ArticleNature communications2026
Systematic multi-omic deconvolution of the clinical heterogeneity of Down syndrome.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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.
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Who cites it
1 citing paper in PubMed.
- Systematic multi-omic deconvolution of the clinical heterogeneity of Down syndrome.Nature communications · 2026Article
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Authors and funding
10 authors.
Funding
Abstract
Persons with Down syndrome, the genetic condition caused by trisomy 21, are at high risk of developing various co-occurring conditions affecting all major organ systems. Recent multi-omic studies have revealed the profound impacts of trisomy 21 on human biology, including strong effects on the transcriptome, proteome, metabolome, and immunome. However, it is unclear whether these changes are conserved effects of trisomy 21 versus effects associated with specific co-occurring conditions. Here we report a multi-omic investigation of 100 clinical phenotypes in a cohort of 356 individuals with Down syndrome, which identifies many phenotype-associated signatures of potential clinical significance. Obesity associates with the largest number of changes in the proteome and metabolome of persons with Down syndrome, with dysregulation of key hormonal, growth signaling, and neurotransmitter systems. Congenital heart defects associate with the strongest changes in the whole blood transcriptome, concurrent with interferon hyperactivity and immune remodeling. Key signatures dysregulated by trisomy 21 are exacerbated in those with seizure disorders, gastrointestinal conditions, and various cardiopulmonary diseases. These analyses implicate immune dysregulation as a driver of diverse clinical phenotypes in Down syndrome beyond canonical autoimmune disorders. Altogether, these results support the development of personalized medicine approaches for the clinical management of Down syndrome.
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