Address for correspondnece: Michael Fossel, M.D., PhD., Clinical Professor of Medicine, Michigan State University, Box 630, Ada, Michigan 49301. Voice: 616-676-8779; fax: 616-676-4099.
mfossel{at}earthlink.net
Ann. N.Y. Acad. Sci. 959: 14-23 (2002).
The most common causes of death and suffering, even in most
underdeveloped nations, are age-related diseases. These diseases
share fundamental and often unappreciated pathology at the cellular
and genetic levels, through cell senescence. In cancer, enforcing
cell senescence permits us to kill cancer cells without significantly
harming normal cells. In other age-related diseases, cell senescence
plays a direct role, and we may be able to prevent and reverse
much of the pathology. While aging is attributed to "wear and
tear," genetic studies show that these effects are avoidable
(as is the case in germ cell lines) and occur only when cells
down-regulate active (and sufficient) repair mechanisms, permitting
degradation to occur. Aging occurs when cells permit accumulative
damage by wear and tear, by altering their gene expression rather
than vice versa. Using telomerase in laboratory settings, we
can currently reset this pattern and its consequences both within
cells and between cells. Doing so resets not only cell behavior
but the pathological consequences within tissues comprising
such cells. We can currently grow histologically young, reconstituted
human skin using old human skin cells (keratinocytes and fibroblasts).
Technically we could now test this approach in joints, vessels,
the immune system, and other tissues. This model is consistent
with all available laboratory data and known aging pathology.
Within the next decade, we will be able to treat age-related
diseases more effectively than ever before.
