More than 500 years ago, Ponce de Leon landed in Florida in search of the fountain of youth — magical waters that reverse aging, prevent illness and grant immortality. He never found it, nor did anyone else, but we have come a long way in understanding the aging process.
We do not know the precise mechanism of aging, but there are some fundamental processes in our bodies that can drive aging. There are several theories of aging.
A widely accepted theory of aging today is called evolutionary senescence, the concept of mutation accumulation. As we age, our cells accumulate mutations in our genetic material or DNA, which affects the ability of tissues to regenerate. Also, some of our genes are designed to enhance reproduction early in life, but can cause problems later. Since genes can only be passed on during reproduction, which generally occurs earlier in life, genes that have negative effects later in life are not removed from the population! A good example is a gene called p53, which controls the fate of damaged cells by preventing their replication or directing them to die. This helps prevent cancer in young people, but it may negatively impact our ability to replace aging cells as we grow older.
Another theory centers on the maintenance of our genomes. As we get older, we accumulate damage to our DNA, which affects cellular function and our ability to renew tissues in the body. Take for example the production of free radical molecules. These highly reactive molecules are normally produced in mitochondria, which use oxygen to produce cellular energy, a process that creates free radical molecules as a by-product. These free radical molecules lead to oxidative damage of DNA and other cellular components.
There also is evidence that the neuroendocrine system (hormones that affect neurological function) influences aging. For example, a reduction in hormone levels can lead to a lengthening of life, at least in experimental animals. We are beginning to suspect that the insulin-related hormonal pathway may play a significant role in aging. Mutations that reduce the amount of this circulating hormone extend life.
A relatively new model of aging involves the replication of chromosomes as cells divide. When cells replicate, specialized structures at the ends of chromosomes called telomeres are shortened.
Shortened telomeres are linked to decreased viability and increased cancer risk. Cells whose telomeres reach a critical length can no longer divide and are described as senescent.
We are expanding our understanding of how aging occurs. The search for a modern-day fountain of youth will require a great deal of dedicated work by biomedical scientists to safely improve and extend human life.