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Elon Musk Outlines His Mission to Link Human Brains With Computers in 4 Years

April 20, 2017 on Fortune
You may find the original article published here.

Tesla founder and Chief Executive Elon Musk said his latest company Neuralink Corp is working to link the human brain with a machine interface by creating micron-sized devices.

Neuralink is aiming to bring to the market a product that helps with certain severe brain injuries due to stroke, cancer lesion, etc, in about four years, Musk said in an interview with website Wait But Why.

“If I were to communicate a concept to you, you would essentially engage in consensual telepathy,” Musk said in the interview published on Thursday.

Artificial intelligence and machine learning will create computers so sophisticated and godlike that humans will need to implant “neural laces” in their brains to keep up, Musk said in a tech conference last year.

“There are a bunch of concepts in your head that then your brain has to try to compress into this incredibly low data rate called speech or typing,” Musk said in the latest interview.

“If you have two brain interfaces, you could actually do an uncompressed direct conceptual communication with another person.”

The technology could take about eight to 10 years to become usable by people with no disability, which would depend heavily on regulatory approval timing and how well the devices work on people with disabilities, Musk was quoted as saying.

In March, the Wall Street Journal reported that Musk had launched a company through which computers could merge with human brains. Neuralink was registered in California as a “medical research” company last July, and he plans on funding the company mostly by himself.

The technology could take about eight to 10 years to become usable by people with no disability, which would depend heavily on regulatory approval timing and how well the devices work on people with disabilities, Musk was quoted as saying.

In March, the Wall Street Journal reported that Musk had launched a company through which computers could merge with human brains. Neuralink was registered in California as a “medical research” company last July, and he plans on funding the company mostly by himself.

MRC scientists discover two repurposed drugs that arrest neurodegeneration in mice

April 20, 2017 on Medical Research CouncilMedical Research Council

You may find the original article published here.

A team of MRC scientists who a few years ago identified a major pathway that leads to brain cell death in mice, have now found two drugs which block the pathway and prevent neurodegeneration. The drugs caused minimal side effects in the mice and one is already licensed for use in humans, so is ready for clinical trials.

Misfolded proteins build up in the brain in several neurodegenerative diseases and are a major factor in dementias such as Alzheimer’s and Parkinson’s as well as prion diseases. Previously, the team found that the accumulation of misfolded proteins in mice with prion disease over-activates a natural defence mechanism, ‘switching off’ the vital production of new proteins in brain cells. They then found switching protein production back on with an experimental drug halted neurodegeneration. However, the drug tested was toxic to the pancreas and not suitable for testing in humans.

In the latest study, published today in Brainopens in new window, the team tested 1040 compounds from the National Institute for Neurological Disorders and Stroke, first in worms (C.elegans) which have a functioning nervous system and are a good experimental model for screening drugs to be used on the nervous system and then in mammalian cells.  This revealed a number of suitable candidate compounds that could then be tested in mouse models of prion disease and a form of familial tauopathy (frontotemporal dementia – FTD), both of which had been protected by the experimental – but toxic – compounds in the team’s previous studies.

The researchers identified two drugs that restored protein production rates in mice – trazodone hydrochloride, a licensed antidepressant, and dibenzoylmethane (DBM), a compound being trialled as an anti-cancer drug. Both drugs prevented the emergence of signs of brain cell damage in most of the prion-diseased mice and restored memory in the FTD mice. In both mouse models, the drugs reduced brain shrinkage which is a feature of neurodegenerative disease.

Professor Giovanna Mallucci, who led the team from the Medical Research Council’s (MRC) Toxicology Unit in Leicester and the University of Cambridge, was today announced as one of the five associate directors of the UK Dementia Research Institute.  She said:

“We know that trazodone is safe to use in humans, so a clinical trial is now possible to test whether the protective effects of the drug we see on brain cells in mice with neurodegeneration also applies to people in the early stages of Alzheimer’s disease and other dementias. We could know in 2-3 years whether this approach can slow down disease progression, which would be a very exciting first step in treating these disorders.

“Interestingly, Trazodone has been used to treat the symptoms of patients in later stages of dementia, so we know it is safe for this group.  We now need to find out whether giving the drug to patients at an early stage could help arrest or slow down the disease through its effects on this pathway.”

The research was funded by the MRC and Professor Mallucci was also funded by a grant from Alzheimer’s Society and Alzheimer’s Drug Discovery Foundation.

Dr Rob Buckle, Chief Science Officer at the MRC, said:

“This study builds on previous work by this team and is a great example of how really innovative discovery science can quite quickly translate into the possibility of real drugs to treat disease.

“The two drugs identified remain experimental but they were shown to protect the mice even when given after the processes underlying neurodegeneration had become established.  We currently have no way of treating these diseases so the prospect of finding drugs that can slow or stop them from progressing is extremely exciting – even more so when this is based on drugs that have already undergone expensive and time consuming testing in unrelated studies to establish that they are likely to be safe to use in humans.”

Dr. Doug Brown, Director of Research and Development at the Alzheimer’s Society, said:

“We’re excited by the potential of these findings. They show that a treatment approach originally discovered in mice with prion disease might also work to prevent the death of brain cells in some forms of dementia. This research is at a very early stage and has not yet been tested in people – but as one of the drugs is already available as a treatment for depression, the time taken to get from the lab to the pharmacy could be dramatically reduced.

“The drug blocks a natural defence mechanism in cells which is overactive in the brains of people with frontotemporal dementia, Alzheimer’s disease and Parkinson’s, so has the potential to work for several conditions. So far it has only been tested in mice with frontotemporal dementia but Alzheimer’s Society is now funding the researchers to test it in models of Alzheimer’s too.”

 

Neuron-recording nanowires could help screen drugs for neurological diseases

Ultimate goal is a neural-lace-like device that can be implanted in the brain to bridge or repair networks

April 18, 2017 on Kurzweil Accelerating Intelligence 

You may find the original article published here.

 

Nanowires-Recording-Neuronal-Activity

A research team* led by engineers at the University of California San Diego has developed nanowire technology that can non-destructively record the electrical activity of neurons in fine detail.

The new technology, published April 10, 2017 in Nano Letters, could one day serve as a platform to screen drugs for neurological diseases and help researchers better understand how single cells communicate in large neuronal networks.

A brain implant

The researchers currently create the neurons in vitro (in the lab) from human induced pluripotent stem cells. But the ultimate goal is to “translate this technology to a device that can be implanted in the brain,” said Shadi Dayeh, PhD, an electrical engineering professor at the UC San Diego Jacobs School of Engineering and the team’s lead investigator.

The technology can uncover details about a neuron’s health, activity, and response to drugs by measuring ion channel currents and changes in the neuron’s intracellular voltage (generated by the difference in ion concentration between the inside and outside of the cell).

The researchers cite five key innovations of this new nanowire-to-neuron technology:

  • It’s nondestructive (unlike current methods, which can break the cell membrane and eventually kill the cell).
  • It can simultaneously measure voltage changes in multiple neurons and in the future could bridge or repair neurons.**
  • It can isolate the electrical signal measured by each individual nanowire, with high sensitivity and high signal-to-noise ratios. Existing techniques are not scalable to 2D and 3D tissue-like structures cultured in vitro, according to Dayeh.
  • It can also be used for heart-on-chip drug screening for cardiac diseases.
  • The nanowires can integrate with CMOS (computer chip) electronics.***

* The project was a collaborative effort between researchers at UC San Diego, the Conrad Prebys Center for Chemical Genomics at the Sanford Burnham Medical Research Institute, Nanyang Technological University in Singapore, and Sandia National Laboratories. This work was supported by the National Science Foundation, the Center for Brain Activity Mapping at UC San Diego, Qualcomm Institute at UC San Diego, Los Alamos National Laboratory, the National Institutes of Health, the March of Dimes, and UC San Diego Frontiers of Innovation Scholar Program. Dayeh’s laboratory holds several pending patent applications for this technology.

** “Highly parallel in vitro drug screening experiments can be performed using the human-relevant iPSC cell line and without the need of the laborious patch-clamp … which is destructive and unscalable to large neuronal densities and to long recording times, or planar multielectrode arrays that enable long-term recordings but can just measure extracellular potentials and lack the sensitivity to subthreshold potentials. … In vivo targeted modulation of individual neural circuits or even single cells within a network becomes possible, and implications for bridging or repairing networks in neurologically affected regions become within reach.” — Ren Liu et al./Nanoletters

*** The researchers invented a new wafer bonding approach to fuse the silicon nanowires to the nickel electrodes. Their approach involved a process called silicidation, which is a reaction that binds two solids (silicon and another metal) together without melting either material. This process prevents the nickel electrodes from liquidizing, spreading out and shorting adjacent electrode leads. Silicidation is usually used to make contacts to transistors, but this is the first time it is being used to do patterned wafer bonding, Dayeh said. “And since this process is used in semiconductor device fabrication, we can integrate versions of these nanowires with CMOS electronics, but it still needs further optimization for brain-on-chip drug screening.”


Abstract of High Density Individually Addressable Nanowire Arrays Record Intracellular Activity from Primary Rodent and Human Stem Cell Derived Neurons

We report a new hybrid integration scheme that offers for the first time a nanowire-on-lead approach, which enables independent electrical addressability, is scalable, and has superior spatial resolution in vertical nanowire arrays. The fabrication of these nanowire arrays is demonstrated to be scalable down to submicrometer site-to-site spacing and can be combined with standard integrated circuit fabrication technologies. We utilize these arrays to perform electrophysiological recordings from mouse and rat primary neurons and human induced pluripotent stem cell (hiPSC)-derived neurons, which revealed high signal-to-noise ratios and sensitivity to subthreshold postsynaptic potentials (PSPs). We measured electrical activity from rodent neurons from 8 days in vitro (DIV) to 14 DIV and from hiPSC-derived neurons at 6 weeks in vitro post culture with signal amplitudes up to 99 mV. Overall, our platform paves the way for longitudinal electrophysiological experiments on synaptic activity in human iPSC based disease models of neuronal networks, critical for understanding the mechanisms of neurological diseases and for developing drugs to treat them.

How close are we to Elon Musk’s brain-computer interface?

By James Wu and Rajesh P.N. Rao, The Conversation, CNN

Updated 7:50 AM ET, Wed April 12, 2017 on CNN.com

You may access the original article published here.

Just as ancient Greeks fantasized about soaring flight, today’s imaginations dream of melding minds and machines as a remedy to the pesky problem of human mortality.

Can the mind connect directly with artificial intelligence, robots and other minds through brain-computer interface (BCI) technologies to transcend our human limitations?

Over the last 50 years, researchers at university labs and companies around the world have made impressive progress toward achieving such a vision.

Recently, successful entrepreneurs such as Elon Musk (Neuralink) and Bryan Johnson (Kernel) have announced new startups that seek to enhance human capabilities through brain-computer interfacing.

How close are we really to successfully connecting our brains to our technologies? And what might the implications be when our minds are plugged in?

VIDEO: How do brain-computer interfaces work and what can they do?

Origins: Rehabilitation and restoration

Eb Fetz, a researcher here at the Center for Sensorimotor Neural Engineering (CSNE), is one of the earliest pioneers to connect machines to minds. In 1969, before there were even personal computers, he showed that monkeys can amplify their brain signals to control a needle that moved on a dial.

Much of the recent work on BCIs aims to improve the quality of life of people who are paralyzed or have severe motor disabilities. You may have seen some recent accomplishments in the news: University of Pittsburgh researchers use signals recorded inside the brain to control a robotic arm. Stanford researchers can extract the movement intentions of paralyzed patients from their brain signals, allowing them to use a tablet wirelessly.

Elon Musk wants to merge man and machine; here’s what he’ll need to work out

Similarly, some limited virtual sensations can be sent back to the brain, by delivering electrical current inside the brain or to the brain surface.

What about our main senses of sight and sound? Very early versions of bionic eyes for people with severe vision impairment have been deployed commercially, and improved versions are undergoing human trials right now. Cochlear implants, on the other hand, have become one of the most successful and most prevalent bionic implants — over 300,000 users around the world use the implants to hear.

The most sophisticated BCIs are “bi-directional” BCIs (BBCIs), which can both record from and stimulate the nervous system. At our center, we’re exploring BBCIs as a radical new rehabilitation tool for stroke and spinal cord injury. We’ve shown that a BBCI can be used to strengthen connections between two brain regions or between the brain and the spinal cord, and reroute information around an area of injury to reanimate a paralyzed limb.

With all these successes to date, you might think a brain-computer interface is poised to be the next must-have consumer gadget.

Still early days

But a careful look at some of the current BCI demonstrations reveals we still have a way to go: When BCIs produce movements, they are much slower, less precise and less complex than what able-bodied people do easily every day with their limbs. Bionic eyes offer very low-resolution vision; cochlear implants can electronically carry limited speech information, but distort the experience of music.

And to make all these technologies work, electrodes have to be surgically implanted — a prospect most people today wouldn’t consider.

Considering ethics now, before radically new brain technologies get away from us

Not all BCIs, however, are invasive. Noninvasive BCIs that don’t require surgery do exist; they are typically based on electrical (EEG) recordings from the scalp and have been used to demonstrate control of cursors, wheelchairs, robotic arms, drones, humanoid robots and even brain-to-brain communication.

VIDEO: The first demonstration of a noninvasive brain-controlled humanoid robot “avatar” named Morpheus in the Neural Systems Laboratory at the University of Washington in 2006. This noninvasive BCI infers what object the robot should pick and where to bring it based on the brain’s reflexive response when an image of the desired object or location is flashed.

But all these demos have been in the laboratory — where the rooms are quiet, the test subjects aren’t distracted, the technical setup is long and methodical, and experiments last only long enough to show that a concept is possible. It’s proved very difficult to make these systems fast and robust enough to be of practical use in the real world.

Even with implanted electrodes, another problem with trying to read minds arises from how our brains are structured. We know that each neuron and their thousands of connected neighbors form an unimaginably large and ever-changing network. What might this mean for neuroengineers?

Imagine you’re trying to understand a conversation between a big group of friends about a complicated subject, but you’re allowed to listen to only a single person. You might be able to figure out the very rough topic of what the conversation is about, but definitely not all the details and nuances of the entire discussion.

Because even our best implants only allow us to listen to a few small patches of the brain at a time, we can do some impressive things, but we’re nowhere near understanding the full conversation.

There is also what we think of as a language barrier. Neurons communicate with each other through a complex interaction of electrical signals and chemical reactions. This native electro-chemical language can be interpreted with electrical circuits, but it’s not easy. Similarly, when we speak back to the brain using electrical stimulation, it is with a heavy electrical “accent.” This makes it difficult for neurons to understand what the stimulation is trying to convey in the midst of all the other ongoing neural activity.

Finally, there is the problem of damage. Brain tissue is soft and flexible, while most of our electrically conductive materials — the wires that connect to brain tissue — tend to be very rigid. This means that implanted electronics often cause scarring and immune reactions that mean the implants to lose effectiveness over time. Flexible biocompatible fibers and arrays may eventually help in this regard.

Co-adapting, cohabiting

Despite all these challenges, we’re optimistic about our bionic future. BCIs don’t have to be perfect. The brain is amazingly adaptive and capable of learning to use BCIs in a manner similar to how we learn new skills like driving a car or using a touchscreen interface. Similarly, the brain can learn to interpret new types of sensory information even when it’s delivered noninvasively using, for example, magnetic pulses.

Ultimately, we believe a “co-adaptive” bidirectional BCI, where the electronics learns with the brain and talks back to the brain constantly during the process of learning, may prove to be a necessary step to build the neural bridge. Building such co-adaptive bidirectional BCIs is the goal of our center.

We are similarly excited about recent successes in targeted treatment of diseases like diabetes using “electroceuticals” — experimental small implants that treat a disease without drugs by communicating commands directly to internal organs.

Do brain interventions to treat disease change the essence of who we are?

And researchers have discovered new ways of overcoming the electrical-to-biochemical language barrier. Injectible “neural lace,” for example, may prove to be a promising way to gradually allow neurons to grow alongside implanted electrodes rather than rejecting them. Flexible nanowire-based probes, flexible neuron scaffolds and glassy carbon interfaces may also allow biological and technological computers to happily coexist in our bodies in the future.

From assistive to augmentative

Elon Musk’s new startup Neuralink has the stated ultimate goal of enhancing humans with BCIs to give our brains a leg up in the ongoing arms race between human and artificial intelligence. He hopes that with the ability to connect to our technologies, the human brain could enhance its own capabilities — possibly allowing us to avoid a potential dystopian future where AI has far surpassed natural human capabilities. Such a vision certainly may seem far-off or fanciful, but we shouldn’t dismiss an idea on strangeness alone. After all, self-driving cars were relegated to the realm of science fiction even a decade and a half ago — and now share our roads.

In a closer future, as brain-computer interfaces move beyond restoring function in disabled people to augmenting able-bodied individuals beyond their human capacity, we need to be acutely aware of a host of issues related to consent, privacy, identity, agency and inequality. At our center, a team of philosophers, clinicians and engineers is working actively to address these ethical, moral and social justice issues and offer neuroethical guidelines before the field progresses too far ahead.

Connecting our brains directly to technology may ultimately be a natural progression of how humans have augmented themselves with technology over the ages, from using wheels to overcome our bipedal limitations to making notations on clay tablets and paper to augment our memories.

Much like the computers, smartphones and virtual reality headsets of today, augmentative BCIs, when they finally arrive on the consumer market, will be exhilarating, frustrating, risky and, at the same time, full of promise.

James Wu is a Ph.D. student in bioengineering and a researcher at the Center for Sensorimotor Neural Engineering at the University of Washington. Rajesh P. N. Rao is a professor of computer science and engineering and director of the Center for Sensorimotor Neural Engineering at the University of Washington.

Copyright 2016 The Conversation. Some rights reserved.