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SENS 目标    传输技术
细胞 太少
太多
变异 染色体
线粒体
舍弃部分 细胞内
细胞外
交叉链 细胞外
为什么只有此七项?

相关信息
文章 网站 主要链接

 

The "seven deadly things" and why there are only seven

"致死七事项"

为什么仅此七项?

SENS is a practical, foreseeable approach to curing aging because all the types of metabolic side-effect whose accumulation is (or is even hypothesised to be) eventually pathogenic are amenable to repair (or in some cases obviation, i.e. disruption of the mechanism by which they become pathogenic) by techniques that, according to the experimentalists who have performed the key work on which those techniques build, can (with adequate funding) probably be implemented in mice within a decade or so.

SENS是用于治愈老化的实用而且前瞻性的方法,因为所有类型的代谢副作用都应该由某些技术来修复(在某些情况下应该排除,也就是说,变成病源性的机制应该破坏):它的积累最终是(或假设是)病源性的,实验家进行了关键的研究工作,确立了某些技术,按他们的说法,这些技术也许可以(若给以足够经费)在十年左右的时间内在小鼠中实现。

 There are seven major categories of such damage, listed below, along with the leading technique or techniques that can address them. Follow the links to read more detail about these techniques. I apologise that these more detailed pages do not yet include references to the literature. In most cases you can find the key references in my relevant publications, which are all available here.

这样的损伤有七个主要类型,列举如下(包括领头技术或适合于某类损伤的技术)。请按链接来阅读这些技术的更多细节。我要道歉的是,这些较详细的网页没有包括原文的参考文献。在大多数情况下,您可以在我的有关文章中发现主要参考文献,它们都能在这里here)找到。

Note: The dates given are when the category of damage in question was first proposed, in the gerontology literature, to be responsible for aging or some major age-related cause of death or debilitation. The earlier ones may not in fact be the first such mention, but they are well-known and often cited as pioneering publications in the area in question.

附注:所列出的日期是:当还在讨论中的损伤类型在老年学文章中第一次被提出会引起老化、或引起一些主要与年龄相关的死亡或虚弱。事实上,较早可能不是最早,但它们已为大家所熟悉,并在我们所讨论领域中常常被引用为先驱文章。

The full citations are below the table. The relevance of these dates is that they are all over 20 years ago. The fact that we have not discovered another major category of even potentially pathogenic damage accumulating with age in two decades, despite so tremendous an improvement in our analytical techniques over that period, strongly suggests that no more are to be found -- at least, none that would kill us in a presently normal lifetime.

本表之下是完整的引用。有关的这些日期全是二十多年前的。在这20年中,尽管我们的分析技术大有改善,但还没有发现另一种主要损伤(哪怕是随龄积累的潜在病源性的),这一事实有力地提示,不会再发现更多的了Ñ至少没有一种能在目前的正常寿命范围内杀死我们。

 

Damage rising
with age

随龄增加的损伤

Date [ref
below]

日期(见以下

参考文献)

Reversible or obviatable by
[see links for more info]

可逆转或可排除的

(请链接以获

得更多资料)

Cell loss, cell atrophy

细胞丧失,细胞萎缩

1955

Stem cells, growth factors, exercise

干细胞,生长因子,锻炼

Nuclear [epi]mutations
(only cancer matters)

核的突变和核的表

突变

(仅与癌症有关)

1959/
1982

WILT (Whole-body Interdiction
of Lengthening of Telomeres)

WILT(阻止全身端粒加长)

Mutant mitochondria

线粒体突变

1972

Allotopic expression of 13 proteins

13种蛋白质异位表达

Cell senescence

细胞衰老

1965

Ablation of unwanted cells

无用细胞的清除

Extracellular crosslinks

or hyperlink

细胞外的交联键

(或称为高联键)

1981

AGE-breaking molecules/enzymes

AGE-破裂的分子/酶

Extracellular junk

细胞外垃圾

1907

Phagocytosis; beta-breakers

巨噬细胞吞噬作用;

β-破碎机

Intracellular junk

细胞内垃圾

1959

Transgenic microbial hydrolases

转基因的微生物水解酶

The above table is to some extent similar to Table 4.3 in Holliday's 1995 book Understanding Ageing, though with important differences resulting from the focus on types of damage rather than types of maintenance. Some of the studies cited here were in fact incorrect in their interpretation of the data they examined, but the point is that they brought the corresponding type of damage to the fore as a candidate component of aging.

上表在某种程度上类似于Holliday1995年《理解老化》一书的表4.3,虽然有重大差别:本表着重于损伤类型、而不是维护类型。这里所引用的某些研究,实际上他们对所查资料的解释是不正确的,但是重要的是,他们把相应类型的损伤,作为老化的候选构件摆了出来。

Alzheimer A. †ber eine eigenartige Erkrankung der Hirnrinde. Allgemeine Zeitschrift fŸr Psychiatrie und psychisch-gerichtliche Medizin, Berlin, 1907, 64: 146-148.
Brody H. Organization of the cerebral cortex III. J Comp Neurol 1955; 102:511-556.
Szilard L. On the nature of the ageing process. Proc Natl Acad Sci USA 1959; 45:35-45.
Strehler BL, Mark DD, Mildvan AS, Gee MV. Rate and magnitude of age pigment accumulation in the human myocardium. J Gerontol 1959; 14:430-439.
Hayflick L. The limited in vitro lifetime of human diploid cell strains. Exp Cell Res 1965; 37:614-636.
Harman D. The biologic clock: the mitochondria? J Am Geriatr Soc 1972;20:145-147.
Monnier VM, Cerami A. Nonenzymatic browning in vivo: possible process for aging of long-lived proteins. Science 1981;211:491-493.
Cutler RG. The dysdifferentiation hypothesis of mammalian aging and longevity. In: The Aging Brain: Cellular and Molecular Mechanisms of Aging in the Nervous System (Gicobini E et al., eds), Raven (New York), 1982, pp. 1-19.



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