Research press release



Ageing: Increasing cellular recycling process extends life and health of mice



これまでの研究でBeth Levineたちは、beclin1タンパク質に特定の変異があるマウスは脳と筋肉におけるオートファジーが増加し、この変異によってアルツハイマー病のマウスモデルの認知機能が改善することを示していた。Levineたちは、今回の研究でbeclin1変異マウスの寿命が延びただけでなく、さまざまな老化関連表現型(例えば、心臓疾患、腎臓疾患、腫瘍の発生)が減少して、健康寿命も延びたことを明らかにした。また、beclin1の変異は、抗老化タンパク質klothoの欠損を原因とするマウスの早期死亡と不妊を救済できることも分かった。


A mutation in a protein crucial to the cellular process of autophagy is shown to increase both healthspan and lifespan in a study in mice published online in Nature this week.

Autophagy, an evolutionarily conserved protein degradation pathway that removes dysfunctional cellular components and recycles their building blocks, promotes increased lifespan in model organisms; however, its role in promoting mammalian longevity is not well understood.

Beth Levine and colleagues previously showed that mice with a specific mutation in the protein beclin1 had increased autophagy in brain and muscle, and that this mutation improved cognitive function in mouse models of Alzheimer’s disease. Here, the same authors report that these mice have not only a longer lifespan, but also an improved healthspan as various ageing-related phenotypes, such as heart and kidney disease and tumour development, are reduced. The same beclin1 mutation is also able to rescue the early lethality and infertility in mice caused by a deficiency of the anti-ageing protein klotho.

The authors conclude that this mutation, which works by releasing beclin1 from its negative regulators, may be an effective mechanism to increase autophagy, prevent premature ageing, improve healthspan and promote longevity in mammals.

doi: 10.1038/s41586-018-0160-9|英語の原文

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