Genetics and Biology of Aging

Background: Aging
Although aging is quite obvious to everybody, on the molecular level it is a fairly complex process a fact that is stressed by the existence of more than 300 theories on aging (Medvedev 1990). Among the most prominent ones are the free radical theory of aging (Harmann 1956), the theory of replicative senescence ( Hayflick 1965) and inflammaging (Franceschi 2000).
The free radical theory of aging which has been considerably improved during the past decades claims that free radicals, mostly radical oxygen species ( ROS ) produced by mitochondria attack lipids, proteins and DNA thereby inflicting damage to the cell. These ROS are the cause of what is generally called oxidative stress. Old defective mitochondria show an increased production of ROS. Over the years it turned out that ROS also trigger senescence and that they are a major cause of inflammaging too.
Inflammaging is characterized by a chronic low level inflammation causing most if not all degenerative diseases. To remove damaged material the process of autophagy takes centre stage. Defective mitochondria as well as defective oxidized proteins are removed by autophagy. When this clearance of dysfunctional mitochondria declines during aging oxidative stress increases leading to wide spread damage including chronic inflammation and cellular senescence.