https://phys.org/news/2020-01-bi ... hways-lifespan.html
Biologists identify pathways that extend lifespan by 500%
by Mount Desert Island Biological Laboratory

Jarod A. Rollins of the MDI Biological Laboratory in Bar Harbor, Maine, is a lead author of a recent scientific paper that identifies synergistic cellular pathways for longevity that amplify lifespan fivefold in C. elegans, a nematode worm used as a model in aging research. The increase in lifespan would be the equivalent of a human living for 400 or 500 years. The discovery of the synergistic effect opens the door to new, more effective anti-aging therapies. Credit: MDI Biological Laboratory
Scientists at the MDI Biological Laboratory, in collaboration with scientists from the Buck Institute for Research on Aging in Novato, Calif., and Nanjing University in China, have identified synergistic cellular pathways for longevity that amplify lifespan fivefold in C. elegans, a nematode worm used as a model in aging research.


The increase in lifespan would be the equivalent of a human living for 400 or 500 years, according to one of the scientists.

The research draws on the discovery of two major pathways governing aging in C. elegans, which is a popular model in aging research because it shares many of its genes with humans and because its short lifespan of only three to four weeks allows scientists to quickly assess the effects of genetic and environmental interventions to extend healthy lifespan.

Because these pathways are "conserved," meaning that they have been passed down to humans through evolution, they have been the subject of intensive research. A number of drugs that extend healthy lifespan by altering these pathways are now under development. The discovery of the synergistic effect opens the door to even more effective anti-aging therapies.

The new research uses a double mutant in which the insulin signaling (IIS) and TOR pathways have been genetically altered. Because alteration of the IIS pathways yields a 100 percent increase in lifespan and alteration of the TOR pathway yields a 30 percent increase, the double mutant would be expected to live 130 percent longer. But instead, its lifespan was amplified by 500 percent.

"Despite the discovery in C. elegans of cellular pathways that govern aging, it hasn't been clear how these pathways interact," said Hermann Haller, M.D., president of the MDI Biological Laboratory. "By helping to characterize these interactions, our scientists are paving the way for much-needed therapies to increase healthy lifespan for a rapidly aging population."

The elucidation of the cellular mechanisms controlling the synergistic response is the subject of a recent paper in the online journal Cell Reports entitled "Translational Regulation of Non-autonomous Mitochondrial Stress Response Promotes Longevity." The authors include Jarod A. Rollins, Ph.D., and Aric N. Rogers, Ph.D., of the MDI Biological Laboratory.

"The synergistic extension is really wild," said Rollins, who is the lead author with Jianfeng Lan, Ph.D., of Nanjing University. "The effect isn't one plus one equals two, it's one plus one equals five. Our findings demonstrate that nothing in nature exists in a vacuum; in order to develop the most effective anti-aging treatments we have to look at longevity networks rather than individual pathways."

The discovery of the synergistic interaction could lead to the use of combination therapies, each affecting a different pathway, to extend healthy human lifespan in the same way that combination therapies are used to treat cancer and HI**kaj Kapahi, Ph.D., of the Buck Institute, has said. Kapahi is a corresponding author of the paper with Rogers and Di Chen, Ph.D., of Nanjing University.

The synergistic interaction may also may explain why scientists have been unable to identify a single gene responsible for the ability of some people to live to extraordinary old ages free of major age-related diseases until shortly before their deaths.

The paper focuses on how longevity is regulated in the mitochondria, which are the organelles in the cell responsible for energy homeostasis. Over the last decade, accumulating evidence has suggested a causative link between mitochondrial dysregulation and aging. Rollins' future research will focus on the further elucidation of the role of mitochondria in aging, he said.

我简单概括下：要想长寿学英文

能让线虫长寿的方法应该超过几十种了吧。。。然而那又有什么用

Biologists identify pathways that extend lifespan by 500% 生物学家发现了可以延长500% 寿命的途径
by Mount Desert Island Biological Laboratory 芒特迪瑟特岛生物实验室

Jarod A. Rollins of the MDI Biological Laboratory in Bar Harbor, Maine, is a lead author of a recent scientific paper that identifies synergistic cellular pathways for longevity that amplify lifespan fivefold in C. elegans, a nematode worm used as a model in aging research. The increase in lifespan would be the equivalent of a human living for 400 or 500 years. The discovery of the synergistic effect opens the door to new, more effective anti-aging therapies. Credit: MDI Biological Laboratory 缅因州巴尔港 MDI 生物实验室的 Jarod a. Rollins 是最近一篇科学论文的主要作者，这篇论文确定了协同作用的细胞通路延长秀丽隐杆线虫寿命的方法，这是一种用作衰老研究模型的线虫。 寿命的延长相当于一个人活400或500年。 协同效应的发现为新的、更有效的抗衰老疗法打开了大门。 提供者: MDI 生物实验室
Scientists at the MDI Biological Laboratory, in collaboration with scientists from the Buck Institute for Research on Aging in Novato, Calif., and Nanjing University in China, have identified synergistic cellular pathways for longevity that amplify lifespan fivefold in C. elegans, a nematode worm used as a model in aging research. Mdi 生物实验室的科学家与来自诺瓦托老化研究所和中国南京大学的科学家合作，已经确定了协同作用的延长寿命的细胞途径，这种途径可以将线虫的寿命延长5倍，这是一种用于老化研究的线虫模型


The increase in lifespan would be the equivalent of a human living for 400 or 500 years, according to one of the scientists. 根据一位科学家的说法，寿命的延长相当于一个人活400到500年

The research draws on the discovery of two major pathways governing aging in C. elegans, which is a popular model in aging research because it shares many of its genes with humans and because its short lifespan of only three to four weeks allows scientists to quickly assess the effects of genetic and environmental interventions to extend healthy lifespan. 这项研究利用了控制秀丽隐杆线虫衰老的两个主要途径的发现，这是衰老研究中的一个流行模型，因为它与人类有许多相同的基因，并且因为它只有三到四周的短寿命，科学家可以快速评估基因和环境干预对延长健康寿命的影响

Because these pathways are "conserved," meaning that they have been passed down to humans through evolution, they have been the subject of intensive research. A number of drugs that extend healthy lifespan by altering these pathways are now under development. The discovery of the synergistic effect opens the door to even more effective anti-aging therapies. 因为这些通路是“保守的” ，也就是说它们是通过进化遗传给人类的，所以它们一直是密集研究的对象。 一些通过改变这些途径来延长健康寿命的药物目前正在开发中。 协同效应的发现为更有效的抗衰老疗法打开了大门

The new research uses a double mutant in which the insulin signaling (IIS) and TOR pathways have been genetically altered. Because alteration of the IIS pathways yields a 100 percent increase in lifespan and alteration of the TOR pathway yields a 30 percent increase, the double mutant would be expected to live 130 percent longer. But instead, its lifespan was amplified by 500 percent. 这项新的研究使用了一种双突变体，其中胰岛素信号(IIS)和 TOR 通路已经被基因改变。 由于 IIS 通路的改变会使寿命增加100% ，而 TOR 通路的改变会使寿命增加30% ，因此这种双突变体的寿命预计会增加130% 。 然而，它的寿命却被放大了500%

"Despite the discovery in C. elegans of cellular pathways that govern aging, it hasn't been clear how these pathways interact," said Hermann Haller, M.D., president of the MDI Biological Laboratory. "By helping to characterize these interactions, our scientists are paving the way for much-needed therapies to increase healthy lifespan for a rapidly aging population." Mdi 生物实验室主席、医学博士赫尔曼 · 哈勒说: “尽管在线虫中发现了控制衰老的细胞通路，但这些通路是如何相互作用的还不清楚。”。 “通过帮助描述这些相互作用，我们的科学家正在为急需的治疗方法铺平道路，以延长快速老龄化人口的健康寿命。”

The elucidation of the cellular mechanisms controlling the synergistic response is the subject of a recent paper in the online journal Cell Reports entitled "Translational Regulation of Non-autonomous Mitochondrial Stress Response Promotes Longevity." The authors include Jarod A. Rollins, Ph.D., and Aric N. Rogers, Ph.D., of the MDI Biological Laboratory. 控制协同反应的细胞机制的阐明是最近发表在在线杂志《细胞报告》上的一篇论文的主题，题为“非自主的线粒体应激反应的翻译调节促进长寿” 作者包括 MDI 生物实验室的 Jarod a. Rollins 博士和 Aric n. Rogers 博士

"The synergistic extension is really wild," said Rollins, who is the lead author with Jianfeng Lan, Ph.D., of Nanjing University. "The effect isn't one plus one equals two, it's one plus one equals five. Our findings demonstrate that nothing in nature exists in a vacuum; in order to develop the most effective anti-aging treatments we have to look at longevity networks rather than individual pathways." “这种协同扩展真的很疯狂，”罗林斯说，他是南京大学蓝博士的第一作者。 “效果不是一加一等于二，而是一加一等于五。 我们的研究结果表明，自然界中没有什么东西是真空存在的; 为了开发最有效的抗衰老治疗方法，我们必须着眼于长寿网络，而不是个体通路。”

The discovery of the synergistic interaction could lead to the use of combination therapies, each affecting a different pathway, to extend healthy human lifespan in the same way that combination therapies are used to treat cancer and HI**kaj Kapahi, Ph.D., of the Buck Institute, has said. Kapahi is a corresponding author of the paper with Rogers and Di Chen, Ph.D., of Nanjing University. 这种协同作用的发现可能会导致联合疗法的使用，每种疗法影响不同的通路，以延长健康人的寿命，就像联合疗法用于治疗癌症一样。 卡帕希是本文的通讯作者，罗杰斯和南京大学陈博士合著

The synergistic interaction may also may explain why scientists have been unable to identify a single gene responsible for the ability of some people to live to extraordinary old ages free of major age-related diseases until shortly before their deaths. 这种协同作用也可能解释为什么科学家们一直无法确定一个单一的基因，这个基因决定了一些人能够在没有与年龄有关的主要疾病的情况下活到特别的老年，直到他们死亡前不久

The paper focuses on how longevity is regulated in the mitochondria, which are the organelles in the cell responsible for energy homeostasis. Over the last decade, accumulating evidence has suggested a causative link between mitochondrial dysregulation and aging. Rollins' future research will focus on the further elucidation of the role of mitochondria in aging, he said. 这篇论文的重点在于线粒体是如何调节寿命的，线粒体是细胞中负责能量稳态的细胞器。 在过去的十年中，越来越多的证据表明线粒体失调和衰老之间存在因果关系。 他说，罗林斯未来的研究将集中在线粒体在衰老中的作用的进一步阐明

感觉我的生命无端的浪费了2分钟。

300岁才能退休🤣

失眠500年可受不了 iOS fly ~

我觉得应该去研究乌龟

人类太复杂了，要延长寿命真的几乎就是逆天而行。

不过，现在大家在研发的各种抗癌药，各种先进细胞治疗工具其实就是长生不老药啊。 iOS fly ~

是不是真的，可以关注一下人类顶端的那几个人的寿命。。。HiPDA·NG

放心 各国首富政要比你们更关心 只要有一丝可能性 要啥给啥

修道。
比如张至顺老道长，104岁仙逝的，那是2015年。
而他差不多是民国时拜师的。
而他的师爷王圆吉，是乾隆年间人。
你们算算，要么他师傅要么他师爷，肯定有一位超级长寿的。
这样的例子，在修道界很常见

线虫和人类差距也太大了
全是噱头，远着呢

魔改人类

很多法老统治时间长达几百年

就怕那时候单身狗会更多…… iOS fly ~

跟咱们三皇五帝时候的历史差不多可靠

首先需要有可信的身份信息记录

反正他们没户口出生证明，想怎么编就怎么编，70岁说90岁，80岁说100岁，也无人能看的出来

话说要是修道能活200年，但是那种生活方式就是能活500年又有什么意义呢？

回复14#zhanghe


zhanghe兄弟是否方便加微信交流？想向你学习一些益寿延年的法门。

如果一种药的最佳剂量，临床试验的结论，成人 一天3次，一次一粒，请问3岁儿童怎么吃法？
15公斤体重的儿童和30公斤的儿童，每天给药量是2倍关系吗？

楼上诸位如果以上问题搞清楚了，就不会把线虫的试验随便放大到人身上了。

性能力也要与时俱进才行，否则后面450年萎着，想想就……

给特朗普先吃上

你抽烟吗？你喝酒吗？你有女朋友吗？
如果都是否定的答案，那活那么久有什么意义？

回复28#零号

对，再配个400岁的老太婆HiPDA·NG

看看长阿含经里就有，人寿2w岁也不稀奇啊 。都是福报。还有身高也很高。杀业重就会短寿。

龟类的平均寿命也就四十岁上下，大型海龟有过100的。所以说啊，想要长寿还得去留学

我40已经觉得活够了，又不太想自我了断。
500年真是折磨啊。 iOS fly ~

不解决癌症问题没戏啊.不是说活得久大概率癌症么,早晚突变.

普通人觉得能战胜癌症就满足了.

人造长寿绝对是世界级的遭难，想想500年后某某某还在的世界吧，欢迎对号入座 iOS fly ~

别，大部分水龟寿命也就20多年。陆龟能超过50年的也是凤毛麟角。

不用抗癌药，人的设计寿命也就40岁左右，活到60就算是高寿，所以几乎所有药物都是在逆天

回复38#ppalm

某种角度说：癌症这个死神还是公平的，无论你是贫穷还是富裕，无论你是无名小卒还是皇亲贵族，癌症死神谁都不放过。我们现在研发的各种天价抗癌药其实也是潜在增加了“不公平”。

歇了吧，真的有效的方法不会这么轻易公布的 iOS fly ~

....
iOS fly ~

返回来看疾病，人类真正有办法可以治愈的寥寥无几。

还是老太太看起来能赢，精神矍铄的很 iOS fly ~

那灭霸就太有用了

太可怕了，平民唯一的自由都要被剥夺了。

别发这种政治贴了，想我们这里被封500年啊。

特没谱活再久也就两届，500就500吧，我只要伊万卡

想要快去排队，摇号

之前据说是换血 iPhone 8+ fly ~

百岁老人可多了去了。。。1