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Would You Survive a Merger with AI?

The idea that humans should merge with AI is very much in the air these days. It is offered both as a way for humans to avoid being outmoded by AI in the workplace, and as a path to superintelligence and immortality. For instance, Elon Musk recently commented that humans can escape being outmoded by AI by “having some sort of merger of biological intelligence and machine intelligence.”1 To this end, he’s founded a company, Neuralink. One of its first aims is to develop “neural lace,” an injectable mesh that connects the brain directly to computers. Neural lace and other AI-based enhancements are supposed to allow data from your brain to travel wirelessly to one’s digital devices or to the cloud, where massive computing power is available.

For many transhumanists, uploading is key to the mind-machine merger.

Perhaps these sorts of enhancements will turn out to be beneficial, but to see if this is the case, we will need to move beyond all the hype. Policymakers, the public, and even AI researchers themselves need a better idea of what is at stake. For instance, if AI cannot be conscious, then if you substituted a microchip for the parts of the brain responsible for consciousness, you would end your life as a conscious being. You’d become what philosophers call a “zombie”—a nonconscious simulacrum of your earlier self. Further, even ifmicrochips could replace parts of the brain responsible for consciousness without zombifying you, radical enhancement is still a major risk. After too many changes, the person who remains may not even be you. Each human who enhances may, unbeknownst to them, end their life in the process.

Josh Mitteldorf — Cracking the Aging Code

New interview with author and researcher Dr. Josh Mitteldorf who runs the aging research blog Aging Matters.


Interview with author and researcher Dr. Josh Mitteldorf who runs the aging research blog ‘Aging Matters’.

Dr. Josh Mitteldorf is an evolutionary biologist and a long-time contributor to the growing field of aging science. His work in this field has focused on theories of aging. He asks the basic question: why do we age and die?

Josh is the co-author of ‘Cracking the Aging Code: The New Science of Growing Old — And What It Means for Staying Young’ : “A revolutionary examination of why we age, what it means for our health, and how we just might be able to fight it.

In Cracking the Aging Code, theoretical biologist Josh Mitteldorf and award-winning writer and ecological philosopher Dorion Sagan reveal that evolution and aging are even more complex and breathtaking than we originally thought. Using meticulous multidisciplinary science, as well as reviewing the history of our understanding about evolution, this book makes the case that aging is not something that “just happens,” nor is it the result of wear and tear or a genetic inevitability. Rather, aging has a fascinating evolutionary purpose: to stabilize populations and ecosystems, which are ever-threatened by cyclic swings that can lead to extinction.

When a population grows too fast it can put itself at risk of a wholesale wipeout. Aging has evolved to help us adjust our growth in a sustainable fashion as well as prevent an ecological crisis from starvation, predation, pollution, or infection.

MitoMouse – Curing Mitochondrial Dysfunction in Mammals

Today, we have launched the MitoMouse project on our fundraising platform Lifespan.io. This project aims to reverse the damage that aging does to the mitochondrial DNA and to restore energy production in our cells with the goal of preventing age-related ill health.

The power stations of the cell

The mitochondria are the power stations of every single cell in our bodies, and they are responsible for converting the nutrients we absorb into energy. The mitochondria are so efficient at doing this that they are responsible for around 90% of the energy that our cells need to function and survive.

Fruit flies live longer with combination drug treatment

A triple drug combination has been used to extend the lifespan of fruit flies by 48% in a new study led by UCL and the Max Planck Institute for Biology of Ageing.

The three drugs are all already in use as : lithium as a mood stabiliser, trametinib as a and rapamycin as an immune system regulator.

The findings, published in Proceedings of the National Academy of Sciences (PNAS), suggest that a combination treatment may one day be helpful at preventing in people.

For the September Journal Club we are taking a look at the new human trial data from the recent senolytics trial at the Mayo Clinic

Click on photo to start video.

A follow on study from their previous human trial targeting IPF. This time the researchers ran a study to see how senolytics influenced diabetic kidney disease and if it actually removes senescent cells in humans.


Senescent cells, which can release factors that cause inflammation and dysfunction, the senescence-associated secretory phenotype (SASP), accumulate with ageing and at etiological sites in multiple chronic diseases. Senolytics, including the combination of Dasatinib and Quercetin (D + Q), selectively eliminate senescent cells by transiently disabling pro-survival networks that defend them against their own apoptotic environment. In the first clinical trial of senolytics, D + Q improved physical function in patients with idiopathic pulmonary fibrosis (IPF), a fatal senescence-associated disease, but to date, no peer-reviewed study has directly demonstrated that senolytics decrease senescent cells in humans.

Reference

Hickson, L. J., Prata, L. G. L., Bobart, S. A., Evans, T. K., Giorgadze, N., Hashmi, S. K., … & Kellogg, T. A. (2019). Senolytics decrease senescent cells in humans: Preliminary report from a clinical trial of Dasatinib plus Quercetin in individuals with diabetic kidney disease. EBioMedicine.

An Interview with Dr. Michael West

At our 2019 Ending Age-related Diseases conference in New York City, we had the pleasure of speaking with Dr. Michael West, the CEO of AgeX Therapeutics.

Dr. West can rightfully be called a pioneer in his field with a substantial background in biomedical and biotechnology corporations. After completing his PhD at Baylor College of Medicine, he founded Geron Corporation in 1990, where he launched and directed programs in telomere biology as it relates to cancer, aging, and human embryonic stem cell technology. He subsequently established the research group that went on to isolate human embryonic stem cells for the first time.

After his time at Geron, Dr. West was chairman and CEO of Advanced Cell Technology, which was acquired by the Japanese company Astellas Pharma in 2016 for $379 Million. Following his success with Advanced Cell Technology and Geron, Dr. West served as the CEO/co-CEO of BioTime Inc. for ten years.

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