33
Essays on Infinite Lifespans
Aubrey de Grey
extends their healthy lifespan by at least two decades. What
will such care comprise?
As I have discussed extensively elsewhere, [8–10] there seem
to be only seven broad categories of molecular and cellular dif-
ference between older and younger people that we need to fix
to achieve two decades of human life extension (“seven deadly
things”). These consist of a decline in the number of cells in
certain tissues and an accumulation of unwanted cells of cer-
tain types, of mutations in our chromosomes, of mutations in
our mitochondria, of random cross-links between long-lived
extracellular proteins and of chemically inert but bulky ‘junk’
in our lysosomes and in extracellular spaces.
Further, I have delineated [8;10–13] approaches to either
repairing or obviating (stopping from being pathogenic
however much they accumulate) all these changes. All these
approaches are already technically feasible. The underly-
ing precursor technologies have already been developed and
the work needed to complete them can be described in con-
siderable detail. I have termed these projects ‘Strategies for
Engineered Negligible Senescence’ (SENS) [8–10], since
their goal is collectively to eliminate from humans the posi-
tive correlation between age and risk of death per unit time
– biogerontologists’ formal definition of senescence.
Unfortunately, most of the first-generation SENS therapies
will be not only risky and laborious but also partial. A thor-
ough survey of this issue exceeds the scope of this essay, so I
will discuss just one illustrative example here: the breaking of
extracellular protein-protein crosslinks.
Most such links are laid down by a process called glycoxi-
dation, in which proteins react with sugars in the circulation
to form adducts that can rearrange and undergo subse-
quent, oxidative reactions forming linkage to a neighboring
protein. [14] Such crosslinks are eventually harmful to long-
lived extracellular structures, especially the artery wall, because