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Stem cells

Down's syndrome link to ageing

Nature volume 501, pages 325–326 (2013)Cite this article

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Triplication of the enzyme USP16 in models of Down's syndrome creates defects in the stem cells resident in adult tissues. This finding provides insight into stem-cell homeostasis during ageing. See Article p.380

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Figure 1: An altered threshold for stress.

Notes

  1. *This article and the paper under discussion1 were published online on 11 September 2013.

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Authors and Affiliations

  1. George P. Souroullas and Norman E. Sharpless are in the Departments of Medicine and Genetics, Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, North Carolina 27599-7295, USA.,

    George P. Souroullas & Norman E. Sharpless

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  1. George P. Souroullas
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  2. Norman E. Sharpless
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Correspondence to Norman E. Sharpless.

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Souroullas, G., Sharpless, N. Down's syndrome link to ageing. Nature 501, 325–326 (2013). https://doi.org/10.1038/nature12558

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  1. Peter Gibson

    The review by Souroullas and Sharpless suggests trisomy found in Down?s syndrome is concerned with an increase in the number of proteins and perhaps none coding RNA. This appears to under estimate the totality of the problem. There are numerous examples where the number of chromosomes has been increased without ill effect. Many animals go in for polyploidy and earthworms are a good example. In secretory cell such as the salivary gland has vastly increased its DNA. One might argue that there is a positive advantage in increasing chromosome numbers. Much of evolution has depended, not on mutations but adjusting chromosome numbers either up or down. The molecular mechanisms that might account for these alterations may be trivial. It is a technical problem. As the authors say Down?s does not show significant defects in DNA metabolism and repair.
    The associations between Alzheimer?s disease and aging have been discussed at length over the decades. The problem is less is known about aging than Alzheimer?s. Alzheimer?s is often been seen as a model for aging. A mass of detrimental molecular alterations are seen in both. Attention has generally been focused on single aspect of these two as for example in Prion diseases.
    An aspect of these problems that has been ignored is the effect of methylation. These appear to have transgenic influences. That is, they control development that extends beyond the lifetime of individuals. One might therefore argue that aging is itself on epigenetic phenomenon. The resulting diseases may be a knock on effect. Attention should perhaps be shifted away from the minutia of how molecules interact to general aspects of a large range of types of animals and how they have in effect dealt with the problem of aging.

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