According to statistics published in the 2006 World Factbook, life expectancy in the United States is 77 years. Don't send out save-the-date cards just yet. Strategies for Engineered Negligible Senescence (SENS) is a medical engineering project striving to remedy and reverse human aging. The SENS strategy is not to interfere with metabolism, like traditional gerontological approaches, but to repair or prevent the accumulating damage and thereby indefinitely postponing the age at which it reaches pathogenic (disease causing) levels. Think of SENS as the cellular police, apprehending and eradicating the "trouble-makers," degenerate molecules and cells, before they spread mortal disorder.

SENS proposes only seven things have been found to damage our bodies, causing age and inevitably death. They are (in no particular order): cell loss, chromosomal mutations, death-resistant cells, mutant mitochondria, extracellular protein crosslinks, extracellular junk and intracellular junk.

Cell Loss
Cell depletion occurs in important tissues such as the brain, the heart and other muscles. The empty spaces are replaced either by neighboring cells that are expanding; foreign, fibrous matter; or nothing at all (which causes the tissue to shrink). I like to think of a particular tissue and its cells as a panel of experts that collaborate on important decisions. Let's use the brain as our example. Brain cells (or brain experts) work together to sustain our thoughts. Cell depletion would be if an expert became dissatisfied with his job, and for whatever reason, quits. Now his empty seat would be filled either by an opportunistic colleague, a foreigner who speaks a different language or by no expert at all. All of these possibilities are detrimental to the "work environment," causing tension among its members.

So how can cell depletion be reversed? One is by naturally stimulating cell division through exercise, causing the muscles to increase in size. Tell those experts to "get on the floor and give you twenty." The second way is by artificially stimulating (e.g. by injection) cell division. Invite slugger Barry Bonds as a guest speaker. The third way is through stem cell therapy; that is, introducing new cells. Dismiss the experts that are bored and replace them with those "who want it more".

Chromosomal Mutations
Chromosomal mutations are changes within our DNA sequence. For the most part, sophisticated means of evolution can naturally maintain such changes- except when cancer is involved. So what we need is a very good cure for cancer. According to the 2002 SENS meeting in Cambridge, UK, Whole-body Interdiction of Lengthening of Telomeres (WILT) is a very ambitious long-term approach. Since all cancers turn on a special enzyme called telomerase to divide indefinitely and eventually grow big enough to kill us, WILT proposes the total elimination of the genes that give rise to telomerase. Further developments on the fight against cancer greatly depend on the progress of stem cell research.

Death-Resistant Cells
Three types of death-resistant cells that accumulate in the aging body to a life-threatening degree are fat cells, certain immune cells and senescent cells. Fat cells tend to grow and/or spread in place of muscle mass that we lose with age, which means you better enjoy those bon bon's while you're still young. Being overweight is relatively harmless; unless of course, it gets to the stage know as "morbidly obese" in which the weight of fats cells put too much strain on the heart. Moreover excess fat within the abdominal cavity, known as visceral fat cells, can cause the body to develop insulin resistance, which eventually leads to Type II diabetes.

The number of white blood cells does not change very much with age, but certain immune cells (e.g. memory cytotoxic T cells) stop working well and become dysfunctional. The number of these cells must be lowered to leave room for more effective immune cells. This is crucial for people with weak immune systems, such as AIDS patients.

Senescent cells ("old cells") accumulate in quite large numbers in the cartilage of our joints. They may become actively toxic, causing irregular cell division and the secretion of too much protein. To get rid of these unwanted cells we can inject something that makes them suicidal or we can convince the immune system to kill them for us.

Mutant Mitochondria
Mitochondria are essentially the lungs of a cell, in that they regulate breathing. These lima bean-shaped organelles take in oxygen and nutrients (i.e. proteins), and convert them into energy. Mitochondria have their own DNA which may become dysfunctional as a result of mutations. Because the DNA's sequence is different than those of chromosomes, a different remedy is also needed. Mitochondria are very complex as its DNA only encodes thirteen proteins out of a thousand through an apparatus called the TIM/TOM complex. If we can replicate the genes that encode the thirteen proteins, we can replace them in the cell if mutations do occur. These replacements will override mutated functions, restoring the TIM/TOM effect.

Extracellular Protein Crosslinks
Extracellular protein crosslinks occur when long-lived proteins just will not go away. Usually all the proteins in our cells remain in an undamaged state because they are constantly being destroyed or recycled; but when they are not, they become more susceptible to chemical reactions. For example, older proteins within an artery wall may chemically bond together, causing the loss of elasticity and essentially high blood pressure. The cure lies in identifying and releasing chemicals that will react with these crosslinks, causing them to break down.

Extracellular Junk
Extracellular junk, unlike extracellular crosslinks, do not chemically react with anything; instead they stockpile like holiday trash along the curbside. Indestructible debris, like amyloid, forms big globular plaques in the brain of Alzheimer's patients. Although the cognitive effects of amyloid are still unknown, I doubt they'll help us remember our sixth grade locker combination. In the works is a vaccine by Elan Pharmaceuticals that stimulates microglia to engulf this accumulating material. Also tiny peptides called beta-breakers may be used to dissolve plaques.

Intracellular Junk
Intracellular junk are stuff inside the cell that cannot be broken down. When lysosomes, the "custodian workers" of the cell, lose their degradation powers, stuff gradually build up. In time the cell stops working right and may cause diseases such as atherosclerosis (a formation of plaques in the artery wall, which eventually burst and cause heart attacks and strokes). A promising solution is to provide cells with natural enzymes, found in soil bacteria and fungi, which will degrade this unyielding material.

So when will SENS grant us a taste of immortality? With adequate funding: in a decade or two. Until then, only the lives of lab rats will be prolonged.