UNIVERSITY OF MINNESOTA · PI LEE, MICHAEL K · 2009 to 2013
$1.5M
NIA NIH HHS P50 AG005146NIA NIH HHS R01 AG029401NIA NIH HHS R01-AG09401NINDS NIH HHS R01 NS038065NINDS NIH HHS R01-NS038065PHS HHS P50 AGO05146
6 · The paper itself

Abstract

The role of amyloid-β (Aβ in the neurodegeneration of Alzheimer's disease remains controversial, to a large extent because of the lack of robust neurodegeneration in mouse models of AD. To address this question, we examined the effects of Aβ antibodies in the recently described monoaminergic (MAergic) axonal degeneration in AβPPswe/PS1dE9 mice. To determine if Aβ accumulation is directly involved in degeneration of MAergic axons, we examined the effects of passive anti-Aβ antibody (7B6) administration on Aβ pathology and MAergic degeneration in AβPPswe/PS1dE9 mice. Injections of monoclonal antibody (mAb) 7B6 into mice (6 to 9 months of age) resulted in a modest reduction of Aβ load in the brains of AβPPswe/PS1dE9 mice. In addition, 7B6 treated AβPPswe/PS1dE9 mice had significantly higher densities of MAergic axons in both cortex and in hippocampus as compared to untreated mutant mice. For example, 7B6 treated mice showed almost 2-fold greater densities of serotonergic (5-HT) axons in the cortex compared to saline treated mice. Similar findings were observed in the catecholaminergic (TH) axons. Our results demonstrate that lowering of Aβ levels via passive Aβ immunotherapy ameliorates ongoing degenerative processes, supporting a causal link between Aβ and neurodegeneration.

Indexed as

Immunization, PassiveAlzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsAntibodies, MonoclonalAxonsBiogenic MonoaminesBrainEnzyme-Linked Immunosorbent AssayImmunohistochemistryMiceMice, TransgenicNerve DegenerationStatistics, NonparametricAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAntibodies, MonoclonalBiogenic Monoamines

Identifiers

PMID20966549
PMCPMC3063938
OpenAlexW1565624092

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.