Evidence map›Paper›PMID 36890585›Full record

ArticleActa neuropathologica communications2023

Neurofibromatosis type 1-dependent alterations in mouse microglia function are not cell-intrinsic.

Francesca Logiacco, Laura Cathleen Grzegorzek, Elizabeth C Cordell, Oliver Popp, Philipp Mertins, David H Gutmann, Helmut Kettenmann, Marcus Semtner

Open access · goldAbstract read
In one paragraph

Article in Acta neuropathologica communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.5field-weighted citation impact, top 37% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
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

8 authors at 4 institutions in 3 countries.

Francesca LogiaccoCellular Neurosciences, Max-Delbrück-Center for Molecular Medicine in the Helmholtz Association, 13125, Berlin, Germany.
Laura Cathleen GrzegorzekCellular Neurosciences, Max-Delbrück-Center for Molecular Medicine in the Helmholtz Association, 13125, Berlin, Germany.
Elizabeth C CordellDepartment of Neurology, Washington University School of Medicine, St. Louis, MO, 63110, USA.
Oliver PoppProteomics Platform, Max-Delbrück-Center for Molecular Medicine in the Helmholtz Association, 13125, Berlin, Germany.
Philipp MertinsProteomics Platform, Max-Delbrück-Center for Molecular Medicine in the Helmholtz Association, 13125, Berlin, Germany.
David H GutmannDepartment of Neurology, Washington University School of Medicine, St. Louis, MO, 63110, USA.
Helmut KettenmannCellular Neurosciences, Max-Delbrück-Center for Molecular Medicine in the Helmholtz Association, 13125, Berlin, Germany.
Marcus SemtnerCellular Neurosciences, Max-Delbrück-Center for Molecular Medicine in the Helmholtz Association, 13125, Berlin, Germany. marcus.semtner@mdc-berlin.de.
Max Delbrück Center · DEWashington University in St. Louis · USBerlin Institute of Health at Charité - Universitätsmedizin Berlin · DEShenzhen Institutes of Advanced Technology · CN

Funding

Defining the Mechanistic Basis for Neurofibromatosis-1 Nervous System Disease HeterogeneityR35NS097211 · NINDS · WASHINGTON UNIVERSITY · PI GUTMANN, DAVID H · 2017 to 2024
$5.7M
Neuronal Regulation of Low-Grade GliomagenesisR01CA258384 · NCI · STANFORD UNIVERSITY · PI David H Gutmann, Michelle Monje-Deisseroth · 2022 to 2026
$3.1M
NCI NIH HHS R01 CA258384NINDS NIH HHS R35 NS097211
6 · The paper itself

Abstract

We previously discovered a sex-by-genotype defect in microglia function using a heterozygous germline knockout mouse model of Neurofibromatosis type 1 (Nf1 ± mice), in which only microglia from male Nf1 ± mice exhibited defects in purinergic signaling. Herein, we leveraged an unbiased proteomic approach to demonstrate that male, but not female, heterozygous Nf1 ± microglia exhibit differences in protein expression, which largely reflect pathways involved in cytoskeletal organization. In keeping with these predicted defects in cytoskeletal function, only male Nf1 ± microglia had reduced process arborization and surveillance capacity. To determine whether these microglial defects were cell autonomous or reflected adaptive responses to Nf1 heterozygosity in other cells in the brain, we generated conditional microglia Nf1-mutant knockout mice by intercrossing Nf1

Indexed as

Neurofibromatosis 1AnimalsBrainMaleMiceMice, KnockoutMicrogliaProteomicsCortexGenetically engineered miceMicrogliaNeurofibrominNF1Purinergic signalingSex differences

Identifiers

PMID36890585
PMCPMC9996880
OpenAlexW4323536760

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.