A Reimagined Research Strategy for Aging

 

Many things go wrong with aging bodies, but at the root of them all is the burden of decades of unrepaired damage to the cellular and molecular structures that make up the functional units of our tissues. As each essential microscopic structure fails, tissue function becomes progressively compromised – imperceptibly at first, but ending in the slide into the diseases and disabilities of aging.

SENS Research Foundation’s strategy to prevent and reverse age-related ill-health is to apply the principles of regenerative medicine to repair the damage of aging at the level where it occurs. We are developing a new kind of medicine: regenerative therapies that remove, repair, replace, or render harmless the cellular and molecular damage that has accumulated in our tissues with time. By reconstructing the structured order of the living machinery of our tissues, these rejuvenation biotechnologies will restore the normal functioning of the body's cells and essential biomolecules, returning aging tissues to health and bringing back the body’s youthful vigor.

 

The Targets

Decades of research in aging people and experimental animals has established that there are no more than seven major classes of such cellular and molecular damage, shown in the table below. We can be confident that this list is complete, first and foremost because of the fact that scientists have not discovered any new kinds of aging damage in nearly a generation of research, despite the increasing number of centers and scientists dedicated to studying the matter, and the use of increasingly powerful tools to examine the aging body. In its own way, each of these kinds of damage make our bodies frail, and contribute to the rising frailty and ill-health that appears in our sixth decade of life and accelerates thereafter.

 

Aging Damage

Year Discovered

Rejuvenation Biotechnology

SENS Strand

Cell loss, tissue atrophy

19551

Stem cells and tissue engineering

RepleniSENS

Cancerous cells

19592, 19823

Removal of telomere-lengthening machinery

OncoSENS

Mitochondrial mutations

19724

Allotopic expression of 13 proteins

MitoSENS

Death-resistant cells

19655

Targeted ablation

ApoptoSENS

Extracellular matrix stiffening

19586, 19817

AGE-breaking molecules; tissue engineering

GlycoSENS

Extracellular aggregates

19078

Immunotherapeutic clearance

AmyloSENS

Intracellular aggregates

19599

Novel lysosomal hydrolases

LysoSENS

 

The specific metabolic processes that are ultimately responsible for causing all of this damage are still only partially understood. The good news is that we don’t need to answer the many open questions about the causes of structural decay in order to develop effective therapies to reverse it. No matter what caused a given unit of damage in the first place, the same regenerative therapeutics can be used to repair it. In other words, it doesn’t matter how a given microscopic lesion occurred, if we apply rejuvenation biotechnologies that restore the machinery of life to proper working order.

The even better news is that we now understand how to fix all of this damage. For each major class of aging damage, a strategy for its removal or repair either already exists in prototype form, or is foreseeable from existing scientific developments: see the specific “Rejuvenation Biotechnology” listed for each kind of aging damage in the Table, and the right-hand navigation bar above.

Even after we have used these new therapies to repair an aging tissue, metabolic processes will continue to cause new damage. This simply means that rejuvenation biotechnologies are not a one-off fix, but will need to be periodically repeated to preserve youthful function. Just as cars need regular rounds of oil changes and spark plug replacements to keep them running smoothly, people will need to go in to rejuvenation clinics to keep up with their regenerative treatments to continue postponing age-related disease.

The entire SENS strategy – from the kinds of aging damage that occur, to their contribution to age-related frailty and illness, to the rejuvenation biotechnologies that can repair and replace the damaged functional units – are described in detail in Ending Aging, by SENS Research Foundation Chief Science Officer Dr Aubrey de Grey and Science Writer Michael Rae. Copies are available from your local bookstore, or from Amazon.com and other online retailers.

Through groundbreaking research in rejuvenation biotechnology, SENS Research Foundation is catalyzing the development of new medical therapies to comprehensively address the disabilities and diseases of aging, leading to a reimagined aging. Please help advance and expand our critical scientific research.

 

References

 1. Brody H. Organization of the cerebral cortex III. J Comp Neurol 1955; 102:511-556.

 2. Szilard L. On the nature of the ageing process. Proc Natl Acad Sci USA 1959; 45:35-45.

 3. 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.

4. Harman D. The biologic clock: the mitochondria? J Am Geriatr Soc 1972;20:145-147.

5. Hayflick L. The limited in vitro lifetime of human diploid cell strains. Exp Cell Res 1965; 37:614-636.

6. Movat HZ, More RH, Haust DM. The diffuse intimal thickening of the human aorta with aging. Am J Pathol 1958;34:1023-1031.

 7. Monnier VM, Cerami A. Nonenzymatic browning in vivo: possible process for aging of long-lived proteins. Science 1981;211:491-493.

8. Alzheimer A. Über eine eigenartige Erkrankung der Hirnrinde. Allgemeine Zeitschrift für Psychiatrie und psychisch-gerichtliche Medizin Berlin 1907; 64: 146-148.

9. 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.