Francesco Catapano, Reem Alkharji, Darren Chambers, Simran Singh, Artadokht Aghaeipour, Jyoti Malhotra, Patrizia Ferretti, Rahul Phadke, Francesco Muntoni
{"title":"发育和成人大脑中肌营养不良蛋白异构体表达的综合时空图。","authors":"Francesco Catapano, Reem Alkharji, Darren Chambers, Simran Singh, Artadokht Aghaeipour, Jyoti Malhotra, Patrizia Ferretti, Rahul Phadke, Francesco Muntoni","doi":"10.1186/s40478-025-01996-z","DOIUrl":null,"url":null,"abstract":"<p><p>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.</p>","PeriodicalId":6914,"journal":{"name":"Acta Neuropathologica Communications","volume":"13 1","pages":"110"},"PeriodicalIF":5.7000,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12096690/pdf/","citationCount":"0","resultStr":"{\"title\":\"A comprehensive spatiotemporal map of dystrophin isoform expression in the developing and adult human brain.\",\"authors\":\"Francesco Catapano, Reem Alkharji, Darren Chambers, Simran Singh, Artadokht Aghaeipour, Jyoti Malhotra, Patrizia Ferretti, Rahul Phadke, Francesco Muntoni\",\"doi\":\"10.1186/s40478-025-01996-z\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>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.</p>\",\"PeriodicalId\":6914,\"journal\":{\"name\":\"Acta Neuropathologica Communications\",\"volume\":\"13 1\",\"pages\":\"110\"},\"PeriodicalIF\":5.7000,\"publicationDate\":\"2025-05-21\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12096690/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Acta Neuropathologica Communications\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1186/s40478-025-01996-z\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"NEUROSCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Acta Neuropathologica Communications","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1186/s40478-025-01996-z","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
A comprehensive spatiotemporal map of dystrophin isoform expression in the developing and adult human brain.
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.
期刊介绍:
"Acta Neuropathologica Communications (ANC)" is a peer-reviewed journal that specializes in the rapid publication of research articles focused on the mechanisms underlying neurological diseases. The journal emphasizes the use of molecular, cellular, and morphological techniques applied to experimental or human tissues to investigate the pathogenesis of neurological disorders.
ANC is committed to a fast-track publication process, aiming to publish accepted manuscripts within two months of submission. This expedited timeline is designed to ensure that the latest findings in neuroscience and pathology are disseminated quickly to the scientific community, fostering rapid advancements in the field of neurology and neuroscience. The journal's focus on cutting-edge research and its swift publication schedule make it a valuable resource for researchers, clinicians, and other professionals interested in the study and treatment of neurological conditions.