PubMed · 6213942
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R Lycett. 1982-08-11. The caring network.. https://pubmed.ncbi.nlm.nih.gov/6213942/
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Down syndrome (DS) results from trisomy for human chromosome 21 and is the most frequent genetic cause of intellectual disability. No effective treatments currently exist that improve neurodevelopment and cognition. Atypical brain development in individuals with DS is apparent before birth, which suggests that the optimal time to begin administration of therapies is prenatally. Human neural progenitor cell (NPC) cultures provide a tractable in vitro model system to examine the effects of trisomy 21 (T21) on neurodevelopment and to measure the effects of pharmacological interventions. Here, we report the results of preclinical studies evaluating 24 candidate therapies. RNA sequencing analyses found that euploid and T21 NPCs showed different transcriptomic responses to five candidate pharmacotherapies. The Rho-associated coiled-coil kinase inhibitor fasudil increased proliferation of T21 NPCs, reduced expression of inflammatory pathway genes in T21 NPCs, and reduced markers of inflammation in LPS-stimulated microglial model systems. These results demonstrate that fasudil can alter multiple T21-associated abnormalities in a beneficial manner, suggesting that fasudil warrants further study as a candidate prenatal pharmacotherapy for DS.
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We have attempted to identify published descriptions and reports of skeletal remains, figurines and paintings of suggested or supposed instances of Down syndrome predating John Langdon Haydon Down's initial account of the condition in 1866. A review of the ascertained material in each of these categories has not provided, in our opinion, convincing evidence of presence of the syndrome, although that possibility is not excluded. In the interests of historical authenticity readers are invited to point out perceived errors or omissions in this presentation.