Evidence map›Paper›PMID 35452678›Full record

ArticleThe Journal of biological chemistry2022

Human brain sialoglycan ligand for CD33, a microglial inhibitory Siglec implicated in Alzheimer's disease.

Anabel Gonzalez-Gil, Ryan N Porell, Steve M Fernandes, Eila Maenpaa, T August Li, Tong Li, Philip C Wong, Kazuhiro Aoki, Michael Tiemeyer, Zaikuan J Yu and 4 more

Open access · goldAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
7.2field-weighted citation impact, top 2% 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

27 citing papers in PubMed, 83 citations in OpenAlex.

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  8. Microglial phagocytosis in Alzheimer disease.Nature reviews. Neurology · 2026
    Review
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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

14 authors at 3 institutions in 1 country.

Anabel Gonzalez-GilDepartment of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Ryan N PorellDepartment of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Steve M FernandesDepartment of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Eila MaenpaaDepartment of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
T August LiDepartment of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Tong LiDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Philip C WongDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA; Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Kazuhiro AokiComplex Carbohydrate Research Center, University of Georgia, Athens, Georgia, USA.
Michael TiemeyerComplex Carbohydrate Research Center, University of Georgia, Athens, Georgia, USA.
Zaikuan J YuDepartment of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Benjamin C OrsburnDepartment of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Namandjé N BumpusDepartment of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Russell T MatthewsDepartment of Neuroscience and Physiology, State University of New York Upstate Medical University, Syracuse, New York, USA.
Ronald L SchnaarDepartment of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA; Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Electronic address: schnaar@jhu.edu.
Johns Hopkins University · USUniversity of Georgia · USSUNY Upstate Medical University · US

Funding

'T V ASSESSMENT - MEMORY DISORDERED PATIENTS'P50AG005146 · NIA · JOHNS HOPKINS UNIVERSITY · PI ALBERT, MARILYN S. · 1985 to 2019
$37.6M
Research Education ComponentP30AG066507 · NIA · JOHNS HOPKINS UNIVERSITY · PI MARILYN S. ALBERT · 2020 to 2026
$29.3M
Using siglecs and their ligands to treat allergic diseases SALTADU19AI136443 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI BOCHNER, BRUCE S · 2018 to 2022
$7.6M
PHARMACOLOGY TRAINING GRANTT32GM008763 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI FREEL MEYERS, CAREN L. · 2000 to 2019
$6.1M
Immersive Training in GlycosciencesK12HL141952 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI HASCALL, VINCENT CHARLES, SCHNAAR, RONALD L · 2018 to 2022
$4.8M
The Chemistry-Biology Interface Program at Johns Hopkins UniversityT32GM080189 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI ROKITA, STEVEN E · 2008 to 2022
$3.5M
Regulation of microglia in Alzheimer's Disease by Siglecs and Siglec ligandsR56AG068089 · NIA · JOHNS HOPKINS UNIVERSITY · PI LI, TONG, SCHNAAR, RONALD L · 2020 to 2020
$786k
Defining the role of keratan sulfate recognition in Alzheimer's Disease progressionR56AG062342 · NIA · UNIVERSITY OF GEORGIA · PI MOREMEN, KELLEY W., SCHNAAR, RONALD L · 2018 to 2018
$777k
NHLBI NIH HHS K12 HL141952NIAID NIH HHS U19 AI136443NIA NIH HHS P30 AG066507NIA NIH HHS P50 AG005146NIA NIH HHS R56 AG062342NIA NIH HHS R56 AG068089NIGMS NIH HHS T32 GM008763NIGMS NIH HHS T32 GM080189
6 · The paper itself

Abstract

Alzheimer's disease (AD) is characterized by accumulation of misfolded proteins. Genetic studies implicate microglia, brain-resident phagocytic immune cells, in AD pathogenesis. As positive effectors, microglia clear toxic proteins, whereas as negative effectors, they release proinflammatory mediators. An imbalance of these functions contributes to AD progression. Polymorphisms of human CD33, an inhibitory microglial receptor, are linked to AD susceptibility; higher CD33 expression correlates with increased AD risk. CD33, also called Siglec-3, is a member of the sialic acid-binding immunoglobulin-type lectin (Siglec) family of immune regulatory receptors. Siglec-mediated inhibition is initiated by binding to complementary sialoglycan ligands in the tissue environment. Here, we identify a single sialoglycoprotein in human cerebral cortex that binds CD33 as well as Siglec-8, the most abundant Siglec on human microglia. The ligand, which we term receptor protein tyrosine phosphatase zeta (RPTPζ)

Indexed as

Alzheimer DiseaseSialic Acid Binding Immunoglobulin-like LectinsAnimalsBrainHumansKeratan SulfateLigandsMiceMicrogliaProtein IsoformsReceptor-Like Protein Tyrosine Phosphatases, Class 5Sialic Acid Binding Ig-like Lectin 3CD33 protein, humanKeratan SulfateLigandsProtein IsoformsReceptor-Like Protein Tyrosine Phosphatases, Class 5Sialic Acid Binding Ig-like Lectin 3Sialic Acid Binding Immunoglobulin-like LectinsAlzheimer's diseasekeratan sulfatemicrogliaphosphacanreceptor protein tyrosine phosphatase zetasialic acidsialyltransferaseSiglec-3Siglec-8Siglec-F

Identifiers

PMID35452678
PMCPMC9130525
OpenAlexW4224260082

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.