Lifeboat Foundation: Safeguarding Humanity
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Category: genetics

Progress always seems to ride a slippery slope. Innovations generally bring a plethora of potential benefits and just as many dangers, the obvious and the hidden. Technologies that tamper with our biological constructs is well underway in the neuro- and biotech industries. Historically, innovations in medicine have usually been beneficial on the aggregate.

But these new breakthroughs go beyond preventing and healing pre-existing causes. Transhuman technologies hold the promise of enhancing who we are as individuals and potentially as an entire species, and the decisions surrounding these technologies are far from simple. Dr. Nayef Al-Rodhan, a philosopher, neuroscientist, and director of the Geneva Center for Security Policy, believes we should be acting now to prepare for the inevitable and the unpredictable ramifications.

Framing Human Motivation

Considering our mixed track record as a species in rolling out groundbreaking innovations, discussing and finding potential solutions to many of the hidden dangers, and obvious ones, seems more than reasonable. One of the more puzzling questions is, where do we begin to have a pragmatic conversation on the ethics of these technologies?

There are plenty of theories about what drive human decisions, not least because human morality is infinitely complex and our minds crave frames through which to make sense of chaos. Dr. Al-Rodhan has his own conception of what drives human motivations. He makes meaning using the lens of “5 P’s” – Power, Pride, Profit, Pleasure, and Permanence – which he posits drive human motivations. “This is my view, the foundation of my outlook…this perceived emotion of self interest drives our moral compass.”

Al-Rodhan’s view of human nature seems to make a lot of sense, bridging the rational with the emotional. Such a frame is particularly helpful when considering technology that undoubtedly taps into our deepest fears and hopes, and invokes rational (and irrational) debate. During a recent TechEmergence interview with Nayef, I asked for his thoughts on the concerns and considerations of this brand of technology in the coming decade.

The Near Business of Enhancement

Al-Rodhan believes that we will see cognitive enhancement primarily through neuropharmacology, or neuro- and psychostimulants. This concept of this technology is nothing new — the military and many other organization have used their stimulants of choice in the past, one of the most pervasive being alcohol. But this new wave of neuro- and psychostimulants will methodically target specific areas in the brain, giving way to the possibility for innovations like increased mood modulation and more cognitive ability within the confines of the brain’s neuronal population.

Neuromodulation has been used in the military, with some efforts to make soldiers less emotional and to require less sleep. The difficulties with side effects are often more pronounced when soldiers return from combat. “They are all messed up due to severe brutality, fear, and some of these agents they are given make them addicts to certain things,” says Nayef, acknowledging that this happens in most all militaries. “The point is that psychostimulants and neuromodulators will make us feel very good, but they are very dangerous because they require addictive behavior…and we need strict oversight mechanisms.”

Nayef says that technologies such as brain machine interface (BMI) are likely beyond the span of a decade, but that implantable microchips (whether bio or biotechnological) are as much of an immediate concern as the introduction of neurostimulants. “The FDA in the United States is entrusted with keeping us on the right path,” says Al-Rodhan.

Finding Common Regulatory Ground

Is it possible to put in place national or international structures for managing these new and emerging technologies? Al-Rodhan believes it is more than possible; however, the primary issue is that our regulation is way behind innovation. Regulatory frameworks are lacking for a number of reasons. The unpopularity in politics is a major obstacle to overcome. In elections, these types of contradictory frameworks are not politically on the front burner for most candidates, and the long-term outlook is limited.

Another area for concern is corporate pharmaceutical entities, which Nayef says are not as well regulated as some might think. Businesses are concerned about the bottom line above all else, which at times yields unfortunate outcomes for the whole of society. “This is part of their role as executive, they’re not too concerned about moral regulation,” says Nayef. As unappealing as it might sound to free market capitalists, the institution that traditionally steps into these frontiers to regulate is government.

A relevant and current example is the science and business of moderating genomes in China, which is already investing a lot of money in this industry. Some effects of this technology may not be so obvious at first, and it is possible that negative ramifications could occur without the correct bioethical oversight. Al-Rodhan asks “what happens if you get a piece of DNA that preludes the biosphere? Who knows what kind of mutation that may produce spontaneously or by merging with other DNA in an organism.” These are the types of questions that governments, academic institutions, corporations, and individual citizens need to be asking, considering the multiple perspectives that emerge from a framework like Al-Rodhan’s that applies across cultural boundaries.

Al-Rodhan describes the process of implementing such regulatory frameworks as a transnational effort, but says that such efforts start with countries like the U.S., Japan, and Europe, where accountable mechanisms already exist. Taking the lead doesn’t guarantee the same priorities will be given elsewhere, but it can provide an example — and ideally a positive one. “We have about a decade to get our act together,” says Al-Rodhan.

Dr Michael Fossel is a PhD and MD heading up telomerase research and therapy and has kindly written a blog article for Bioviva detailing the work both they and his company Telocyte are doing to fight back against Alzheimer’s.

How Alzheimer’s Can Be Prevented and Cured…

Michael Fossel, MD, PhD

As I said in my medical textbook on aging, “If age is a thief, then the greatest treasure we lose is ourselves.” We fear Alzheimer’s not simply because it takes away our health, but because it steals our souls.

Once, we thought it was simply “old age” that gradually killed the cells that carry information and memory. These are brain cells that make us who we are and define our consciousness.

Only in the past two decades, have we gradually come to realize that it’s not the neurons, which are merely the innocent bystanders in the tragedy,

but the microglial cells that cause the disease. It’s our microglia, not our neurons that steal our very souls.

Alzheimer’s disease begins in our glial cells. These cells together form.

90% of our brains, while neurons are only a small minority in the nervous system.

One set of these glial cells, the microglia, have the critical job of protecting the neurons and supporting them metabolically. These are the cells that, among dozens of other functions, are responsible for clearing metabolic waste products and recycling the extracellular proteins that surround the neurons.

Unfortunately, as we age, the microglial cells not only fail to divide, but gradually lose telomere length. By itself, telomere loss is unimportant,

but this loss begins a cascade of crucial changes in our cells.

As these telomeres shorten, they trigger a gradual shift in gene expression throughout the entire microglial cell. While the genes remain unchanged,

the “tune they play” i.e. the epigenetic pattern of gene expression becomes a sinister song. Proteins that are critical to DNA repair, to making our mitochondria work, to holding free radical damage to a minimum, begin to become scant. Where once, a young microglial cell would recycle proteins quickly and efficiently– including beta amyloid proteins — as the cell ages, the rate of turnover slows to a crawl.

The problem is much like many other things in life. If cell phones were replaced not every two years, but every twenty years, few of them would work. If a garden is weeded not every week, but once every two years, it would be engulfed in weeds. If we showered not once a day, but once every year, few of us would have friends.

Cells are no different: if we recycle proteins quickly, there is little damage, but if we recycle proteins slowly, then the damage begins to become obvious. Our cells don’t age because they are damaged; rather our cells permit damage to accumulate because they age. Shorter telomeres cause changes in gene expression, slower cell recycling, with the end results being old, damaged cells.

In Alzheimer’s disease, the microglia is the earliest change, the key change that begins the entire cascade of pathology to dementia. As our microglial cells slow down, they no longer keep up with the damage around them and the result is a gradual accumulation of damaged and denatured proteins.

The disaster begins.

At first, only trivial amounts of beta amyloid begin to accumulate in small aggregates, but then they grow larger, gathering into huge amyloid plaques.

Where once they could barely be seen, they now become visible under a microscope. But the problem is not simply these plaques themselves, but their effect on the neurons. Beta amyloid protein is critical to cell function, but only in small amounts, not in the vast plaques that now surround the besieged neuron. These growing plaques are toxic to neurons,

making it harder and harder for these cells to survive, let alone function normally.

Tau proteins likewise begin to form tangles and the neurons can no longer maintain themselves. At first, they begin to lose the ability to transmit nerve impulses, then they become more and more damaged internally, until the neurons die, first only a few, then in larger populations, leaving only scars, inflammation, and empty space. One-by-one our neurons are snuffed out, submerged under the rising effects of beta amyloid and tau proteins,

and all of this, the plaques, the tangles, and the dying neurons characteristic of Alzheimer’s can be traced back to the failing microglial cells.

As I write this, there have been more than 1,300 clinical Alzheimer’s trials looking at potential interventions. Many deal only with nursing care, but of those that try to intervene in the actual pathology, most have amyloid as their target, and a few target tau proteins. Small wonder then,

that none of these trials has ever been able to slow, let alone stop, or even reverse the disease. Every one of them is aimed at the wrong target.

Instead of trying to reverse the primary problem — the changes within the aging microglial cell — they aim at what are merely symptoms and results rather than causes. Imagine what would happen if we tried to cure bacterial infections by aiming merely at fevers, rather than aiming at the bacterial themselves. Current clinical trials are much the same: instead of aiming at the cause, they aim at the result.

Can we do better?

Almost certainly, we can. We know that the changes in gene expression that define aging in our cells are controlled by the changing telomere lengths as these cells divide.

We also know that if we reset the telomere to the original length, we not only reset gene expression, but end up with a cell that looks and acts like a young cell.

We have even done this not only in human tissues, in the lab, but in animals such as mice and rats. When we reset telomere lengths in the aging rodent brain, the animals begin to act normally again and we see the brains returning toward normal volume and function.

Can we do the same for human patients? Can we cure Alzheimer’s disease? We almost certainly can. We now not only understand how the disease works, and we not only have been able to show we can manage to intervene in animals,

but we already have the tools we need to cure Alzheimer’s disease in those we love.

Telomeres can be reset using telomerase, and enzymes comprising hTERT and hTERC. hTERT stands for human telomerase reverse transcriptase. hTERC

stands for human telomerase RNA component. Both of these telomere length extending enzymes can be delivered into the human brain, using either liposomes or viral vectors, much as has already been done in animal trials.

Once we can reverse the disease, once we can cure Alzheimer’s, it will change from the most frightening of illnesses to one we can deal with:

easily prevented, easily cured, and (much as it once erased our personal memories) a forgotten thing of the past.

There are at least two biotech projects currently aimed at human trials,

one via standard FDA-sponsored research (Telocyte), the other using a faster and less formal, “offshore” approach (BioViva). We support both approaches, wanting an effective therapy for Alzheimer’s that is both safe and rapidly available to all.

BioViva is seeking funding to initiate the use of these kinds of microglial telomere lengthening therapies in human test subjects immediately. If successful, we might not just eradicate Alzheimer’s disease, but also the cognitive impairment that strikes all people as they age past 30.

Maximum Life Foundation is raising $250,000 to give a grant to BioViva to test these therapies on human volunteers. 100% of donations earmarked for this study will be sent to BioViva with nothing subtracted for overhead.

The grant would cover this initial phase of the study and more.

To make your tax-deductible donation to this special fund aimed at quickly testing these telomere lengthening approaches in aging humans, go to www. MaxLife.org, or send your check to:

Maximum Life Foundation (BioViva)

2324 Colony Plaza Newport Beach,

CA 92660

Tele: (800) 881‑5346.

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Italian neurosurgeon Sergio Canavero grabbed the world’s attention this past winter when he announced his plans to perform the first human head transplant. Many doubted that such an outrageous procedure would ever see the light of day. Now, Canavero has a date on the books.

Thirty-year-old Russian computer scientist Valery Spiridonov is set to become the world’s first head transplant patient in December 2017. Spiridonov suffers from a rare genetic muscle-wasting condition known as Werdnig-Hoffmann disease. There’s currently no known treatment.

As you might not want to imagine, the procedure will be filled with challenges and uncertainties. There’s the hair-raising possibility that the head will reject the body or vice versa. The spinal cord might not fuse properly. Even if everything goes well, there’s no telling whether Spiridonov’s mental capacities or personality will remain the same. He’s embarking on totally uncharted medical territory.

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In April 2015, a paper by Chinese scientists about their attempts to edit the DNA of a human embryo rocked the scientific world and set off a furious debate. Leading scientists warned that altering the human germ line without studying the consequences could have horrific consequences. Geneticists with good intentions could mistakenly engineer changes in DNA that generate dangerous mutations and cause painful deaths. Scientists — and countries — with less noble intentions could again try to build a race of superhumans.

Human DNA is, however, merely one of many commercial targets of ethical concern. The DNA of every single organism — every plant, every animal, every bacterium — is now fair game for genetic manipulation. We are entering an age of backyard synthetic biology that should worry everybody. And it is coming about because of CRISPRs: clustered regularly interspaced short palindromic repeats.

Discovered by scientists only a few years ago, CRISPRs are elements of an ancient system that protects bacteria and other single-celled organisms from viruses, acquiring immunity to them by incorporating genetic elements from the virus invaders. CRISPRs evolved over millions of years to trim pieces of genetic information from one genome and insert it into another. And this bacterial antiviral defense serves as an astonishingly cheap, simple, elegant way to quickly edit the DNA of any organism in the lab.

Until recently, editing DNA required sophisticated labs, years of experience, and many thousands of dollars. The use of CRISPRs has changed all that. CRISPRs work by using an enzyme — Cas9 — that homes in on a specific location in a strand of DNA. The process then edits the DNA to either remove unwanted sequences or insert payload sequences. CRISPRs use an RNA molecule as a guide to the DNA target. To set up a CRISPR editing capability, a lab only needs to order an RNA fragment (costing about $10) and purchase off-the-shelf chemicals and enzymes for $30 or less.

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The human being — especially in so-called “advanced civilizations” — is the animal that molds itself into its own pet.

Peter Sloterdijk is Germany’s most controversial thinker and media theorist. He has dared to challenge long-established divisions in traditional philosophy of body and soul, subject and object, culture and nature. His 1999 lecture on “Regulations for the Human Park,” in which he argued that genetic engineering was a continuation of human striving for self-creation, stirred up a tempest in a country known for Nazi eugenics. At the same time, he himself has concluded that “the taming of man has failed” as civilization’s potential for barbarism has grown ever greater. His seminal books include “Critique of Cynical Reason” and his trilogy, “Spheres.”

At a recent Berggruen Center on Philosophy and Culture symposium on humans and technology at Cambridge University’s St. John’s School of Divinity, The WorldPost discussed with Sloterdijk the end of borders between humans and technology, the cloud, singularity and identity in the age of globalization.

For years now, you have been arguing that a new type of being was coming into existence, as the human species fuses with its technological prosthetics — “anthropo-technology.” In this new being, man and machine are becoming one integrated, operative system linked by information.

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You may have heard of precision medicine in the news, but what actually is it, and what could it mean for the future of healthcare?

In the past, medicine was geared for the masses and was applied to large numbers of people, on the basis of average effectiveness. If a particular substance was ineffective on 10% of the population, it could still pass through and be prescribed anyway. Before genomics, it was tricky to understand or postulate why people had such varied responses to medication, but now we have the right tools — things are changing.

While all humans have extremely similar genes in percentage terms, there are distinct differences in each of us that create our particular vulnerabilities and characteristics. We also respond differently to many treatments; a cure for one might be mediocre for another. This is particularly true for cancer. With the Precision Medicine Initiative taking off, taking into account genetics, lifestyle and environment is beginning to give us an edge — making medicine more accurate and effective.

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California researchers opened the world’s largest publicly available stem cell bank Tuesday, which will aid in the search for cures for genetic diseases such as Alzheimer’s, epilepsy and autism.

Universities from around the state will contribute adult skin samples to the bank, while the Buck Institute for Research in Novato will store the material.

The Stem Cell Bank is funded through a $32 million grant awarded in 2013 by the California Institute for Regenerative Medicine, which itself was established in 2004 through voter approval of Proposition 71. That measure provided an initial $3 billion in state bonds to the institute.

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A key mystery of the DNA replication process has been unraveled by researchers from King Abdullah University of Science and Technology (KAUST).

Before a bacterium can divide, it must make a copy of its genetic material, the circular DNA molecules that resemble bunched rubber bands, through a process called DNA replication. In this process, the two strands of DNA making up the circular DNA molecule unwind and separate to become templates for generating new strands.

To ensure the process is well regulated, the bacterium has set a number of “roadblocks,” or termination sites on the DNA, to ensure the permanent stoppage of replication forks, Y-shaped structures formed between the strands as the DNA molecule splits.

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THE genome is written in an alphabet of just four letters. Being able to read, study and compare DNA sequences for humans, and thousands of other species, has become routine. A new technology promises to make it possible to edit genetic information quickly and cheaply. This could correct terrible genetic defects that blight lives. It also heralds the distant prospect of parents building their children to order.

The technology is known as CRISPR-Cas9, or just CRISPR. It involves a piece of RNA, a chemical messenger, designed to target a section of DNA; and an enzyme, called a nuclease, that can snip unwanted genes out and paste new ones in. Other ways of editing DNA exist, but CRISPR holds the promise of doing so with unprecedented simplicity, speed and precision.

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Cancerous melanoma cells, shown with their cell bodies (green) and nuclei (blue), are nestled in tiny hollow lumens (tubes) within the cryogel (red) structure. (credits: Thomas Ferrante, Sidi A. Bencherif / Wyss Institute at Harvard University)

A new biologically inspired “injectable cryogel whole-cell cancer vaccine” combines patient-specific harvested cancer cells and immune-stimulating chemicals or biological molecules to help the body attack cancer. It has been developed by scientists at Harvard’s Wyss Institute and Dana-Farber Cancer Institute.

This new approach is simpler and more economical than other cancer cell transplantation therapies, which harvest tumor cells and then genetically engineer them to trigger immune responses once they are transplanted back into the patient’s body, the researchers say.

The research, headed by Wyss Core Faculty member David Mooney, Ph.D., was reported online in an open-access paper in Nature Communications on August 12.

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