Research Biology of Aging and
DNA Repair
As people grow older, those who were
once healthy gradually become less physically and
mentally fit and more vulnerable to illness and death.
Scientists are studying what causes these biological
changes and why they occur at different rates in different
people. One basic unanswered question includes
whether aging is a single process with several different
results, or whether aging manifests itself as separate
processes in different body systems – such as
the immune system, bones, muscles, etc. Below
are some current scientific thoughts about the biology
of aging and why our lab is interested in researching
this field of study.
The aging process begins, at least in
part, when the rate at which cells divide begins to
slow down. Fewer immune system cells in an individual
can lead to higher disease susceptibility. Fewer
bone cells can lead to osteoporosis, and fewer skin
cells can lead to wrinkles. However, reduced
cell proliferation doesn’t have any bearing
on the health of the heart or the brain, as these
organs do not have cells which replicate much, if
at all. The mechanisms which sustain heart and
brain tissues are therefore of great research interest.
Scientists are working to identify biomarkers
in order to obtain key indicators of a person’s
life status and expectancy. Much focus is on
cell replication rate which may serve as an excellent
biomarker of aging. Studies involving caloric
restriction and oxidative stress support this theory.
Animals placed on a low calorie diet for an extended
period of time maintain or increase cell replication
rates, and show little or no aging. Alternatively,
damage from toxic free radicals causes cell replication
to slow or cease, and cells age or die.
Because a cell senesces or dies when
damage to its DNA is too great for it to copy or divide
properly, many scientists are devoting their time
to the study of intricate DNA repair systems.
DNA repair systems identify DNA damage and correct
it before too many improper base pairings, deletions,
etc. is reproduced and accumulates within the cell.
Accumulation of uncorrected DNA damage over several
years may lead to aging, and eventual cell death.
Supporting studies show internal and external toxins,
such as ultra-violet light or cigarette smoke, ensue
in oxidative damage, engender inefficient DNA repair
systems, and decrease lifespan. Humans with
genetic diseases resulting in greater spontaneous
DNA damage and/or inefficient repair systems often
show premature signs of aging. And animals with
faster rates of DNA repair generally have longer lives
than those with slower DNA repair rates.
Once a factor affecting cell replication
rate is understood, a biomarker has been identified.
A drug or dietary additive then can be developed and
used to slow the aging process.
