Evidence map›Paper›PMID 16630540›Full record

ArticleBiochemical and biophysical research communications2006

Amelioration of amyloid load by anti-Abeta single-chain antibody in Alzheimer mouse model.

Ken-ichiro Fukuchi, Mary Ann Accavitti-Loper, Hong-Duck Kim, Kazuki Tahara, Yunpeng Cao, Terry L Lewis, Robert C Caughey, Helen Kim, Robert Lalonde

Open access · greenAbstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

19 citing papers in PubMed, 44 citations in OpenAlex.

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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

9 authors at 5 institutions in 3 countries.

Ken-ichiro FukuchiDepartment of Cancer Biology and Pharmacology, University of Illinois College of Medicine at Peoria, Box 1649, Peoria, IL 61656, USA. kfukuchi@uic.edu
Mary Ann Accavitti-Loper
Hong-Duck Kim
Kazuki Tahara
Yunpeng Cao
Terry L Lewis
Robert C Caughey
Helen Kim
Robert Lalonde
University of Alabama at Birmingham · USUniversity of Illinois Urbana-Champaign · USChina Medical University · CNIllinois College · USUniversité de Rouen Normandie · FR

Funding

Alzheimer Vaccines: Noninvasive Vaccination by DNA-Base*R01NS043947 · NINDS · UNIVERSITY OF ILLINOIS AT CHICAGO · PI FUKUCHI, KEN-ICHIRO · 2001 to 2005
$1.7M
NINDS NIH HHS NS43947NINDS NIH HHS R01 NS043947
6 · The paper itself

Abstract

Parenteral immunization of transgenic mouse models of Alzheimer disease (AD) with synthetic amyloid beta-peptide (Abeta) prevented or reduced Abeta deposits and attenuated their memory and learning deficits. A clinical trial of immunization with synthetic Abeta, however, was halted due to brain inflammation, presumably induced by a toxic Abeta, T-cell- and/or Fc-mediated immune response. Another issue relating to such immunizations is that some AD patients may not be able to raise an adequate immune response to Abeta vaccination due to immunological tolerance or age-associated decline. Because peripheral administration of antibodies against Abeta also induced clearance of amyloid plaques in the model mice, injection of humanized Abeta antibodies has been proposed as a possible therapy for AD. By screening a human single-chain antibody (scFv) library for Abeta immunoreactivity, we have isolated a scFv that specifically reacts with oligomeric Abeta as well as amyloid plaques in the brain. The scFv inhibited Abeta amyloid fibril formation and Abeta-mediated cytotoxicity in vitro. We have tested the efficacy of the human scFv in a mouse model of AD (Tg2576 mice). Relative to control mice, injections of the scFv into the brain of Tg2576 mice reduced Abeta deposits. Because scFvs lack the Fc portion of the immunoglobulin molecule, human scFvs against Abeta may be useful to treat AD patients without eliciting brain inflammation.

Indexed as

Alzheimer DiseaseAmyloidAmyloid beta-PeptidesAnimalsBrainBrain ChemistryDisease Models, AnimalHumansImmunoglobulin Variable RegionLearning DisabilitiesMemory DisordersMiceMice, TransgenicMuscle, SkeletalPeptide FragmentsAmyloidAmyloid beta-Peptidesamyloid beta-protein (1-42)Immunoglobulin Variable RegionPeptide Fragments

Identifiers

PMID16630540
PMCPMC2475574
OpenAlexW2005885974

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.