Many things go wrong with aging bodies, but only a few of them are primary changes in the structure of the body itself — that is, aging damage. Other changes (such as increases in inflammation and oxidative stress) are the secondary consequences of this primary change: either the direct results of those damaged components' inability to carry out their normal role in metabolism, or the body's adaptive or maladaptive attempts to compensate for those changes. Thus, by removing, repairing, replacing, or rendering harmless the damage, we restore the normal functioning of the body's cells and essential biomolecules, and the secondary changes are given the chance to return to their normal, youthful baseline.
Scientists have spent decades looking for such changes in aging bodies, this research has led to the conclusion that there are no more than seven major classes of such cellular and molecular damage, shown in the table below.
|Aging Damage||Discovery||SENS Solution|
|Cell loss, tissue atrophy||19551||Stem cells and tissue engineering (RepleniSENS)|
(only cancer matters)
|19592, 19823||Removal of telomere-lengthening machinery (OncoSENS)|
|Mutant mitochondria||19724||Allotopic expression of 13 proteins (MitoSENS)|
|Death-resistant cells||19655||Targeted ablation (ApoptoSENS)|
|Tissue stiffening||19586, 19817||AGE-breaking molecules (GlycoSENS); tissue engineering|
|Extracellular aggregates||19078||Immunotherapeutic clearance (AmyloSENS)|
|Intracellular aggregates||19599||Novel lysosomal hydrolases (LysoSENS)|
We can be confident that this list is complete, first and foremost because of fact that scientists have not discovered any new kinds of aging damage in nearly a generation, despite the facts that research into aging has been slowly accelerating and that we have had ever-increasingly powerful tools with which to investigate the aging body.
The specific metabolic processes that are ultimately responsible for all of this damage are still poorly understood. However, as is discussed on the SENS, An Engineering Solution page, this ignorance doesn't matter for "engineering" purposes. All that matters is our ability to periodically fix the damage, at the right time: after it has formed, but before it builds up to levels high enough to interfere with our youthful functioning.
The even better news is that we know how to fix all of this damage today. For each major aging lesion, a SENS solution for its removal or repair either already exists in prototype form, or is foreseeable from existing scientific developments. The links at the top of this page give more information about these solutions.
Within each class of aging damage, SENS will initially target the specific kinds of damage that make our bodies frail and limit our healthy lifespan within our first hundred years. This first wave of therapies will not repair all of the damage of aging, but will rejuvenate our bodies and add significantly to healthy human longevity. Once we have achieved a first generation of SENS therapies, our next targets will be forms of aging damage that take longer to cause us problems, renewing the lease on healthy life that the first wave of therapies gave us.
Thanks to the generous support of our donors and volunteers, SENS Foundation is now funding scientific research in the areas that are currently the greatest bottlenecks to the achievement of this first wave of therapies, including projects in LysoSENS, MitoSENS, OncoSENS and ApoptoSENS, and are working on a collaboration in GlycoSENS. With exciting preliminary results from these projects, and with increasing support from our generous donors, SENS Foundation is active in identifying and pursuing additional research projects. To support this critical SENS research, please join the ranks of SENS Foundation's supporters.
- 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.
- 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.
- Harman D. The biologic clock: the mitochondria? J Am Geriatr Soc 1972;20:145-147.
- Hayflick L. The limited in vitro lifetime of human diploid cell strains. Exp Cell Res 1965; 37:614-636.
- Movat HZ, More RH, Haust DM. The diffuse intimal thickening of the human aorta with aging. Am J Pathol 1958;34:1023-1031.
- Monnier VM, Cerami A. Nonenzymatic browning in vivo: possible process for aging of long-lived proteins. Science 1981;211:491-493.
- Alzheimer A. Über eine eigenartige Erkrankung der Hirnrinde. Allgemeine Zeitschrift für Psychiatrie und psychisch-gerichtliche Medizin Berlin 1907; 64: 146-148.
- 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.