Evidence map›Paper›PMID 18091561›Full record

ArticleJournal of neuropathology and experimental neurology2008

Limited clearance of pre-existing amyloid plaques after intracerebral injection of Abeta antibodies in two mouse models of Alzheimer disease.

Stina M Fangmark Tucker, David R Borchelt, Juan C Troncoso

Open access · bronzeAbstract read
In one paragraph

Article in Journal of neuropathology and experimental neurology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-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

13 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Mouse models of Anti-Aβ immunotherapies.Molecular neurodegeneration · 2025
    Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Currents concepts on the immunopathology of amyloidosis.Clinical reviews in allergy & immunology · 2010
    Review
  12. Article
  13. 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

3 authors at 1 institution in 1 country.

Stina M Fangmark TuckerDepartment of Pathology, Johns Hopkins School of Medicine, Baltimore, Maryland, USA.
David R Borchelt
Juan C Troncoso
Johns Hopkins University · US

Funding

'T V ASSESSMENT - MEMORY DISORDERED PATIENTS'P50AG005146 · NIA · JOHNS HOPKINS UNIVERSITY · PI HUGANIR, RICHARD L · 1985 to 2019
$37.6M
Repair and Regeneration in Alzheimer's DiseaseR01NS047225 · NINDS · UNIVERSITY OF FLORIDA · PI BORCHELT, DAVID R, SAVONENKO, ALENA · 2004 to 2012
$3.2M
NIA NIH HHS P50 AG005146NIA NIH HHS P50AG005146NINDS NIH HHS R01 NS047225NINDS NIH HHS R01NS47225
6 · The paper itself

Abstract

Recent studies have demonstrated the potential utility of antibodies for the treatment of Alzheimer disease (AD). In transgenic mouse models of AD, peripheral and intracerebral administration of Abeta-specific antibodies reduces amyloid burdens to varied extents. The mechanism may involve clearance of pre-existing amyloid plaques or prevention of new amyloid formation. Here, we have used two transgenic models, the inducible CamKII-ttAxtetAPP/swe/ind (Line 107) and the APPswe/PS1dE9 (Line 85), to test the ability of intracerebral injection of Abeta antibodies to clear amyloid. Because the production of Abeta peptides in the Line 107 model is inducible, whereas production in Line 85 mice is constitutive, we could study the effects of antibody on pre-existing plaques versus continuous plaque formation. In Line 85, injection of antibody resulted in modest but statistically significant reductions in amyloid burden (average, 14%-16%). However, injected antibodies had no effect on amyloid burden in Line 107 under conditions in which the production of Abeta was suppressed, indicating that pre-existing plaques are not rapidly cleared. These results indicate that intracerebral injection of Abeta antibodies produces modest reductions in amyloid deposition in these two models and that the mechanism may involve prevention of amyloid formation rather than clearance of pre-existing plaques.

Indexed as

Immunization, PassiveAlzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsCalcium-Calmodulin-Dependent Protein Kinase Type 2Disease Models, AnimalDose-Response Relationship, DrugEnzyme-Linked Immunosorbent AssayHumansImmunoglobulin GMiceMice, Inbred C57BLMice, TransgenicPlaque, AmyloidAmyloid beta-PeptidesAmyloid beta-Protein PrecursorCalcium-Calmodulin-Dependent Protein Kinase Type 2Immunoglobulin G

Identifiers

PMID18091561
PMCPMC3972013
OpenAlexW2038383390

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.