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Scientists funded by the NIH BRAIN Initiative hope to diagram all of the circuits in the brain. One group will attempt to identify all of the connections among the retina’s ganglion cells (red), which transmit visual information from bipolar cells (green) and photoreceptors (purple) to the brain. (credit: Josh Morgan, Ph. D. and Rachel Wong, Ph. D./University of Washington)

The National Institutes of Health and the Kavli Foundation separately announced today (Oct. 1, 2015) commitments totaling $185 million in new funds supporting the BRAIN Initiative — research aimed at deepening our understanding of the brain and brain-related disorders, such as traumatic brain injuries (TBI), Alzheimer’s disease, and Parkinson’s disease.

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We all know that self-driving cars are cute and tend to be safer — at least according to Google’s self-released reports to date — but this new report has the self-driving revolution holding massive potential as one of the greatest things to happen to public health in the 21st century.

As The Atlantic reports, automated cars could save up to 300,000 lives per decade in the United States. Their reporting is based on this research paper by consulting firm McKinsey & Co., which is filled with fascinating ways that self-driving cars will help us accident-prone humans by midcentury.

From the McKinsey report (bold added by us to highlight the mind-blowing data):

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Sensors and robotics are two exponential technologies that will disrupt a multitude of billion-dollar industries.

This post (part 3 of 4) is a quick look at how three industries — transportation, agriculture, and healthcare/elder care — will change this decade.

Before I dive into each of these industries, it’s important I mention that it’s the explosion of sensors that is fundamentally enabling much of what I describe below.

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Aubrey de Grey wants to save lives. He wants to save as many as he possibly can, as soon as he can, and to do it he is going to fix ageing.

The prominent scientist and futurologist is on a crusade to beat ageing and when he does it will mean that we stay healthy and live longer – possibly for up to hundreds of years.

But, as de Grey emphasises, his primary goal is not just making people live longer; he wants us to live healthily, he wants to restore us to a state of health that is “fully functional in every way”. The ability to live for hundreds of years is just a side effect.

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Not everyone wants to sleep in. A growing transhumanism community wants to sleep less, and better, and they’re going to great lengths to make it happen.

For those unaware, transhumanism is an intellectual and cultural movement that aims to improve the human condition, to push beyond our biological limitations, largely through technological advancements. They’re particularly focused on extreme longevity. But with treatments for an extended healthy life still works in progress (and playing out on a very long timeline), some transhumanists have turned their attention to sleep.

The average well-rested person sleeps eight hours a day. The average American lives 79 years. That’s a little more than just 50 years being awake. Life is much shorter than you realized — at least if you agree with your typical sleep-hacker that sleeping is wasted downtime.

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Our gut and the microbiome play a crucial role in our health, but could better understanding of that role help us avoid disease and live longer?

The microbiome weighs 2–3 pounds and contains 10 times more cells than our own, but we’ve neglected our microbial tenants for a long time. These little denizens help us break down food, provide key nutrients and even play a role in inflammation and the integrity of our intestinal tract. It’s no surprise then that fermented foods and probiotics are gaining popularity as we become more aware of how important our gut is. Recent evidence even links poor digestive health to chronic inflammation and Parkinson’s disease.

New research suggests that both gut integrity, and the amount and type of bacteria that reside within it, can actually predict an individual’s health. They may even quicken or slow the pace of aging.

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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., or send your check to:

Maximum Life Foundation (BioViva)

2324 Colony Plaza Newport Beach,

CA 92660

Tele: (800) 881‑5346.

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Everything starts to go downhill as we get older and muscle is no exception; even simple tasks become challenging as we lose bone and muscle. Now research has identified a protein behind this age-related decline and therapeutic molecules that can fight it, helping individuals stay healthy and strong for longer.

A team at the Univesity of Iowa has discovered that a protein called ATF4 might be behind muscular decline. ATF 4 is a transcription factor, which means it tells the body to activate or regulate certain genes. ATF4 seems to change skeletal muscle with age, reducing protein synthesis and overall mass.

”Many of us know from our own experiences that muscle weakness and atrophy are big problems as we become older”

What can we do about it?

Researchers also identified two molecules that dramatically reduce this age-related decline in mice: ursolic acid from apple peels, and tomatidine, present in green tomatoes. When elderly mice were fed either of these compounds, muscle mass was increased by 10% and muscle strength by 30% — essentially restoring their muscles to a youthful state.

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