First shown in the 1960's, cells are able to undergo a process known as autophagy where cells can recycle old or damaged proteins. Autophagy ("self-eating") is a tightly regulated catabolic process where the cell degrades its own cellular components through its lysosomal machinery. Autophagy is responsible for the degradation of long lived proteins and organelles, as well as the maintenance of cell homeostasis. Similarly, autophagy has been shown to play a physiological role in the defence against metabolic stress, DNA damage, and chromosomal instability. Briefly, this process is accomplished through the formation of double membrane vesicles called autophagosomes which engulf cytoplasm and organelles. These autophagosomes then fuse with lysosomes to form autolysosomes where degradation occurs [16]. The genes involved in this process are unified under the common name of Atg (autophagy-related) where key autophagy genes include Atg6 (Beclin-1), Atg7, Atg8 (LC3) and Atg12. There is accumulating evidence that this process can allow the cell to survive harsh conditions by activating this process and has also been linked to healthy aging. The autophagy gene Beclin-1 has also been shown to be a haploinsufficient tumor suppressor.

Therefore, it is my hypothesis that these super seniors have greater levels of autophagy. To test this, I propose to do an array comparative genomic hybridization (arrayCGH) or high-resuloution CGH study where we look for copy number variations of essential autophagy genes such as Beclin-1. Since these super seniors are healthy, the control group will not be age matched. However, the group will try to be matched based on other variables such as sex, ethnicity, their current health/fitness and occupation in order to get as similar a group as possible. In addition, the sample sizes will have to be quite large to account for the heterogeneity in the test and control populations.