Evidence map›Paper›PMID 36306731›Full record

ArticleCell2022

Microglia are SYK of Aβ and cell debris.

Dorothy P Schafer, Jacob M Stillman

Abstract readComment
PubMed Publisher
In one paragraph

Article in Cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

10 citing papers in PubMed, 21 citations in OpenAlex.

  1. PTP1B inhibition promotes microglial phagocytosis in Alzheimer's disease models by enhancing SYK signaling.Proceedings of the National Academy of Sciences of the United States of America · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Dorothy P SchaferDepartment of Neurobiology, Brudnik Neuropsychiatric Research Institute, University of Massachusetts Chan Medical School, Worcester, MA, USA. Electronic address: dorothy.schafer@umassmed.edu.
Jacob M StillmanDepartment of Neurobiology, Brudnik Neuropsychiatric Research Institute, University of Massachusetts Chan Medical School, Worcester, MA, USA; University of Massachusetts Chan Morningside Graduate School of Biomedical Sciences, Neuroscience Program, Worcester, MA, USA.
University of Massachusetts Chan Medical School · US

Funding

Microglia-dependent mechanisms governing neural circuit plasticityR01MH113743 · NIMH · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI Dorothy Patricia Schafer · 2017 to 2026
$4.9M
How Do Synaptic Connections Change in Demyelinating Disease?R01NS117533 · NINDS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI SCHAFER, DOROTHY PATRICIA · 2021 to 2025
$2.2M
Dissecting the impact of senescence on microglia function and neurodegenerationRF1AG068281 · NIA · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI SCHAFER, DOROTHY PATRICIA, ZHANG, HONG · 2020 to 2020
$1.7M
Training in the Molecular Basis of Autoimmunity and AutoinflammationT32AI132152 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI Katherine A. Fitzgerald, Ann Marshak-Rothstein · 2018 to 2026
$1.6M
NIAID NIH HHS T32 AI132152NIA NIH HHS RF1 AG068281NIMH NIH HHS R01 MH113743NINDS NIH HHS R01 NS117533
6 · The paper itself

Abstract

During neurodegenerative disease, resident CNS macrophages termed "microglia" assume a neuroprotective role and engulf toxic protein aggregates and cell debris. In this issue of Cell, two groups independently show how spleen tyrosine kinase (SYK) acts downstream of microglial surface receptors to propagate this neuroprotective program in vivo.

Indexed as

MicrogliaNeurodegenerative DiseasesHumansMacrophagesSyk KinaseSyk KinaseSYK protein, human

Identifiers

PMID36306731
OpenAlexW4307816925

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.