Evidence map›Paper›PMID 21141969›Full record

ArticleMolecular pharmaceutics2011

Receptor-mediated abeta amyloid antibody targeting to Alzheimer's disease mouse brain.

Qing-Hui Zhou, Ailing Fu, Ruben J Boado, Eric Ka-Wai Hui, Jeff Zhiqiang Lu, William M Pardridge

Abstract read
In one paragraph

Article in Molecular pharmaceutics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

22 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
  2. Vamp3/syntaxin 4 mediates the basolateral membrane fusion of TfR transcytosis across the BBB and is exploited by pathogenicProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  3. The blood-brain barrier: a help and a hindrance.Brain : a journal of neurology · 2025
    Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
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  10. Article
  11. Article
  12. Article
  13. Review
  14. Agile delivery of protein therapeutics to CNS.Journal of controlled release : official journal of the Controlled Release Society · 2014
    Review
  15. Non-viral gene therapy that targets motor neurons in vivo.Frontiers in molecular neuroscience · 2014
    Article
  16. Review
  17. Article
  18. Developing therapeutic antibodies for neurodegenerative disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2013
    Review
  19. Article
  20. Immunologic privilege in the central nervous system and the blood-brain barrier.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2013
    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

6 authors at 1 institution in 1 country.

Qing-Hui ZhouDepartment of Medicine, UCLA, Los Angeles, California 90024, USA.
Ailing Fu
Ruben J Boado
Eric Ka-Wai Hui
Jeff Zhiqiang Lu
William M Pardridge
ArmaGen (United States) · US

Funding

Monoclonal Antibody Drug Development for Alzheimer?s DiseaseR01AG032244 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI PARDRIDGE, WILLIAM M · 2008 to 2012
$1.6M
NIA NIH HHS R01 AG032244NIA NIH HHS R01-AG032244
6 · The paper itself

Abstract

The goal of this work is the reduction in the Abeta amyloid peptide burden in brain of Alzheimer's disease (AD) transgenic mice without the concomitant elevation in plasma Abeta amyloid peptide. An anti-Abeta amyloid antibody (AAA) was re-engineered as a fusion protein with a blood-brain barrier (BBB) molecular Trojan horse. The AAA was engineered as a single chain Fv (ScFv) antibody, and the ScFv was fused to the heavy chain of a chimeric monoclonal antibody (mAb) against the mouse transferrin receptor (TfR), and this fusion protein was designated cTfRMAb-ScFv. The cTfRMAb-ScFv protein penetrates mouse brain from blood via transport on the BBB TfR, and the brain uptake is 3.5% of injected dose/gram brain following an intravenous administration. Double transgenic APPswe,PSEN1dE9 mice were studied at 12 months of age. The mice were shown to have extensive Abeta amyloid plaques in cerebral cortex based on immunocytochemistry. The mice were treated every 3-4 days by intravenous injections of either saline or the cTfRMAb-ScFv fusion protein at an injection dose of 1 mg/kg for 12 consecutive weeks. The brain Aβ¹⁻⁴² concentration was reduced 40% in the fusion protein treated mice, without any elevation in plasma Aβ¹⁻⁴² concentration. No cerebral microhemorrhage was observed in the treated mice. These results show that brain-penetrating antibody pharmaceutics can be developed for brain disorders such as AD following the re-engineering of the antibody as a fusion protein that is transported across the BBB via receptor-mediated transport.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsAntibodies, MonoclonalBlood-Brain BarrierBrainEnzyme-Linked Immunosorbent AssayImmunohistochemistryMaleMiceMice, TransgenicPlaque, AmyloidReceptors, TransferrinAmyloid beta-PeptidesAntibodies, MonoclonalReceptors, Transferrin

Identifiers

PMID21141969
PMCPMC3034812
OpenAlexW2056672961

What OpenQuestion holds

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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.