The SENS Research Foundation (SRF), cofounded by biogerontologist and advocate Aubrey de Grey, funds work on the foundation science needed for tomorrow's rejuvenation therapies. We age and die because the operation of our metabolism generates various forms of cellular and molecular damage, some fraction of which goes unrepaired. Like rust, it accumulates and degrades the operation of organs and tissues to cause age-related disease and, ultimately, death. Work aimed at treating and repairing the root causes of aging is arguably the most important research presently taking place today: even if we combine every other cause of human suffering and death into one total, that toll is only half of the harm caused by aging.
In addition to funding research, the SENS Research Foundation staff and supporters also engage in advocacy relating to rejuvenation research: education, raising awareness, and fundraising. Too few scientists are engaged, there is far too little funding considering the gains that might be obtained comparatively soon with a suitable large-scale research program, and the public is largely ignorant and indifferent, even as they age to death, with more than hundred thousand lives lost to aging every day.
One aspect of the Foundation's outreach efforts is a growing YouTube video library of lectures and presentations by researchers in the field. A recent addition has Aubrey de Grey walking through the role of mitochondrial DNA damage, the present state of knowledge in the field, and what might be done to reverse this contribution to degenerative aging:
In this video, SRF Chief Science Officer Dr. Aubrey de Grey discusses mitochondrial mutations, their role in aging, and the SENS approach to combating their deleterious effects. Dr. de Grey opens his lecture by describing the structure of mitochondrial DNA (mtDNA) in humans. In particular, he explains that only thirteen protein-encoding mitochondrial genes actually reside in mitochondria. Throughout the course of human evolution, over a thousand other mitochondrial genes have migrated to the nuclear genome.
Next, he explains the major theories developed between the 1970 and the present that aimed to explain the role of mtDNA mutations in aging. During his discussion of the most recent theoretical ground, Dr. de Grey explains his own contribution to the field: an alternative hypothesis to explain how clonal expansion of mutant mitochondria might occur. He then turns to therapeutic strategies and discusses the three main mechanisms by which scientists might intervene in mitochondrial aging.
Dr. de Grey closes by describing the mechanism SRF finds most promising: inserting the thirteen protein-encoding mitochondrial genes into the nucleus modified in such a way that the corresponding RNA transcripts or protein-products can be imported into the mitochondria.