A new study published by scientists at the Salk Institute recently shows how that changes in the nucleolus of progeria cells and normally aged cells share some characteristics that may allow them to be used as a biomarker for biological age[1].

What is Progeria?

Hutchinson-Gilford progeria is a rare genetic disease that causes people to suffer from aging-like symptoms on an accelerated timescale compared to regular aging. Whilst it shares similarities with regular aging it is not accelerated aging per se, but the outcome is much the same.

The condition is due to a rare mutation in one of the structural proteins in the cell nucleus, lamin A, but it was not clear how a single defective protein in the nucleus causes the various aging-like features typical of this disease.

The research

The researchers first investigated if the mutation was causing the lamin A protein to become more unstable and thus shorter lived. After measuring the level of protein turnover in progeria cells and healthy cells, they found out that it was not just lamin A that was being affected by the disease.

The looked at all the proteins in the nucleus and rather than just the mutant lamin A experiencing rapid turnover, they saw a wide change in overall protein stability in progeria cells. This was quite a surprise for the researchers and suggests a change in protein metabolism with a broad range of effects just from one mutation to lamin A.

Next, the researchers looked at the nucleolus, which creates protein-assembling structures called ribosomes, was enlarged in the prematurely aging cells compared to healthy cells. Not only that, the team also discovered that the size of the nucleolus also increases in size with age.

This suggests that it may be possible to use the size of the nucleolus as a potential biomarker of aging as well as a possible target for therapies to counter progeria and even regular aging.


Whilst the first part of the experiment showing how one mutation caused a wide change in protein metabolism is intriguing, it was only the case in progeria cells.

The changes to the nucleolus size in both progeria and normal cells is of the most interest here in relation to regular aging. The observation is good news as there is an urgent need for effective aging biomarkers and for academia to reach a consensus on what panel of biomarkers is best to use in the lab for aging research.

The development of accurate and cost-effective biomarkers is something of great interest to the research community and here at LEAF, we are supporting the AgeMeter and MouseAge projects to develop new aging biomarkers.


[1] Buchwalter. A. & Hetzer. M (2017) Nucleolar expansion and elevated protein translation in premature aging. Nature Communications 8, Article number: 328


About the author

Steve Hill

Steve serves on the LEAF Board of Directors and is the Editor in Chief, coordinating the daily news articles and social media content of the organization. He is an active journalist in the aging research and biotechnology field and has to date written over 500 articles on the topic as well as attending various medical industry conferences. In 2019 he was listed in the top 100 journalists covering biomedicine and longevity research in the industry report – Top-100 Journalists covering advanced biomedicine and longevity created by the Aging Analytics Agency. His work has been featured in H+ magazine, Psychology Today, Singularity Weblog, Standpoint Magazine, and, Keep me Prime, and New Economy Magazine. Steve has a background in project management and administration which has helped him to build a united team for effective fundraising and content creation, while his additional knowledge of biology and statistical data analysis allows him to carefully assess and coordinate the scientific groups involved in the project. In 2015 he led the Major Mouse Testing Program (MMTP) for the International Longevity Alliance and in 2016 helped the team of the SENS Research Foundation to reach their goal for the OncoSENS campaign for cancer research.
  1. September 2, 2017

    I’m very much pro active in slowing down my aging
    Fasting,eating healthy, keystonic state ,ta 65 etc
    I’m 60 next April,and find I have to pull out my license
    To show Proof

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