What do we know right now?

Evolutionary biologists have known for some time that round worms, yeast cells, and fruit flies all age differently and have different life spans, e.g., the fruit fly, Drosophila melanogaster, lives for about 30 or 40 days; whereas animals like field mice live three years, dolphins 25, elephants almost 50, and the Galapagos tortoises can make it to 100.

Ever heard of the Frenchwoman Jeanne Calment? She was the oldest person ever documented, dying in August 1997 at age 122. (Madame Calment supposedly gave up smoking just a few years ago because she couldn’t see well enough to light her cigarettes. Don’t tell your parents that’s in here, and don’t smoke because you will have a better chance of making it to old age if you don’t.)

But these life spans pale in comparison to those of some species of giant trees who live hundreds of years. (N.B. Life span is the maximum length a species can live, whereas life expectancy is usually less and varies from organism to organism.)

So what makes all this work?

To be honest, we still don't know for sure. However, scientists like Judith Campisi, Ph.D., (head of the Department of Cell and Molecular Biology at the University of California at Berkeley) are testing the hypothesis that the answer may lie in our cells. Actually cells senesce (the process of becoming old) at different rates among different organisms and among different people. Molecular biologists know that our cells can duplicate up to 50 times in vitro (meaning in a test tube or laboratory dish) before they stop, or become senescent cells.

Leonard Hayflick discovered this almost 40 years ago, but only recently have geneticists (scientists who study our heredity) been able to isolate genes that can cause certain cells to act differently, either age faster, that is, go through their 50 duplications sooner, or extend the number of divisions to 100+. What these scientists are looking for is the senescent factor (SF), which may be the underlying cause of why our billions of cells stop dividing and thus age. The elusive SF has been viewed from either a "damage" theory or a "programmed" theory point of view.

The Theory of Aging

Damage theories are based on the assumption that aging is the result of accumulated errors from such sources as free radicals. Now free radicals aren’t protestors who’ve been released from jail. They are, according to Denham Harman’s 1956 theory, atoms, ions, and molecules that contain an unpaired electron. Based on Harman’s idea, the underlying cause of aging and aging-related increases in diseases like cancer, is the accumulation of structural damage to our cells from being constantly bombarded by metabolically generated free radicals. Oxygen free radicals are thought to greatly increase the severity of, if not cause, such life-shortening diseases as diabetes, strokes, and heart attacks. Since longer-lived species have lower rates of free radical generation than do shorter-lived ones, then life span may be dependent upon our ability to prevent oxidative damage.

By contrast, programmed theories suggest the SF is genetically regulated. While both theories are correct to a certain degree, they are interconnected and have been thought to create a fixed, maximum life span of between 120-130 years.

Now even the presumption of a fixed life span is being questioned. Two researchers at MIT in Cambridge, MA, Drs. David Sinclair and Leonard Guarente believe they have discovered the "Holy Grail" of aging, the SF.

Believe it or not, it may all be a big mistake. These two scientists think that bits of extra DNA – deoxyribonucleic acid, the building blocks of life – accumulate within our cells’ nuclei, and that this "junk" DNA builds up to levels that clog normal cell action.

Our mothers have been telling us that junk food is bad for us, now junk DNA may be, too! Actually, what Drs. Sinclair and Guarente published in the prestigious journal, Cell, was about brewer’s yeast cells; however, they believe that this buildup of junk DNA from too many repeats of our ribosomes – protein producing factories inside a cell’s nucleus – is what also causes Werner’s syndrome in humans, which is a fatal disease of premature aging.

Persons afflicted with Werner’s syndrome are normal until they become teenagers, then they start developing signs of accelerated aging like very wrinkled skin and die in their 30s. If the Cell paper’s conclusion is correct, then knowing what the SF is may lead scientists to find ways to slow down the mechanism of cellular senescence, or aging.

Our Research

At Baylor College of Medicine’s Huffington Center on Aging in Houston, Texas, research teams led by Dr. Roy G. Smith are using animal models to study how the aging nervous system can restore pituitary-regulated growth hormone levels to more youthful pulsatile rhythms and how to prevent neuronal loss leading to such neurodegenerative diseases as Parkinson's and Alzheimer's. At the University of 'Texas in San Antonio, former HCOA researchers, Drs. James and Olivia Pereira-Smith, are studying the role that the SF plays in reducing the number of cell divisions on such aging-related health problems as osteoporosis (thinning bones that break easily), declining immune function, cancer, liver impairment, growth hormone declines, skin changes, and cardiovascular disease.

These scientists know that at least four genes are involved in cellular senescence and that three of them lie on human chromosomes 1,4, and 7; they’ve even cloned the gene on chromosome 4 for further study. They have also discovered a protein – remember proteins are mainly those amino acids that form the principal component of our cells – that inhibits DNA synthesis on the surface of membranes of senescent cells.

Is this the SF? We’ll know soon, so check later editions of Encarta to find out.

Previous

Top

Next