{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,12]],"date-time":"2026-06-12T05:54:56Z","timestamp":1781243696274,"version":"3.54.1"},"reference-count":49,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2022,9,7]],"date-time":"2022-09-07T00:00:00Z","timestamp":1662508800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100021566","name":"Fundaci\u00f3n Isabel Gemio","doi-asserted-by":"publisher","award":["2018\/0200"],"award-info":[{"award-number":["2018\/0200"]}],"id":[{"id":"10.13039\/501100021566","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Annals of Neurology"],"published-print":{"date-parts":[[2022,11]]},"abstract":"<jats:sec><jats:title>Objective<\/jats:title><jats:p>Duchenne muscular dystrophy (DMD) exon 45\u201355 deletion (del45\u201355) has been postulated as a model that could treat up to 60% of DMD patients, but the associated clinical variability and complications require clarification. We aimed to understand the phenotypes and potential modifying factors of this dystrophinopathy subset.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>This cross\u2010sectional, multicenter cohort study applied clinical and functional evaluation. Next generation sequencing was employed to identify intronic breakpoints and their impact on the <jats:italic>Dp140<\/jats:italic> promotor, intronic long noncoding RNA, and regulatory splicing sequences. DMD modifiers (<jats:italic>SPP1, LTBP4, ACTN3<\/jats:italic>) and concomitant mutations were also assessed. Haplotypes were built using <jats:italic>DMD<\/jats:italic> single nucleotide polymorphisms. Dystrophin expression was evaluated via immunostaining, Western blotting, reverse transcription polymerase chain reaction (PCR), and droplet digital PCR in 9 muscle biopsies.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>The series comprised 57 subjects (23 index) expressing Becker phenotype (28%), isolated cardiopathy (19%), and asymptomatic features (53%). Cognitive impairment occurred in 90% of children. Patients were classified according to 10 distinct index\u2010case breakpoints; 4 of them were recurrent due to founder events. A specific breakpoint (D5) was associated with severity, but no significant effect was appreciated due to the changes in intronic sequences. All biopsies showed dystrophin expression of &gt;67% and traces of alternative del45\u201357 transcript that were not deemed pathogenically relevant. Only the <jats:italic>LTBP4<\/jats:italic> haplotype appeared associated the presence of cardiopathy among the explored extragenic factors.<\/jats:p><\/jats:sec><jats:sec><jats:title>Interpretation<\/jats:title><jats:p>We confirmed that del45\u201355 segregates a high proportion of benign phenotypes, severe cases, and isolated cardiac and cognitive presentations. Although some influence of the intronic breakpoint position and the <jats:italic>LTBP4<\/jats:italic> modifier may exist, the pathomechanisms responsible for the phenotypic variability remain largely unresolved. 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