Evidence map›Paper›PMID 42365367›Full record

ArticleJournal of neuroinflammation2026

Csf1r-mediated depletion of myeloid cells prevents dopaminergic neuron loss during chronic colitis.

Rebecca Katharina Kutscherauer, Marie Andert, Iris Stolzer, Emely Elisa Neumaier, Mark Dedden, Pavel Kielkowski, Wei Xiang, Alexander Grotemeyer, Marco Prinz, Takahiro Masuda and 7 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of neuroinflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

17 authors.

Rebecca Katharina KutscherauerDepartment of Molecular Neurology, Universitätsklinikum Erlangen, Friedrich- Alexander-Universität Erlangen-Nürnberg, University Hospital Erlangen, Erlangen, Germany.
Marie AndertDepartment of Molecular Neurology, Universitätsklinikum Erlangen, Friedrich- Alexander-Universität Erlangen-Nürnberg, University Hospital Erlangen, Erlangen, Germany.
Iris StolzerDepartment of Medicine 1, Universitätsklinikum Erlangen, Friedrich-Alexander- Universität Erlangen-Nürnberg, Erlangen, Germany.
Emely Elisa NeumaierDepartment of Medicine 1, Universitätsklinikum Erlangen, Friedrich-Alexander- Universität Erlangen-Nürnberg, Erlangen, Germany.
Mark DeddenDepartment of Medicine 1, Universitätsklinikum Erlangen, Friedrich-Alexander- Universität Erlangen-Nürnberg, Erlangen, Germany.
Pavel KielkowskiDepartment of Chemistry, Ludwig-Maximilians-Universität München, München, Germany.
Wei XiangDepartment of Molecular Neurology, Universitätsklinikum Erlangen, Friedrich- Alexander-Universität Erlangen-Nürnberg, University Hospital Erlangen, Erlangen, Germany.
Alexander GrotemeyerDepartment of Molecular Neurology, Universitätsklinikum Erlangen, Friedrich- Alexander-Universität Erlangen-Nürnberg, University Hospital Erlangen, Erlangen, Germany.
Marco PrinzInstitute of Neuropathology, Medical Faculty, University of Freiburg, Freiburg, Germany.
Takahiro MasudaDivision of Molecular Neuroimmunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
Klaus-Peter KnobelochInstitute of Neuropathology, Medical Faculty, University of Freiburg, Freiburg, Germany.
Veit RothhammerDepartment of Neurology, Universitätsklinikum Erlangen, Friedrich-Alexander- Universität Erlangen-Nürnberg, Erlangen, Germany.
Sebastian ZundlerDepartment of Medicine 1, Universitätsklinikum Erlangen, Friedrich-Alexander- Universität Erlangen-Nürnberg, Erlangen, Germany.
Johannes C M SchlachetzkiDepartment of Neurosciences, University of California, San Diego, USA.
Jürgen WinklerDepartment of Molecular Neurology, Universitätsklinikum Erlangen, Friedrich- Alexander-Universität Erlangen-Nürnberg, University Hospital Erlangen, Erlangen, Germany.
Claudia GüntherDepartment of Medicine 1, Universitätsklinikum Erlangen, Friedrich-Alexander- Universität Erlangen-Nürnberg, Erlangen, Germany.
Patrick SüßDepartment of Molecular Neurology, Universitätsklinikum Erlangen, Friedrich- Alexander-Universität Erlangen-Nürnberg, University Hospital Erlangen, Erlangen, Germany. patrick.suess@uk-erlangen.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammatory bowel disease (IBD) predisposes to neuropsychiatric comorbidity and increases the risk of Parkinson's Disease (PD). Although the gut-immune-brain axis was proposed as a link between IBD and PD and a driver of PD immunopathogenesis, the regional pattern and single-cell landscape of the brain immune response during colitis and its contribution to PD pathology remain poorly defined. Here, we observe a loss of dopaminergic neurons and synuclein pathology in the substantia nigra pars compacta of adult mice with chronic colitis. By confocal microscopy and integrated multi-omics, we reveal a complex midbrain-specific immune response to chronic colitis. Single-cell mapping of the midbrain immune landscape showed an inflammatory shift of microglial clusters including an expansion of interferon-response microglia, CD8

Indexed as

ColitisDopaminergic NeuronsMyeloid CellsReceptors, Granulocyte-Macrophage Colony-Stimulating FactorAnimalsChronic DiseaseMaleMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMicrogliaCsf1r protein, mouseReceptors, Granulocyte-Macrophage Colony-Stimulating FactorColony-stimulating factor 1 receptorGut-immune-brain axisInflammatory bowel diseaseMicrogliaParkinson’s Disease

Identifiers

PMID42365367
PMCPMC13309958

What Socratic 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 Socratic graph.