Lifeboat Foundation

Remember that paralyzed guy from Southern California who managed to walk on his own accord thanks to a revolutionary technique that bridged the gap in his severed spinal column with a wireless Bluetooth link? A team of doctors at Ohio’s Case Western Reserve University have reportedly accomplished the same feat with a patient’s arms.

The team described its initial findings at a meeting of the Society for Neuroscience in Chicago on Tuesday. The system works much like that of the earlier team at UC Irvine: a brain-control interface (BCI) reads the patient’s brain waves emanating from his motor cortex, converts them into actionable electrical signals and wirelessly transmits them to an actuator “sewn into” the patient’s arm. This actuator is comprised of 16 filament wires that generate electrical impulses, which cause various muscle groups to contract when stimulated. The patient thinks about moving his arm and it does so — well, sorta.

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One robot has been given a simulated version of the brain cells that let animals build a mental map of their surroundings.

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To whom it may concern,

Cryonics is a legitimate science-based endeavor that seeks to preserve human beings, especially the human brain, by the best technology available. Future technologies for resuscitation can be envisioned that involve molecular repair by nanomedicine, highly advanced computation, detailed control of cell growth, and tissue regeneration.

With a view toward these developments, there is a credible possibility that cryonics performed under the best conditions achievable today can preserve sufficient neurological information to permit eventual restoration of a person to full health.

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Dr Michael Fossel comments on the recent Bioviva announcement of the first human gene therapy against aging.

The other day, a friend of mine, Liz Parrish, the CEO and founder of BioViva, made quite a splash when she injected herself with a viral vector containing genes for both telomerase and FST. Those in favor of what Liz did applaud her for her courage and her ability to move quickly and effectively in a landscape where red tape and regulatory concerns have – in the minds of some – impeded innovation and medical care. Those opposed to what Liz did have criticized her for moving too rapidly without sufficient concern for safety, ethics, or (from some critics) scientific rationale.

Many people have asked me to comment, both as an individual and as the founder of Telocyte. This occurs for two reasons. For one thing, I was the first person to ever advocate the use of telomerase as a clinical intervention, in discussions, in published journal articles, and in published books. My original JAMA articles (1997 and 1998), my first book on the topic (1996), and my textbook (2004) all clearly explained both the rational of and the implications for using telomerase as a therapeutic intervention to treat age-related disease. For another thing, Liz knew that our biotech firm, Telocyte, intends to do almost the same thing, but with a few crucial differences: we will only be using telomerase (hTERT) and we intend to pursue human trials that have FDA clearance, have full IRB agreement, and meet GMP (“Good Medical Production”) standards.

We cannot help but applaud Liz’s courage in using herself as a subject, a procedure with a long (and occasionally checkered) history in medical science. Using herself as the subject undercuts much of the ethical criticism that would be more pointed if she used other patients. Like many others, we also fully understand the urgent need for more effective therapeutic interventions: patients are not only suffering, but dying as we try to move ahead. In the case of Alzheimer’s disease, for example (our primary therapeutic target at Telocyte), there are NO currently effective therapies, a history of universal failure in human trials for experimental therapies, and an enormous population of patients who are currently losing their souls and their lives to this disease. A slow, measured approach to finding a cure is scarcely welcome in such a context.

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Bigger isn’t always better, but in this case it might be. Research has found that a large hippocampus gives you a memory boost and may shield you from dementia.

The hippocampus is rooted deep in the brain and deals with a range of things, but it’s also a major seat of neurogenesis; making new brain cells. The seahorse shaped structure plays a leading role in translating your experiences to long term memory and it’s made up of two sides. The left helps you record language, and the right hippocampus deals with spatial memory, like an interior google map.

The seat of memory?

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Electrocorticography (ECoG) was pioneered in the early 1950s by Wilder Penfield and Herbert Jasper, neurosurgeons at the Montreal Neurological Institute. The two developed ECoG as part of their groundbreaking Montreal procedure, a surgical protocol used to treat patients with severe epilepsy. The cortical potentials recorded by ECoG were used to identify epileptogenic zones – regions of the cortex that generate epileptic seizures. These zones would then be surgically removed from the cortex during resectioning, thus destroying the brain tissue where epileptic seizures had originated. Penfield and Jasper also used electrical stimulation during ECoG recordings in patients undergoing epilepsy surgery under local anesthesia. This procedure was used to explore the functional anatomy of the brain, mapping speech areas and identifying the somatosensory and somatomotor cortex areas to be excluded from surgical removal. This week we learned that Google has filed a patent relating to this medical field titled “Microelectrode Array for an Electrocorticogram.”

Google’s patent FIG. 6 noted above shows an application of the microelectrode array 1 according to the invention when recording an electrocorticogram of a human being. The microelectrode array is wirelessly connected to an electronic control device 10, which comprises in particular an amplifier for the electrode signals and a data acquisition system. The microelectrode array, implanted e.g. below the patient’s scalp, has an energy receiving coil 60 and an antenna 61 for bidirectional data transfer between the microelectrode array 1 and the electronic control device. It is also possible for the energy receiving coil simultaneously to be used as an antenna, such that no separate antenna is required.

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In the last few years, the topic of artificial intelligence (AI) has been thrust into the mainstream. No longer just the domain of sci-fi fans, nerds or Google engineers, I hear people discussing AI at parties, coffee shops and even at the dinner table: My five-year-old daughter brought it up the other night over taco lasagna. When I asked her if anything interesting had happened in school, she replied that her teacher discussed smart robots.

The exploration of intelligence — be it human or artificial — is ultimately the domain of epistemology, the study of knowledge. Since the first musings of creating AI back in antiquity, epistemology seems to have led the debate on how to do it. The question I hear most in this field from the public is: How can humans develop another intelligent consciousness if we can’t even understand our own?

It’s a prudent question. The human brain, despite being only about 3 pounds in weight, is the least understood organ in the body. And with a billion neurons — with 100 trillion connections — it’s safe to say it’s going to be a long time before we end up figuring out the brain.

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We all have different circadian rhythms but they slow down during aging, and we may be able to do something about it.

Your body is in a state of constant flux and the circadian rhythm is its master regulator, controlling everything from sleep cycles to appetite and beyond. Jet lag is a side effect of a confused internal cycle as it adjusts to a new timetable. Shift work and irregular patterns of activity can also potentially cause some serious problems if sustained for a long period, including raising risk of type 2 diabetes, dementia and all cause mortality.

When researchers studied aging mice, they saw a progressive decline in levels of molecules called polyamines. These are involved with a number of processes, but particularly in cell growth and circadian rhythm. The drop in polyamines also coincided with a slowing of their circadian cycle — which increased disease risk.

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Can we, as adults, grow new neurons? Neuroscientist Sandrine Thuret says that we can, and she offers research and practical advice on how we can help our brains better perform neurogenesis—improving mood, increasing memory formation and preventing the decline associated with aging along the way.

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