Evidence map›Paper›PMID 40568906›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

Inhibition of Phosphodiesterase 10A by MP-10 Rescues Behavioral Deficits and Normalizes Microglial Morphology and Synaptic Pruning in A Mouse Model of FOXP1 Syndrome.

Henning Fröhlich, Jing Wang, Ferdinand Althammer, Tim Schubert, Nina Kluck, Valery Grinevich, Stefanie Schmitteckert, Christian P Schaaf, Gudrun A Rappold

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

9 authors.

Henning FröhlichInstitute of Human Genetics, Heidelberg University, 69120, Heidelberg, Germany.ORCID 0000-0002-9757-2034
Jing WangInstitute of Human Genetics, Heidelberg University, 69120, Heidelberg, Germany.
Ferdinand AlthammerInstitute of Human Genetics, Heidelberg University, 69120, Heidelberg, Germany.
Tim SchubertInstitute of Human Genetics, Heidelberg University, 69120, Heidelberg, Germany.
Nina KluckInstitute of Human Genetics, Heidelberg University, 69120, Heidelberg, Germany.
Valery GrinevichDepartment of Neuropeptide Research in Psychiatry, Central Institute of Mental Health, Medical Faculty Mannheim, Heidelberg University, 69120, Mannheim, Germany.
Stefanie SchmitteckertInstitute of Human Genetics, Heidelberg University, 69120, Heidelberg, Germany.
Christian P SchaafInstitute of Human Genetics, Heidelberg University, 69120, Heidelberg, Germany.
Gudrun A RappoldInstitute of Human Genetics, Heidelberg University, 69120, Heidelberg, Germany.

Funding

Deutsche Forschungsgemeinschaft 517366075Deutsche Forschungsgemeinschaft FR 3990/3-1
6 · The paper itself

Abstract

FOXP1 syndrome caused by FOXP1 haploinsufficiency is characterized by intellectual disability, speech, and language impairment, autistic features, and neuropsychiatric abnormalities such as anxiety and hyperactivity. Behavioral changes in patients are mirrored in Foxp1

Indexed as

Forkhead Transcription FactorsMicrogliaNeuronal PlasticityPhosphoric Diester HydrolasesRepressor ProteinsAnimalsBehavior, AnimalDisease Models, AnimalMaleMiceForkhead Transcription FactorsFoxp1 protein, mousePde10a protein, mousePhosphoric Diester HydrolasesRepressor ProteinsFOXP1 syndromemouse modelMP‐10 (PF‐2545920)Pde10atreatment

Identifiers

PMID40568906
PMCPMC12462984

What OpenQuestion holds

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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.