Evidence map›Paper›PMID 33644757›Full record

ArticleBrain communications2021

Distinct microglial response against Alzheimer's amyloid and tau pathologies characterized by P2Y12 receptor.

Jun Maeda, Takeharu Minamihisamatsu, Masafumi Shimojo, Xiaoyun Zhou, Maiko Ono, Yukio Matsuba, Bin Ji, Hideki Ishii, Masanao Ogawa, Hiroyasu Akatsu and 11 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Brain communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
5.4field-weighted citation impact, top 3% 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

47 citing papers in PubMed, 77 citations in OpenAlex.

  1. Article
  2. Immune-mediated excitotoxicity in brain disorders.Nature reviews. Immunology · 2026
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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

21 authors at 5 institutions in 2 countries.

Jun MaedaDepartment of Functional Brain Imaging, National Institute of Radiological Sciences, National Institutes for Quantum and Radiological Science and Technology, Chiba, Japan.
Takeharu MinamihisamatsuDepartment of Functional Brain Imaging, National Institute of Radiological Sciences, National Institutes for Quantum and Radiological Science and Technology, Chiba, Japan.
Masafumi ShimojoDepartment of Functional Brain Imaging, National Institute of Radiological Sciences, National Institutes for Quantum and Radiological Science and Technology, Chiba, Japan.
Xiaoyun ZhouDepartment of Functional Brain Imaging, National Institute of Radiological Sciences, National Institutes for Quantum and Radiological Science and Technology, Chiba, Japan.
Maiko OnoDepartment of Functional Brain Imaging, National Institute of Radiological Sciences, National Institutes for Quantum and Radiological Science and Technology, Chiba, Japan.
Yukio MatsubaLaboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science, Saitama, Japan.
Bin JiDepartment of Functional Brain Imaging, National Institute of Radiological Sciences, National Institutes for Quantum and Radiological Science and Technology, Chiba, Japan.ORCID https://orcid.org/0000-0002-9672-6441
Hideki IshiiDepartment of Advanced Nuclear Medicine Science, National Institute of Radiological Sciences, National Institutes for Quantum and Radiological Science and Technology, Chiba, Japan.
Masanao OgawaDepartment of Advanced Nuclear Medicine Science, National Institute of Radiological Sciences, National Institutes for Quantum and Radiological Science and Technology, Chiba, Japan.
Hiroyasu AkatsuDepartment of Neuropathology, Choju Medical Institute, Fukushimura Hospital, Aichi, Japan.
Daita KanedaDepartment of Neuropathology, Choju Medical Institute, Fukushimura Hospital, Aichi, Japan.
Yoshio HashizumeDepartment of Neuropathology, Choju Medical Institute, Fukushimura Hospital, Aichi, Japan.
John L RobinsonCenter for Neurodegenerative Disease Research, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104-2674, USA.
Virginia M-Y LeeCenter for Neurodegenerative Disease Research, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104-2674, USA.
Takashi SaitoDepartment of Neurocognitive Science, Institute of Brain Science, Nagoya City University Graduate School of Medical Sciences, Aichi, Japan.
Takaomi C SaidoLaboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science, Saitama, Japan.
John Q TrojanowskiCenter for Neurodegenerative Disease Research, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104-2674, USA.
Ming-Rong ZhangDepartment of Advanced Nuclear Medicine Science, National Institute of Radiological Sciences, National Institutes for Quantum and Radiological Science and Technology, Chiba, Japan.
Tetsuya SuharaDepartment of Functional Brain Imaging, National Institute of Radiological Sciences, National Institutes for Quantum and Radiological Science and Technology, Chiba, Japan.
Makoto HiguchiDepartment of Functional Brain Imaging, National Institute of Radiological Sciences, National Institutes for Quantum and Radiological Science and Technology, Chiba, Japan.
Naruhiko SaharaDepartment of Functional Brain Imaging, National Institute of Radiological Sciences, National Institutes for Quantum and Radiological Science and Technology, Chiba, Japan.
National Institutes for Quantum Science and Technology · JPInstitute for Neurodegenerative Disorders · USRIKEN Center for Brain Science · JPFukushimura Hospital · JPNagoya City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Microglia are the resident phagocytes of the central nervous system, and microglial activation is considered to play an important role in the pathogenesis of neurodegenerative diseases. Recent studies with single-cell RNA analysis of CNS cells in Alzheimer's disease and diverse other neurodegenerative conditions revealed that the transition from homeostatic microglia to disease-associated microglia was defined by changes of gene expression levels, including down-regulation of the P2Y12 receptor gene (

Indexed as

Alzheimer’s diseaseamyloid pathologymicrogliaP2Y12 receptortauopathy

Identifiers

PMID33644757
PMCPMC7901060
OpenAlexW3128664180

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.