Aubrey de Grey on the program:

"I am overjoyed to be co-hosting the second "Undoing Aging" conference together with Michael Greve just one year after the first, thanks to the generosity and hard work of Michael’s Forever Healthy Foundation and their team. 

​It is now entirely appropriate to be holding conferences on rejuvenation biotechnology every year, given how rapidly the field and the industry have grown relative to a decade ago, when my conferences in Cambridge were biannual. As you will see below, we are again assembling a huge variety of world-leading speakers whose research spans all aspects of rejuvenation biotechnology."

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Undoing Aging 2019 program

Thursday, 28th

12:00   Registration

1:00   Snacks

1:20   Welcome: Aubrey de Grey & Michael Greve

​Opening Keynote

​1:30 - 2:30 Nir Barzilai, Albert Einstein College of Medicine

​3:00 - 4:00 ​Session 1: Short talks from submitted abstract

tba ​

Rejuvenation outside the cell

The aging of the organism cannot be reduced to the aging of cells, because the body also consists of extracellular material. In some cases, this material is secreted and deposited locally, and in other cases it circulates in the blood and performs important functions far from where it was made. Sometimes the material consists of cells, sometimes small molecules, sometimes proteins. Messy, huh? And what's worse, all of these categories go downhill with age. We will hear about a range of research geared to fixing that.

4:00 - 5:30 Session 2: Cells in the circulation

Graham Pawelec, University of Tübingen Medical School Janko Nikolich-Zugich, University of Arizona Doris Lambracht-Washington, University of Texas, Southwestern

6:00 - 7:30 ​Session 3: Extracellular moleculesDamage outside the cell

Joshua McClure, MaxWell Biosciences Alvaro Mata, Queen Mary University of London tba​

7:30 ​Welcome Reception & Networking

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Friday, 29th

8:30 ​Coffee & Bites

Restoring cellular youth

​Many aspects of aging arise from a decline in the number of cells of a given type, which in turn often arises from a decline in the number or function of their progenitor cells. Telomere shortening has been heavily implicated in this, and researchers have long sought methods to lengthen telomeres in progenitor cells without at the same time elevating cancer risk. At present we are also seeing the emergence of various other ways to deliver this restoration of “stemness”.

9:30 - 11:00 Session 4: Cell TherapyRegenerative medicine

Adelaida Palla, Stanford University Dongsheng Cai, Albert Einstein College of Medicine Mike West, AgeX Therapeutics ​

​11:30 - 1:00 ​Session 5: DNA Maintenance

​Jerry Shay, University of Texas Southwestern Medical Center Joachim Lingner, Ecole Polytechnique Fédéral de Lausanne Laura Niedernhofer, University of Minnesota ​

1:00 ​Lunch

​2:00 - 3:30 ​Session 6: Short talks from submitted abstractsAbstracts

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​Senolysis

​It has been two decades since West and Campisi began to suggest that senescent cells might be more than just disabled, but actively toxic. Since 2011, their idea has not only been confirmed in the lab but has spawned a huge range of ideas for eliminating such cells, many of which are already being pursued in startups. The rate of progress is such that a single session at UA can no longer do justice to it - so, we're having two!

4:00 - 5:30 ​Session 7: Senolysis I

tba Judith Campisi, Buck Institute for Research on Aging Paul Robbins, University of Minnesota Medical School​ ​

​6:00 - 7:30 Session 8: Senolysis II

Dmitry Bulavin, Institute for Research on Cancer and Aging, Nice Aaron Wolfe, Antoxerene tba

Special lecture: Calment Controversy

​Nikolay Zak, Moscow Society of Naturalists

7:30 ​Networking

  
​Saturday, 30th

8:30 Coffee & Bites

Molecular vandalism

Many of our cells decline with age in function and/or number as a result of spontaneous, destructive chemical reactions. One of the most problematic examples is Alzheimer's disease. A huge contributor to this process is spontaneous oxidation, which disrupts the structure and function of bioactive molecules as diverse as lipids, proteins and DNA. In the morning sessions we will hear about efforts to counteract all these processes.

9:30 - 11:00 ​Session 9:  New approaches to neurodegeneration

Julie Andersen, Buck Institute for Research on Aging Evan Snyder, Sanford Burnham Prebys Institute Ruth Itzhaki, Manchester University ​

11:30 - 13:00 ​Session 10:  Counteracting oxidation

​Mikhail Shchepinov, Retrotope Amutha Boominathan, SENS Research Foundation tba​

1:00 ​Lunch

2:00 - 3:30 ​Session 11: Short talks from submitted abstracts

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Getting the SENS therapies to their target

​The SENS strands are defined as types of aging damage that can be matched to corresponding, generic repair strategies. However, these strategies will only be useful if they reach their target. This requires the development of novel, powerful methods to direct both pharmaceuticals and macromolecules within the body - and it also requires aggressive efforts to ensure that, once such therapies are developed, they can actually be administered to as many elderly people as possible as soon as possible.

4:00 - 5:30 ​Session 12: Getting molecules and cells where they are needed

​​Ruby Yanru Chen-Tsai, Applied Stem Cell Chongxi Xu, Techfields Pharma ​Lusine Danielyan, University of Tübingen

6:00 - 7:30 ​Session 13: Clinical translation

Richard Barker, New Medicine Partners ​Daria Khaltourina, International Longevity Alliance tba

7:30 Party