Research press release




特定の早老症候群は、DNA修復機構の欠陥を原因とし、DNA損傷の持続と老化促進を引き起こす。これと同じようなDNA修復機構の欠陥を有するマウスは、寿命が約4~6か月以下だが、食餌制限による抗老化応答に似た生存応答の兆候も示している。今回、Jan Hoeijmakersたちは、DNA修復欠損マウスに食餌制限を行うことで、こうした防御応答を増強できることを明らかにした。このマウスの食物摂取量を30%制限したところ、残りの寿命が3倍の長さになり、数々の老化促進の特徴が抑制された。例えば、食餌制限をしたマウスは、自由に食物を摂取したマウスと比べて、保持される神経細胞が50%多かった。


Dietary restriction slows accelerated ageing and protects against DNA damage in mice that model certain human progeroid syndromes - disorders that cause premature ageing. These findings, reported in Nature this week, help us to learn more about the beneficial effects of dietary restriction and may aid the discovery of treatments for ageing disorders.

Certain progeroid syndromes are driven by faulty DNA repair machinery, which leads to persistent DNA damage and accelerated ageing. Mice with similarly compromised DNA repair have lifespans limited to around 4-6 months or less, but also show signs of a survival response that resembles the anti-ageing response induced by dietary restriction. Jan Hoeijmakers and colleagues find that these protective responses can be enhanced by restricting the diet of DNA-repair-deficient mice. A 30% restriction in food intake is shown to triple the remaining lifespan of these mice and supresses numerous features of accelerated ageing; for example, mice subjected to dietary restriction retained 50% more nerve cells compared with their counterparts that could eat as much as they wanted.

The authors propose that therapies mimicking the effects of dietary restriction could be used to treat progeroid syndromes and possibly neurodegeneration. However, it remains to be confirmed if the dietary restriction effect is preserved from mice to man.

doi: 10.1038/nature19329

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