Evidence map›Paper›PMID 40400011›Full record

ArticleActa neuropathologica communications2025

A comprehensive spatiotemporal map of dystrophin isoform expression in the developing and adult human brain.

Francesco Catapano, Reem Alkharji, Darren Chambers, Simran Singh, Artadokht Aghaeipour, Jyoti Malhotra, Patrizia Ferretti, Rahul Phadke, Francesco Muntoni

Abstract read
In one paragraph

Article in Acta neuropathologica communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

  1. Article
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  5. Behavioral improvement in dystrophicMolecular therapy. Nucleic acids · 2025
    Article
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  8. Review
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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

9 authors.

Francesco CatapanoThe Dubowitz Neuromuscular Centre, Developmental Neurosciences Programme, Great Ormond Street Institute of Child Health, University College London, 30 Guilford Street, London, WC1N 1EH, UK.
Reem AlkharjiDevelopmental Biology and Cancer Department, UCL Great Ormond Street Institute of Child Health, London, WC1N 1EH, UK.
Darren ChambersThe Dubowitz Neuromuscular Centre, Developmental Neurosciences Programme, Great Ormond Street Institute of Child Health, University College London, 30 Guilford Street, London, WC1N 1EH, UK.
Simran SinghThe Dubowitz Neuromuscular Centre, Developmental Neurosciences Programme, Great Ormond Street Institute of Child Health, University College London, 30 Guilford Street, London, WC1N 1EH, UK.
Artadokht AghaeipourThe Dubowitz Neuromuscular Centre, Developmental Neurosciences Programme, Great Ormond Street Institute of Child Health, University College London, 30 Guilford Street, London, WC1N 1EH, UK.
Jyoti MalhotraSarepta Therapeutics Lnc., Cambridge, MA, USA.
Patrizia FerrettiDevelopmental Biology and Cancer Department, UCL Great Ormond Street Institute of Child Health, London, WC1N 1EH, UK.
Rahul PhadkeThe Dubowitz Neuromuscular Centre, Developmental Neurosciences Programme, Great Ormond Street Institute of Child Health, University College London, 30 Guilford Street, London, WC1N 1EH, UK.
Francesco MuntoniThe Dubowitz Neuromuscular Centre, Developmental Neurosciences Programme, Great Ormond Street Institute of Child Health, University College London, 30 Guilford Street, London, WC1N 1EH, UK. f.muntoni@ucl.ac.uk.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mutations in the dystrophin gene (DMD) cause the severe muscle-wasting disease Duchenne muscular dystrophy (DMD). Additionally, there is a high incidence of intellectual disability and neurobehavioural comorbidities in individuals with DMD. Similar behavioural abnormalities are found in mdx dystrophic mouse models. Unlike muscle, several dystrophin isoforms are expressed in the human brain, but a detailed map of regional and cellular localisation of dystrophin isoforms is missing. This is crucial in understanding the neuropathology of DMD individuals, and for evaluating the translatability of pre-clinical findings in DMD mouse models receiving genetic therapy interventions. Here, we provide a comprehensive dystrophin expression profile in human brains from early development to adulthood. We reveal expression of dp427p2, dp427c, dp427m and dp40 isoforms in human embryonic brains, not previously reported. We also detected dp427p2 expression and developmental regulation in human brain across the lifespan. In addition we showed by in situ hybridisation that dp140 was greatly downregulated in adult brains. Importantly, our data also demonstrate expression of DMD transcripts in human motor neurons and co-expression of different dystrophin isoforms within single neurons in both developing and adult brains. Finally, we show localisation of DMD transcripts with GAD1+ GABAergic-associated transcripts in neurons including cerebellar Purkinje cells and interneurons, as well as in the majority of neocortical and hippocampal SLC17A7+ glutamatergic neurons, suggesting a role for dystrophin in signalling at the neuronal inhibitory and excitatory synapses.

Indexed as

BrainDystrophinAdolescentAdultChildChild, PreschoolFemaleGlutamate DecarboxylaseHumansInfantMaleMiddle AgedMuscular Dystrophy, DuchenneProtein IsoformsYoung AdultDystrophinGlutamate DecarboxylaseProtein IsoformsDuchenne muscular dystrophyDystrophinGABAergic neuronGlutamergic neuronsHuman brainIntellectual disabilityPurkinje neurons

Identifiers

PMID40400011
PMCPMC12096690

What Socratic holds

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LicenceCC BY-NC-ND
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Registered trials

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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.