Aubrey de Grey

Aubrey David Nicholas Jasper de Grey (born 20 April 1963) is an English author and theoretician in the field of gerontology, and the Chief Science Officer of the SENS Research Foundation. He is editor-in-chief of the academic journal Rejuvenation Research, author of The Mitochondrial Free Radical Theory of Aging (1999) and co-author of Ending Aging (2007). He is perhaps best known for his view[neutrality' is 'disputed] that human beings could, in theory, live to lifespans far in excess of that which any authenticated cases have lived to today.

De Grey's research focuses on whether regenerative medicine can thwart the aging process. He works on the development of what he calls "Strategies for Engineered Negligible Senescence" (SENS), a tissue-repair strategy intended to rejuvenate the human body and allow negligible senescence. To this end, he has identified seven types of molecular and cellular damage caused by essential metabolic processes. SENS is a proposed panel of therapies designed to repair this damage.

De Grey is a fellow of the Gerontological Society of America, the American Aging Association, the Institute for Ethics and Emerging Technologies, and an advisor to the Singularity Institute for Artificial Intelligence. He has been interviewed in recent years in a number of news sources, including CBS 60 Minutes, the BBC, The New York Times, Fortune Magazine, The Washington Post, TED, Popular Science, The Colbert Report, Time, and the Skeptics' Guide to the Universe.

The Seven Types of Aging Damage Proposed by de Grey (The Seven Deadly Things)
Main article: Strategies for Engineered Negligible Senescence


 * 1) Mutations - in Chromosomes causing cancer due to nuclear mutations/epimutations:These are changes to the nuclear DNA (nDNA), the molecule that contains our genetic information, or to proteins which bind to the nDNA. Certain mutations can lead to cancer, and, according to de Grey, non-cancerous mutations and epimutations do not contribute to aging within a normal lifespan, so cancer is the only endpoint of these types of damage that must be addressed.


 * 1) Mutations - in Mitochondria:Mitochondria are components in our cells that are important for energy production. They contain their own genetic material, and mutations to their DNA can affect a cell’s ability to function properly. Indirectly, these mutations may accelerate many aspects of aging.


 * 1) Junk - inside of cells, aka intracellular aggregates:Our cells are constantly breaking down proteins and other molecules that are no longer useful or which can be harmful. Those molecules which can’t be digested simply accumulate as junk inside our cells. Atherosclerosis, macular degeneration and all kinds ofneurodegenerative diseases (such as Alzheimer's disease) are associated with this problem.


 * 1) Junk - outside of cells, aka extracellular aggregates:Harmful junk protein can also accumulate outside of our cells. The amyloid senile plaque seen in the brains of Alzheimer’s patients is one example.


 * 1) Cells - too few, aka cellular loss:Some of the cells in our bodies cannot be replaced, or can only be replaced very slowly - more slowly than they die. This decrease in cell number causes the heart to become weaker with age, and it also causes Parkinson's disease and impairs the immune system.


 * 1) Cells - too many, aka Cell senescence:This is a phenomenon where the cells are no longer able to divide, but also do not die and let others divide. They may also do other things that they’re not supposed to, like secreting proteins that could be harmful. Cell senescence has been proposed as cause or consequence of type 2 diabetes. Immune senescence is also caused by this.[citation needed]
 * 2) Extracellular protein crosslinks:Cells are held together by special linking proteins. When too many cross-links form between cells in a tissue, the tissue can lose its elasticity and cause problems including arteriosclerosis and presbyopia.