SENS

For those concerned with preserving life despite the many reasonable arguments to the contrary, Strategies for Engineering Negligible Senescence is a project spearheaded by Cambridge biomedical gerontologist Aubrey de Grey. SENS takes a goal-directed approach to eliminating aging, rather than a curiosity-driven approach to observing the body’s predetermined pattern of decline, malfunction, and collapse.



Aubrey de Grey defines SENS in contradistinction to traditional methods in geriatric treatment. Geriatrics attempts to stop damage from causing pathology, while biomedical gerontology would provide anti-aging medicine, rejuvenating the body rather than merely slowing down the aging process.


Aubrey de Grey, the face of SENS

SENS targets seven deadly causes of aging and proposes advanced treatments to counteract their effects. Here are the perceived problems and their required solutions:

1. Cell atrophy

Counteracting the loss of cells would require the addition of growth factors. Real traction cannot be made in this area without prevalent stem cell research. The Geron Corporation developed techniques for extending telomeres in 1998 and proved that they prevented cellular senescence, but a greater chance of developing cancer might be a trade-off of such methods.

2. Cellular mutations

Genetic mutations leading to cancer formation would need to be targeted. One possible method of reducing mutations is by introducing whole-body interdiction of lengthening telomeres.

3. Mitochondrial mutations

Mitochondria are prone to undergoing mutations due to their highly oxidative environment. The loss of mitochondrial function is thought to be a major cause of progressive cellular deterioration. To correct the problem, genes existing in the mitochondria could be preserved by copying them onto the chromosomes in the nucleus.

4. Cellular senescence

Programmed apoptosis would involve eliminating senescent cells through the intervention of cell therapies or vaccines, making room for healthy cells.

5. Extracellular cross-links

Chemical bonds between extracellular structures become brittle and weak with age. Enzymes and small-molecule drugs might be developed to break links caused by glycation (sugar-bonding).

6. Extracellular junk

This would involve removing the buildup of toxic substances such as Alzheimer’s-causing amyloid plaque. Junk found outside the cell might be removed by enhancing the immune system’s use of specialized cells called phagocytes, which serve to remove foreign bodies and thus fight infection. Microscopic surgical processes and small molecule drugs capable of breaking chemical beta-bonds might also prove beneficial.

7. Intracellular junk

Removing junk from inside of cells would require adding new enzymes to the cell’s natural digestion organ, the lysosome. These enzymes could be taken from bacteria or molds.


To accelerate research in radical life extension, the Methuselah Mouse Prize is being offered to scientists capable of extending the lifespan of mice. The prize is currently $3.6 million

Perhaps the main impediment standing in the way of SENS development is the entrenched position of death advocacy in our culture. Mistaking the necessity of death for an inherent human virtue, critics of SENS cling to any number of false justifications for the continuing existence of senescence.

"[T]he common wisdom is quite strong - even among friends and associates," writes SENS advocate Ray Kurzweil. "[T]he common wisdom regarding life cycle and the concept that life won’t be much different in the future than it is today still permeates people’s thinking. Thoughts and statements regarding life’s brevity and senescence are still quite influential. The deathist meme, that death gives meaning to life, is alive and well."

On the contrary, the struggle to eliminate senescence deserves our every effort. Even if SENS proves not to be up to the task, obviously we'll never know until we try.