Berger began working with Vasilis Marmarelis, a biomedical engineer at USC, to begin making a brain prosthesis. They first worked with hippocampal slices from rats. Knowing that neuronal signals move from one end of the hippocampus to the other, the researchers sent random pulses into the hippocampus, recorded the signals at various locales to see how they were transformed, and then derived mathematical equations describing the transformations. They implemented those equations in computer chips.
Next, to assess whether such a chip could serve as a prosthesis for a damage hippocampal region, the researchers investigated whether they could bypass a central component of the pathway in the brain slices. Electrodes placed in the region carried electrical pulses to an external chip, which performed the transformations normally done in the hippocampus. Other electrodes delivered the signals back to the slice of brain.
Then the researchers took a leap forward by trying this in live rats, showing that a computer could in fact serve as an artificial component of the hippocampus. They began by training the animals to push one of two levers to receive a treat, recording the series of pulses in the hippocampus as they chose the correct one. Using those data, Berger and his team modeled the way the signals were transformed as the lesson was converted into a long-term memory, and they captured the code believed to represent the memory itself. They proved that their device could generate this long-term memory code from input signals recorded in rats’ brains while they learned the task. Then they gave the rats a drug that interfered with their ability to form long-term memories, causing them to forget which lever produced the treat. When the researchers pulsed the drugged rats’ brains with the code, the animals were again able to choose the right lever.
Last year, the scientists published primate experiments involving the prefrontal cortex, a part of the brain that retrieves the long-term memories created by the hippocampus. They placed electrodes in the monkey brains to capture the code formed in the prefrontal cortex that they believed allowed the animals to remember an image they had been shown earlier. Then they drugged the monkeys with cocaine, which impairs that part of the brain. Using the implanted electrodes to send the correct code to the monkeys’ prefrontal cortex, the researchers significantly improved the animal’s performance on the image-identification task.
Within the next two years, Berger and his colleagues hope to implant an actual memory prosthesis in animals. They also want to show that their hippocampal chips can form long-term memories in many different behavioral situations. These chips, after all, rely on mathematical equations derived from the researchers’ own experiments. It could be that the researchers were simply figuring out the codes associated with those specific tasks. What if these codes are not generalizable, and different inputs are processed in various ways? In other words, it is possible that they haven’t cracked the code but have merely deciphered a few simple messages.
Berger allows that this may well be the case, and his chips may form long-term memories in only a limited number of situations. But he notes that the morphology and biophysics of the brain constrain what it can do: in practice, there are only so many ways that electrical signals in the hippocampus can be transformed. “I do think we’re going to find a model that’s pretty good for a lot of conditions and maybe most conditions,” he says. “The goal is to improve the quality of life for somebody who has a severe memory deficit. If I can give them the ability to form new long-term memories for half the conditions that most people live in, I’ll be happy as hell, and so will be most patients.”
Despite the uncertainties, Berger and his colleagues are planning human studies. He is collaborating with clinicians at his university who are testing the use of electrodes implanted on each side of the hippocampus to detect and prevent seizures in patients with severe epilepsy. If the project moves forward as envisioned, Berger’s group will piggyback on the trial to look for memory codes in those patients’ brains.
http://www.technologyreview.com/featuredstory/513681/memory-implants/ (via fuckyeahdarkextropian)
paging Johnny Mnemonic!
As announced today, the Defense Advanced Research Projects Agency (DARPA) has issued a $2.9 million contract to researchers at Harvard’s Wyss Institute for Biologically Inspired Engineering to develop a flexible robotic exoskeleton that can be worn by soldiers — and eventually civilians — to make them stronger and more resilient. The suit could even help people with mobility issues and paralysis to move again.
In that sense, the Soft Exosuit, as it’s known, is similar in its goals to other robotic exoskeletons we’ve seen and written about before. But unlike many of those suits — which tend to be bulky, heavy and somewhat cumbersome — the Soft Exosuit is specifically designed to be as light and flexible as possible. It fits mostly around a wearer’s waist and legs and is made up primarily of textiles woven into straps which contain microprocessors, sensors, and a power supply. The motors that provide additional force and mobility are also located in a strap that goes around the wearer’s waist.
A team led by Dr. Michael Rudnicki, senior scientist at the Ottawa Hospital Research Institute and professor of medicine at the University of Ottawa, found that as muscle stem cells age, their reduced function is a result of a progressive increase in the activation of a specific signalling pathway. Such pathways transmit information to a cell from the surrounding tissue. The particular culprit identified by Dr. Rudnicki and his team is called the JAK/STAT signalling pathway.
"What’s really exciting to our team is that when we used specific drugs to inhibit the JAK/STAT pathway, the muscle stem cells in old animals behaved the same as those found in young animals," said Dr. Michael Rudnicki, a world leader in muscle stem cell research. "These inhibitors increased the older animals’ ability to repair injured muscle and to build new tissue."
What’s happening is that our skeletal muscle stem cells are not being instructed to maintain their population. As we get older, the activity of the JAK/STAT pathway shoots up and this changes how muscle stem cells divide. To maintain a population of these stem cells, which are called satellite cells, some have to stay as stem cells when they divide. With increased activity of the JAK/STAT pathway, fewer divide to produce two satellite cells (symmetric division) and more commit to cells that eventually become muscle fibre. This reduces the population of these regenerating satellite cells, which results in a reduced capacity to repair and rebuild muscle tissue.
At NASA’s Moffett Field, about four miles from Google’s headquarters in Mountain View, Calif., the agency has been developing a drone traffic management program that would in effect be a separate air traffic control system for things that fly low to the ground — around 400 to 500 feet for most drones.
Much like the air traffic control system for conventional aircraft, the program would monitor the skies for weather and traffic. Wind is a particular hazard, because drones weigh so little compared with regular planes.
The system would also make sure the drones do not run into buildings, news helicopters or other lower-flying objects — a more challenging task than for an airplane flying at 30,000 feet. There would also be no-fly zones, such as anywhere near a major airport.
“One at a time you can make them work and keep them safe,” said Parimal H. Kopardekar, a NASA principal investigator who is developing and managing that program. “But when you have a number of them in operation in the same airspace, there is no infrastructure to support it.”
Unlike the typical image of an air traffic control center — a dark room full of people wearing headphones and staring at radar screens — NASA’s system, like the drones themselves, would dispense with the people and use computers and algorithms to figure out where they can and cannot fly.
Google plans to spend the next year improving its drone’s ability to navigate between two points, as well as its “detect and avoid” system, the network of sensors that keeps it from running into things, according to a spokeswoman. The company expects it to be “a few years but less than a decade” before people can realistically use it.
But for drones to make it into cities, the technology of delivery could end up taking a back seat to everything else.
“There is the technology piece and then there is the public acceptance piece, and both have to evolve,” Dr. Kopardekar said. “If they are taken over by some rogue elements, how do you manage them? How do you have them safely land and take off in the presence of a grandma doing landscaping and kids playing soccer?”
Marine carotenoids found in local seaweeds and kelp may be particularly powerful foods. One marine carotenoid in the Okinawan diet that holds particular promise is astaxanthin, a natural product which is available as a supplement, derived mainly from micro-algae. The compound has powerful, broad-ranging anti-oxidative and anti-inflammatory properties. Research indicates astaxanthin may benefit those suffering from inflammation-related conditions including arthritis and rheumatoid disorders, metabolic disease, as well as cardiovascular, neurological, and liver diseases.
However, one of the most intriguing characteristics about astaxanthin is what is doesn’t do. It doesn’t have the nasty side effects that conventional anti-inflammatory therapies such as steroids and aspirin (and related compounds) exhibit. Its safety profile is strong. Lately Astaxanthin has become the darling of some “celebrity” doctors, but it isn’t some passing fad. Over 1,000 peer-reviewed publications are available on astaxanthin and more than several hundred have been published in just the last three years, reflecting a growing scientific interest.
Astaxanthin has also been shown to beneficially activate the FOXO3 gene — which is strongly associated with human longevity. Astaxanthin, along with other marine carotenoids such as polysaccharide fucoidan, xanthophyll fucoxanthin have some amazing qualities such as inhibiting cancer growth, fostering reduction in bad cholesterol, and lowering triglycerides.
In a sense these compounds trigger our biological systems into mimicking an ancient survival mechanism called caloric restriction. Caloric restriction has been unequivocally proven to make organisms live longer. It sounds counter-intuitive but the less you eat (up to about 30% less than usual), the longer you live so long as you maintain a diet adequate in macro- and micronutrients. A diet that contains compounds that turn on caloric restriction’s biological mechanisms may also make you live longer and healthier.
In other words, if you consume dietary compounds that mimic caloric restriction’s biological effects (“CR mimetics”), you can activate the same genes that caloric restriction activates, thus getting the benefits of caloric restriction without the deprivation. Our studies, and those of others, have shown strong support for this.