Evidence map›Paper›PMID 28755839›Full record

ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2018

Peripheral complement interactions with amyloid β peptide in Alzheimer's disease: 2. Relationship to amyloid β immunotherapy.

Andrés Crane, William D Brubaker, Jenny U Johansson, Abhishek Trigunaite, Justine Ceballos, Bonnie Bradt, Courtney Glavis-Bloom, Tanya L Wallace, Andrea J Tenner, Joseph Rogers

Open access · greenAbstract read
In one paragraph

Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 7% 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, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

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  16. Elovanoids counteract oligomeric β-amyloid-induced gene expression and protect photoreceptors.Proceedings of the National Academy of Sciences of the United States of America · 2019
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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

10 authors at 2 institutions in 1 country.

Andrés CraneBiosciences Division, SRI International, Menlo Park, CA, USA.
William D BrubakerBiosciences Division, SRI International, Menlo Park, CA, USA.
Jenny U JohanssonBiosciences Division, SRI International, Menlo Park, CA, USA.
Abhishek TrigunaiteBiosciences Division, SRI International, Menlo Park, CA, USA.
Justine CeballosBiosciences Division, SRI International, Menlo Park, CA, USA.
Bonnie BradtBiosciences Division, SRI International, Menlo Park, CA, USA.
Courtney Glavis-BloomBiosciences Division, SRI International, Menlo Park, CA, USA.
Tanya L WallaceBiosciences Division, SRI International, Menlo Park, CA, USA.
Andrea J TennerDepartments of Molecular Biology and Biochemistry and Neurobiology and Behavior, University of California, Irvine, Irvine, CA, USA.
Joseph RogersBiosciences Division, SRI International, Menlo Park, CA, USA. Electronic address: joseph.rogers@sri.com.
SRI International · USUniversity of California, Irvine · US

Funding

PRESENCE AND ROLE OF IMMUNE MARKERS IN ALZHEIMER'S BRAINR01AG007367 · NIA · SUN HEALTH RESEARCH INSTITUTE · PI ROGERS, JOSEPH B · 1988 to 2014
$3.3M
Function and polymorphisms of complement receptor 1 (CR1) in Alzheimer's diseaseR01AG039750 · NIA · SRI INTERNATIONAL · PI ROGERS, JOSEPH B · 2011 to 2015
$2.6M
NIA NIH HHS R01 AG007367NIA NIH HHS R01 AG039750
6 · The paper itself

Abstract

introductionOur previous studies have shown that amyloid β peptide (Aβ) is subject to complement-mediated clearance from the peripheral circulation, and that this mechanism is deficient in Alzheimer's disease. The mechanism should be enhanced by Aβ antibodies that form immune complexes (ICs) with Aβ, and therefore may be relevant to current Aβ immunotherapy approaches.

methodsMultidisciplinary methods were employed to demonstrate enhanced complement-mediated capture of Aβ antibody immune complexes compared with Aβ alone in both erythrocytes and THP1-derived macrophages.

resultsAβ antibodies dramatically increased complement activation and opsonization of Aβ, followed by commensurately enhanced Aβ capture by human erythrocytes and macrophages. These in vitro findings were consistent with enhanced peripheral clearance of intravenously administered Aβ antibody immune complexes in nonhuman primates. DISCUSSION: Together with our previous results, showing significant Alzheimer's disease deficits in peripheral Aβ clearance, the present findings strongly suggest that peripheral mechanisms should not be ignored as contributors to the effects of Aβ immunotherapy.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsAntibodiesCell AdhesionCells, CulturedComplement System ProteinsDose-Response Relationship, DrugErythrocytesFemaleHumansImmunologic FactorsImmunotherapyMacaca fascicularisMacrophagesMaleAmyloid beta-PeptidesAntibodiesComplement System ProteinsImmunologic FactorsAlzheimer's diseaseAmyloid β peptideAβ immunotherapyBloodComplementComplement receptor 1ErythrocyteHumanMacrophage

Identifiers

PMID28755839
PMCPMC5881571
OpenAlexW2737953625

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.