Evidence map›Paper›PMID 29792870›Full record

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

Peripheral complement interactions with amyloid β peptide in Alzheimer's disease: Polymorphisms, structure, and function of complement receptor 1.

Jenny U Johansson, William D Brubaker, Harold Javitz, Andrew W Bergen, Denise Nishita, Abhishek Trigunaite, Andrés Crane, Justine Ceballos, Diego Mastroeni, Andrea J Tenner and 2 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
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 31 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 4 pooled it
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

31 citing papers in PubMed, 4 syntheses or guidelines pooled it, 42 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

12 authors at 5 institutions in 1 country.

Jenny U JohanssonBiosciences Division, SRI International, Menlo Park, CA, USA.
William D BrubakerBiosciences Division, SRI International, Menlo Park, CA, USA.
Harold JavitzEducation Division, SRI International, Menlo Park, CA, USA.
Andrew W BergenBiosciences Division, SRI International, Menlo Park, CA, USA.
Denise NishitaBiosciences Division, SRI International, Menlo Park, CA, USA.
Abhishek TrigunaiteBiosciences Division, SRI International, Menlo Park, CA, USA.
Andrés CraneBiosciences Division, SRI International, Menlo Park, CA, USA.
Justine CeballosBiosciences Division, SRI International, Menlo Park, CA, USA.
Diego MastroeniThe Biodesign Institute, Arizona State University, Tempe, AZ, USA.
Andrea J TennerDepartments of Molecular Biology and Biochemistry, Pathology, and Neurobiology and Behavior, University of California, Irvine, CA, USA.
Marwan SabbaghAlzheimer's and Memory Disorders Division, Barrow Neurological Institute, Phoenix, AZ, USA.
Joseph RogersBiosciences Division, SRI International, Menlo Park, CA, USA. Electronic address: joseph.rogers@sri.com.
SRI International · USArizona State University · USBarrow Neurological Institute · USMenlo School · 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

introductionGenome-wide association studies consistently show that single nucleotide polymorphisms (SNPs) in the complement receptor 1 (CR1) gene modestly but significantly alter Alzheimer's disease (AD) risk. Follow-up research has assumed that CR1 is expressed in the human brain despite a paucity of evidence for its function there. Alternatively, erythrocytes contain >80% of the body's CR1, where, in primates, it is known to bind circulating pathogens.

methodsMultidisciplinary methods were employed.

resultsConventional Western blots and quantitative polymerase chain reaction failed to detect CR1 in the human brain. Brain immunohistochemistry revealed only vascular CR1. By contrast, erythrocyte CR1 immunoreactivity was readily observed and was significantly deficient in AD, as was CR1-mediated erythrocyte capture of circulating amyloid β peptide. CR1 SNPs associated with decreased erythrocyte CR1 increased AD risk, whereas a CR1 SNP associated with increased erythrocyte CR1 decreased AD risk. DISCUSSION: SNP effects on erythrocyte CR1 likely underlie the association of CR1 polymorphisms with AD risk.

Indexed as

Polymorphism, Single NucleotideAgedAged, 80 and overAlzheimer DiseaseAmyloid beta-PeptidesApolipoproteins EErythrocytesFemaleGenetic Predisposition to DiseaseHumansMaleMicrogliaNeocortexProspective StudiesProtein IsoformsReceptors, Complement 3bAmyloid beta-PeptidesApolipoproteins ECR1 protein, humanProtein IsoformsReceptors, Complement 3bAmyloid β peptideClearanceComplement C3b/C4b receptor 1Complement receptor 1CR1ErythrocyteImmune adherenceRed blood cellSingle nucleotide polymorphism

Identifiers

PMID29792870
PMCPMC6231989
OpenAlexW2803583953

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.