OncoSENS at Albert Einstein College of Medicine
Ruling out epimutations as a cause of aging
Along with mutations in our cellular DNA, some cells also suffer "epimutations:" permanent damage to the structures that control the expression of the underlying genes. SENS Research Foundation has identified biomedical strategies to keep the body healthy and functioning normally despite the low level of mutations that accumulate with age; the same strategies will also work for epimutations, if their rate of accumulation is similarly low. To give the first assurance that the rate of epimutation-hampered cell accumulation over the adult lifespan is low enough for the strategy to be comprehensive, SENS Research Foundation is funding research at Albert Einstein College of Medicine to put new methods to use in determining that rate more definitively.
Biological aging is accompanied by an accumulation of cells that have suffered mutations - permanent damage to their genetic DNA code. Other cells accumulate that have undergone the closely-related "epimutations": damage to the "scaffolding" that helps the cell to control which genes are turned on and off at any time.
Mutations and epimutations are the main drivers of two dangerous age-changes that we can overcome with SENS regenerative engineering: a comprehensive solution to cancer and the loss of cells available for tissue regeneration due to the cell's protective defense mechanisms of cellular senescence and apoptosis (cellular "suicide").
Beyond these effects, only a very few cells survive and accumulate with age despite harboring mutations - too few to pose a barrier to the first great leap in healthy lifespan. But it's been harder to be sure of the same for cells with epimutations, since tracking the number of such cells that accumulate with age has proven challenging.
Because of the importance of knowing that the SENS rejuvenation engineering platform is comprehensive, SENS Research Foundation is funding research by Dr. Silvia Gravina in the laboratory of Dr. Jan Vijg (Chair, Department of Genetics, Albert Einstein College of Medicine) to resolve this issue, using newly-developed techniques to see how many such cells accumulate with age in the brains of aging mice.