• The first person to receive implant from brain-chip confirmed – Neuralink

    The first human patient has received an implant from brain-chip startup Neuralink on Sunday and is recovering well, the company’s billionaire founder Elon Musk said.

    “Initial results show promising neuron spike detection,” Musk said in a post on the social media platform X on Monday.

    Spikes are activity by neurons, which the National Institute of Health describes as cells that use electrical and chemical signals to send information around the brain and to the body.

    The U.S. Food and Drug Administration had given the company clearance last year to conduct its first trial to test its implant on humans, a critical milestone in the startup’s ambitions to help patients overcome paralysis and a host of neurological conditions.

    In September, Neuralink said it received approval for recruitment for the human trial.

    The study uses a robot to surgically place a brain-computer interface (BCI) implant in a region of the brain that controls the intention to move, Neuralink said previously, adding that its initial goal is to enable people to control a computer cursor or keyboard using their thoughts alone.

    The implants’ “ultra-fine” threads help transmit signals in participants’ brains, Neuralink has said.

    The first product from Neuralink would be called Telepathy, Musk said in a separate post on X.

    The startup’s PRIME Study is a trial for its wireless brain-computer interface to evaluate the safety of the implant and surgical robot.

    Neuralink did not immediately respond to a Reuters request for further details.

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    The company has faced calls for scrutiny regarding its safety protocols. Reuters reported earlier this month that the company was fined for violating U.S. Department of Transportation (DOT) rules regarding the movement of hazardous materials.

    The company was valued at about $5 billion last June, but four lawmakers in late November asked the U.S. Securities and Exchange Commission to investigate whether Musk had misled investors about the safety of its technology after veterinary records showed problems with the implants on monkeys included paralysis, seizures and brain swelling.

    Musk wrote in a social media post on Sept. 10 that “no monkey has died as a result of a Neuralink implant.” He added that the company chose “terminal” monkeys to minimize risk to healthy ones.

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  • Millions with Genetic Variant Raising Risk of ‘Implosive’ Cell Death

     

    A team of researchers has identified a genetic issue that takes the cellular brakes off necroptosis – the type of programmed cell death that usually alerts the immune system to the presence of invaders. However, it can trigger an excessive inflammatory response if uncontrolled.

    In the latest study, researchers estimate that this genetic variant, a single-base change in the gene encoding a protein called MLKL, can be found in up to 3 percent of people. That amounts to millions of people worldwide.

    Furthermore, the researchers didn’t associate this MLKL gene variant with any one particular disease, though after characterizing its effects in cell cultures and animal models, They claimed it could increase people’s risk of inflammatory diseases such as diabetes, especially when combined with other genetic and environmental factors.

    Cells die all the time in our bodies in different ways. Many of these deaths happen without much fanfare. Other deaths happen under duress of an infection self-implode. Their disintegrated remains trigger the immune system into a state of heightened vigilance.

    Two things can cause problems in the human body. One is that cancer can occur if cells don’t die. The second is that unleashing too much inflammation can occur if cells go boom more often than they should.

    For most humans, the MLKL will stop when the body tells it to stop, but 2 to 3 percent of people have a form of MLKL that is less responsive to stop signals. That statement is from Sarah Garnish, a cell biologist at the Walter and Eliza Hall Institute of Medical Research (WEHI) in Melbourne, Australia. She is part of the latest study.

    She said this adds up to many millions of people carrying a copy of this gene variant when the number is considered globally.

    The latest study has been published in Nature Communications.

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  • Why a leading theory has been branded ‘pseudoscience’

    Consciousness: why a leading theory has been branded ‘pseudoscience’

    Hubis/Shutterstocl

    Philip Goff, Durham University

    Civil war has broken out in the field of consciousness research. More than 100 consciousness researchers have signed a letter accusing one of the most popular scientific theories of consciousness – the integrated information theory – of being pseudoscience.

    Immediately, several other figures in the field responded by critiquing the letter as poorly reasoned and disproportionate.

    Both sides are motivated by a concern for the long-term health and respectability of consciousness science. One side (including the letter signatories) is worrying that the association of consciousness science with what they perceive to be a pseudoscientific theory will undermine the credibility of the field.

    The other side is pressing that what they perceive as unsupported charges of pseudoscience will ultimately result in the whole science of consciousness being perceived as pseudoscience.

    Integrated information theory – often referred to as IIT – is a very ambitious theory of consciousness proposed by neuroscientist Giulio Tononi. It ultimately aims to give mathematically precise conditions for when any system – a brain or some other lump or matter – is or is not conscious.

    The theory revolves around a mathematical measure of integration of information, or interconnections, labelled with the Greek letter ϕ. The basic idea is that a system becomes conscious at the precise moment when there is more ϕ in the system as a whole than in any of its parts.

    IIT implies that many more things are conscious than we ordinarily suppose. This means it gets close to a kind of “panpsychism” – the view that consciousness pervades the physical universe. Having said that, there are big differences between IIT and the new wave of Bertrand Russell-inspired panpsychism which has recently been making waves in academic philosophy, and which has been the focus of much of my research.

    IIT even implies, as pointed out by the computer scientist Scott Aaronson, that an inactive grid of connected logic gates would be conscious.

    The signatories of the letter worry that, while certain aspects of IIT may have been tested, the theory as a whole has not. Therefore, they argue, there is little experimental support for these bold and counter-intuitive implications. Opponents of the letter say that this is true of all current theories of consciousness, and reflects challenges with current neuroimaging techniques.

    Adversarial collaboration

    All of this follows the announcement over the summer of the first results of an “adversarial collaboration” between IIT and another popular theory of consciousness, known as the global workspace theory.

    According to this theory, information in the brain becomes conscious when it is in a “global workspace”, which means it is available to be used by many and varied systems throughout the brain – perceptual areas, long-term memory and motor control – for a wide variety of tasks. In contrast, if certain information is only available to a single system in the brain to perform a highly specific task, such as to regulate breathing, then that information is not conscious.

    The idea of an adversarial collaboration is that the proponents of each of the rival theories design experiments together, and agree in advance on which results would favour each theory.

    The hope is that agreeing in advance about what the results would mean will prevent theorists from interpreting whatever results come up as fitting with their preferred theory. This first round of experimental results turned out to be mixed. Some confirmed certain parts of IIT, and some backed up particular aspects of global workspace theory. On balance, there was arguably a slight advantage to IIT.

    The announcement of these ambiguous results was accompanied by the neuroscientist Christof Koch – a prominent proponent of IIT – publicly conceding defeat on a bet he made 25 years ago with philosopher David Chalmers, that the science of consciousness would be all wrapped up by now.

    Image of Christof Koch.
    Christof Koch giving a TED talk.
    CC BY-NC-ND

    One factor which may be playing a big role, although it has not been explicitly mentioned in any of these online skirmishes, is that IIT does not merely justify itself through scientific experimentation. It also involves philosophical reflection.

    IIT begins with five “axioms”, which its proponents claim each of us can know through attention to our own conscious experience. These include that conscious experience is unified – that we don’t experience, say, colours and shapes separately but as aspects of a single, unbroken experience.

    The theory then translates these axioms into five corresponding “postulates” – properties which it claims are required for a physical system to embody consciousness. For example, IIT explains the unity of our conscious experience in terms of the integration of the physical system.

    Opponents of IIT may in part be motivated by a desire to sharply distinguish the science from the philosophy of consciousness, thus ensuring the former is perceived – in particular by funders – as a serious scientific enterprise.

    Beyond science

    The problem is that consciousness is not merely a scientific issue. The task of science is to explain publicly observable phenomena. But consciousness is not a publicly observable phenomenon: you can’t look inside someone’s brain and see their feelings and experiences. Of course, science theorises about unobservable phenomena, such as fundamental particles, but it only does this to explain what can be observed. In the unique case of consciousness, the phenomenon we are trying to explain is not publicly observable.

    Instead, consciousness is known about privately, through the immediate awareness each of us has of our own feelings and experience. The downside of this is that it’s very hard to experimentally demonstrate which theory of consciousness is correct. The upside is that, in contrast to other scientific phenomena, we have direct access to the phenomenon, and our direct access may provide insights into its nature.

    Crucially, to accept that our knowledge of consciousness is not limited to what we can glean from experiments is to accept that we need both science and philosophy to deal with consciousness. In my new book Why? The Purpose of the Universe, I explore how such a partnership could be achieved.

    IIT is not perfect, either in its scientific or its philosophical aspects. But it is pioneering in accepting the need for science and philosophy to work hand in glove to crack the mystery of consciousness.The Conversation

    Philip Goff, Associate Professor of Philosophy, Durham University

    This article is republished from The Conversation under a Creative Commons license. Read the original article.

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  • Elon Musks satellites litter space…

    NEEDING SPACE

    ‘Terrifying’ video reveals Elon Musk’s huge army of satellites as scientists warn of Starlink’s ‘hidden danger’

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  • NASA – 7 years, billions of kilometres, a handful of dust

    7 years, billions of kilometres, a handful of dust: NASA just brought back the largest-ever asteroid sample

    NASA

    Eleanor K. Sansom, Curtin University and Nick Timms, Curtin University

    After a journey of billions of kilometres, NASA’s OSIRIS-REx mission has culminated in a small black capsule blazing through the sky before touching down in the Utah desert.

    Inside is likely to be the largest ever sample of dust and rock returned from an asteroid. Extracted and brought back with great technical ingenuity from an asteroid called Bennu, scientists will now study in search of clues about the origins of the Solar System and life itself.

    The seven-year mission took OSIRIS-REx to a near-Earth carbon-rich asteroid, which it orbited for two and a half years, mapping its surface and measuring properties such as its density and spin. This “rubble pile” asteroid also has a (very) small chance of one day impacting Earth, so getting intricate measurements of its orbit and other dynamics was also a mission goal.

    The origins of the Solar System – and life

    Most asteroids are the rocky leftovers of failed planets and destructive collisions in the early Solar System, orbiting in a belt between Mars and Jupiter. They vary drastically in size, shape and composition, and finding out what they are made of can help us learn more about how the planets formed.

    These primitive bodies – some more than 4.5 billion years old – can also shed light on the origins of life, because they tell us about the distribution of water, minerals and other elements such as carbon.

    There is also an element of self-interest in studying these asteroids, to understand the risk they may pose if they are heading Earth’s way.

    Using telescopes on Earth, we can get a rough idea of what an asteroid’s surface is made of. However, to do an in-depth chemical analysis we need to get hold of some actual samples.

    Most of the asteroid samples we have are meteorites – lumps of space rock that have crashed into Earth. There are more than 70,000 meteorites in collections around the world, but we know the origins of less than 0.1% of them.

    What’s more, we know the samples we have are not very representative of the kinds of asteroids in space. Part of the reason for this is that some kinds of asteroids are better than others at surviving the fiery descent through the atmosphere.

    But some meteorites don’t appear to correspond to any known type of asteroid. So where do they come from?

    Using dedicated camera networks such as Australia’s Desert Fireball Network we can observe incoming asteroids, recover meteorite samples and track their paths back through space to determine their origins. This process can deliver relatively uncontaminated samples to the lab.

    Even still, linking a meteorite to a known parent asteroid, or even a type of asteroid observed via telescope, is very difficult.

    Bringing pieces of space back to Earth

    Sample return missions are the gold standard for analysing the makeup of extraterrestrial bodies. They can bring pieces from a different planet or asteroid back to Earth to study.

    The first such mission was to the Moon, bringing back lunar samples for analysis. We learned the Moon was made from the same material as the Earth, and that it likely formed from the orbiting debris after a giant impact.

    Sample return missions are technically very challenging. Not only does a spacecraft have to travel hundreds of millions of kilometres from Earth, but it has to match speed with the target (not just zoom past), find a safe landing site, touch down to collect a sample (without crashing), stow the sample in a sealed capsule, take off again, and return to Earth. Much of this process needs to be autonomous, as the time delay for communications with Earth is too long for remote control.

    Other than the lunar samples returned by the Apollo missions, OSIRIS-REx is the fourth mission to return extraterrestrial material back to Earth.

    NASA’s Stardust mission, launched in 1999, returned microscopic samples from the trail of comet Wild-2. The Hayabusa mission, launched in 2003 by the Japanese space agency, JAXA, returned less than 1 milligram from asteroid Itokawa. JAXA’s Hayabusa2 (launched 2014) returned 5.4 grams of sample from asteroid Ryugu.

    NASA estimates OSIRIS-REx has brought back around 250 grams from asteroid Bennu, by far the largest sample yet recovered. We will know for sure once the sample is carefully examined at Johnson Space Centre over the coming days.

    The sound of fireballs

    We and our colleagues at Curtin University are heavily involved in the global effort to find out what asteroids are really made of, having participated in or analysed samples from all of these sample return missions and leading the Global Fireball Observatory.

    There are six OSIRIS-REx mission scientists from Curtin (including one of us – Nick Timms), and they will be among those receiving the first wave of samples in the coming weeks.

    The re-entry of the capsule also had its own incredible science value. It was essentially a human-made fireball.

    Fireballs, or really bright shooting stars from large space rocks, are quite rare and impossible to predict. This is why we use dedicated camera networks to observe large areas of sky (The Desert Fireball Network observes nearly three million square kilometres of Australian skies every night).

    When objects from outer space enter the atmosphere, travelling much faster than the speed of sound, they ignite the air to create a fireball and also trigger other less-studied phenomena such as shockwaves – which can be hazardous.

    A sample return is a great opportunity to set out seismic sensors and other instruments to analyse the shockwave, which can tell us more about the physics of re-entry and why some meteorites survive while others don’t make it. This was done for the Hayabusa2 sample return in 2020, and researchers from Sandia Labs and the University of Southern Queensland had detectors set up in Utah for the OSIRIS-REx return.

    What’s next?

    Like Hayabusa2, the OSIRIS-REx spacecraft itself isn’t finished yet. Both of these spacecraft dropped their precious samples to Earth and have continued on with the aim of future asteroid fly-bys.

    The mission, now renamed “OSIRIS-APEX”, has already begun to redirect itself towards an asteroid called Apophis, which it will intercept not long after the asteroid zooms past Earth in April 2029.The Conversation

    Eleanor K. Sansom, Research Associate, Curtin University and Nick Timms, Associate Professor, Curtin University

    This article is republished from The Conversation under a Creative Commons license. Read the original article.

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  • A magnetic therapy for depression gains precision – Knowable Mag

    A magnetic therapy for depression gains precision

    Approved over a decade ago, transcranial magnetic stimulation (TMS) is moderately effective. Tailoring the treatment to individual brains may improve results.

    9.7.2023

    In the mid-1970s, a British researcher named Anthony Barker wanted to measure the speed at which electrical signals travel down the long, slender nerves that can carry signals from the brain to muscles like those in the hand, triggering movement. To find out, he needed a way to stimulate nerves in people.

    Researchers had already used electrodes placed on the skin to generate a magnetic field that penetrated human tissue — this produced an electric current that activated the peripheral nerves in the limbs. But the technique was painful, burning the skin. Barker, at the University of Sheffield in England, and his colleagues started to work on a better method.

    In 1985, with promising results under their belts, they tried positioning the coil-shaped magnetic device they’d developed on participants’ heads. The coil emitted rapidly alternating magnetic pulses over the brain region that controls movement, generating weak electrical currents in the brain tissue and activating neurons that control muscles in the hand. After about 20 milliseconds, the participants’ fingers twitched.

    The technique, now called transcranial magnetic stimulation (TMS), has proved a vital tool for investigating how the human brain works. When targeted to specific brain regions, TMS can temporarily inhibit or enhance various functions – blocking the ability to speak, for instance, or making it easier to commit a series of numbers to memory. And when brain imaging technologies such as functional magnetic resonance imaging (fMRI) emerged in the 1990s, researchers could now “see” inside people’s brains as they received TMS stimulation. They could also observe how neural pathways respond differently to stimulation in psychiatric illnesses like schizophrenia and depression.

    In recent decades, this fundamental research has yielded new treatments that alter brain activity, with TMS therapies for depression at the fore. In 2008, the US Food and Drug Administration approved NeuroStar, the nation’s first TMS depression device, and many other countries have since sanctioned the approach.

    Yet even though TMS is now a widely available depression treatment, many questions remain about the method. It’s not clear how long the benefits of TMS can last, for example, or why it appears to work for some people with depression but not others. Another challenge is disentangling the effects of TMS from the placebo effect — when someone believes that they will benefit from treatment and gets better even though they’re receiving a “sham” form of stimulation.

    Whether TMS can “cure” depression “is an open question — there’s evidence for and against,” says David Pitcher, a cognitive neuroscientist at the University of York who wrote a 2021 overview in the Annual Review of Psychology on using TMS to study human cognition. But as researchers fine-tune the approach and run more sophisticated clinical trials, TMS is emerging as a powerful tool for dissecting depression’s complexities — and for some people, loosening its grip.

    From electric fish to magnets

    TMS may be relatively new, but using electricity as medicine is ancient. As early as the 1st century CE, Roman physicians recommended using live electric torpedo fish to treat headache. Almost two millennia later, in the 1930s, physicians discovered that inducing brain seizures with electricity could reduce symptoms of schizophrenia and other forms of mental illness.

    That was the beginning of electroconvulsive therapy (ECT) — pejoratively known as shock therapy. The practice spread rapidly despite the risk of memory loss, confusion and injuries from muscle spasms. Administering ECT without fully informing patients about the therapy and its risks also raised ethical concerns, an issue that medicine as a whole was seriously grappling with at the time.

    Eventually, muscle relaxants, anesthetics and more stringent consent protocols improved ECT, although side effects such as headache and temporary short-term memory loss are still reported. ECT remains one of the most effective treatments for people who don’t respond to first-line antidepressant treatments such as serotonin reuptake inhibitors (SSRIs), a group of drugs that includes Zoloft and Prozac.

    Yet both those drugs and ECT are difficult to control precisely, because they affect the whole brain. A more targeted approach is deep brain stimulation (DBS), which involves directly stimulating neurons with electrodes that are surgically implanted in regions known to affect mood and motivation. DBS has shown promise in pilot studies and was approved for investigative use in 2022, but has yet to receive clinical approval.

    TMS, by contrast, requires no surgery and has fewer side effects than ECT, says Alvaro Pascual-Leone, a neurologist at Harvard Medical School. Though it’s not as easy to target to a specific brain region as DBS, it is much more precise than antidepressant drugs or ECT.

    Pascual-Leone began investigating magnetic stimulation to treat major depressive disorder in the early 1990s. It excited him because of the ability to noninvasively focus the stimulation, and its few and relatively minor side effects, which commonly include scalp discomfort, tingling, spasms and lightheadedness and, rarely, seizures and hearing loss.

    Although its mechanisms aren’t fully understood, TMS appears to act by reconfiguring neural circuits, kickstarting more typical communication between different brain areas, says Noah S. Philip, a psychiatrist at Brown University who researches TMS for treating depression.

    At rest, people with depression often have reduced activity levels in an area of the brain called the dorsolateral prefrontal cortex (DLPFC) compared with non-depressed individuals, neuroimaging studies have shown. The region is a primary site for TMS therapy, says Philip. A hub for short-term memory, planning and abstract reasoning, the DLPFC is connected to several brain circuits implicated in depression: the salience network, which helps to focus attention on some things and ignore others; the default mode network, which is active when a person is not engaged in any particular task; and the executive network, key to planning, decision-making and impulse control. Together, these circuits underlie our ability to focus on relevant information and switch our attention between self-directed thinking and our environment.

    Scientists think that abnormal communication between the networks can lead to the constant rumination, self-criticism and tendency to overly focus on negative aspects in life that people with depression often experience. Using fMRI to measure how nodes in the networks communicate before and after TMS, Philip, among other researchers, has found that multiple sessions of TMS can restore more typical activity. He says the change can endure beyond a year and can possibly be maintained longer with additional TMS treatments.

    The sustained effects of TMS are likely due to the remodeling of neuronal connections brought on by microscopic changes to brain cells, Philip says. Studies have shown that TMS can stimulate neurons to sprout new dendrites, the branched appendages that receive signals from other neurons.

    An early clinical trial found that people with severe depression who received daily TMS for several weeks were up to four times as likely to go into remission as participants in control groups, who were fitted with a TMS device but didn’t receive actual stimulation. In later studies that lacked control groups — meaning both the patients and the doctors knew TMS was being administered — 30 percent to 40 percent of patients who hadn’t improved with medications went into remission, defined by a low score on a standard measure such as the Hamilton Depression Rating Scale. That’s roughly on par with the number of people who respond well to antidepressant medications, according to a 2013 review in Current Opinion in Psychiatry.

    Still, many questions remain — including whether better results can be gained by targeting specific regions in individual patients. “Some people with depression experience sadness, others have more of a lack of motivation or apathy,” says Pascual-Leone. “Some people eat too much; others eat too little.” Unlike more general treatments, he says, TMS holds such targeting potential.

    Bespoke brain stimulation

    In many clinics and research labs, the process of determining where to place TMS coils on a person’s head is relatively simple. The FDA-sanctioned method harks back to Barker’s original experiments: A participant sticks their thumb out like a hitchhiker, and technicians move the magnetic coil around their scalp until the electrical stimulation hits a part of the motor cortex that makes their thumb involuntarily twitch. Using this spot as their landmark, the technicians then move the coil to a position that targets the left DLPFC.

    The approach is moderately effective, but many researchers think it doesn’t adequately account for the large variations in brain structure among individuals. Increasingly, scientists are using fMRI and other brain imaging technologies to tailor TMS stimulation to each person’s unique brain structure and observe how it affects their neural activity patterns. “An exciting advance in the last 10 years with TMS is to use it on patients, then neuroimage their brain to look at changes in the connectivity between the DLPFC and the areas we know it’s connected to,” says Pitcher of the University of York.

    A team of investigators at Stanford University, led by psychiatrist Nolan Williams, director of the Stanford Brain Stimulation Lab, is one of the groups developing this combined approach. In a small 2021 study, the team used fMRI scans, which measure changes in blood flow associated with brain activity, to locate a small subregion in the DLPFC in individual patients. This subregion’s activity shows an inverse relationship to that of another brain area, the subgenual cingulate (SGC): In people who are experiencing depression, the SGC’s activity is boosted while the DLPFC subregion’s activity is lowered. Conversely, the more active the node in the DLPFC, the less active the SGC becomes. The SGC, for its part, appears to influence the default mode network, anchoring people in negative patterns of self-rumination.

    In the Stanford study, Williams and colleagues targeted the DLPFC subregion in 29 people with what’s known as treatment-resistant depression: They scored “moderate to severe” on a standard assessment that considers how they responded to previous depression treatments and the duration and severity of their symptoms. The group received an experimental, accelerated treatment regimen with more than one daily TMS session. To control for a potential placebo effect, some group members were randomly assigned to receive sham stimulation that sounded and felt like TMS but didn’t deliver the electromagnetic pulses.

    After five days of treatment, 79 percent of the participants who received the focused TMS experienced remission, compared with 13 percent of the control group. The team also observed that stimulating the area of the DLPFC that’s most strongly connected with the SGC normalizes the relevant connections among the three regions. “You see it when you scan people after,” Williams says.

    One participant in his early sixties, Tommy Van Brocklin, had battled depression for about 45 years. In recent years, the medication he had been taking stopped working.

    The five-day treatment made him feel “like a tree being pecked by a woodpecker,” because of the knocking sounds that the TMS device emits, he jokes. But on day three, he noticed a difference in his mood: “Everything seemed to kind of kick into gear, and it was good.”

    The researchers believe this individualized approach to TMS treatment could be a fast, effective intervention for suicidal patients. In 2022, Williams’s method passed an important regulatory hurdle: The FDA granted permission to commercialize it.

    Seeing such high remission rates after just five days of treatment — a highly practical intervention — is exciting, says William T. Regenold, director of a research unit that studies noninvasive neuromodulation at the US National Institute of Mental Health. He and his colleagues are currently conducting a clinical trial investigating changes in brain activity in severely depressed patients who receive TMS along with talk therapy. “The idea is to have a synergistic effect between the psychotherapy and the TMS,” he says.

    By adjusting the treatment to each person’s brain anatomy, the Stanford study’s success is “very aligned with the notions of precision medicine — of individually targeted interventions,” says Pascual-Leone.

    But there’s still much work ahead. One urgent challenge is to tease out the benefits of stimulation from the placebo effect; some research suggests that this effect plays a role in the improvements that many experience from TMS. This problem isn’t unique to brain stimulation, but is common to all depression treatments. Several meta-analyses of the placebo effect for antidepressant medications, for example, have found that people who get inactive pills experience a 20 percent to 40 percent improvement in their symptoms, typically measured by one of several standard questionnaires.

    Research groups are starting to achieve clearer, more impressive outcomes using brain scans to guide individualized stimulation, as the Stanford team did. But they’ll need more studies to determine if TMS will find similar success in larger populations, as well as in groups such as teenagers, the elderly and people who have conditions that often accompany depression, such as anxiety and post-traumatic stress. Some labs are experimenting with the design of TMS devices — comparing figure-8-shaped magnetic coils to ones shaped like butterfly wings, for example — and altering the frequency of stimulation to see how that alters brain activity and treatment outcomes.

    Still, many fundamental questions about TMS remain. Although scientists know it disrupts normal neuronal firing, “we don’t really understand how TMS works in a mechanistic way” to alter brain states like mood, says Pitcher. One reason is that researchers can’t record activity from a single neuron in a human being and do TMS at the same time, he says. It’s not clear why certain frequencies of TMS appear to ramp up activity in some brain regions, while turning it down in other areas — or how the new neuronal connections spurred by TMS affect the different brain networks.

    “Fortunately, we can do that work, advancing science while helping people with disabling diseases,” says Pascual-Leone. “That’s an amazing position to be in.”

    This article originally appeared in Knowable Magazine, an independent journalistic endeavor from Annual Reviews. Sign up for the newsletter.

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  • Kidneys Grown With Human Cells in Pig Embryos

    Chinese scientists are growing kidneys containing human cells in pig embryos. This is a first instance that could help address organ donation shortages.

    However, this development raises ethical issues – especially since some human cells were also found in the pigs’ brains, experts said.

    Researchers from the Guangzhou Institutes of Biomedicine and Health focused on kidneys because they are one of the first organs to develop, and the most commonly transplanted in human medicine.

    For example, rat organs have been produced in mice, and mouse organs have been produced in rats, but previous attempts to grow human organs in pigs have not succeeded, an expert claimed.

    This new approach improves the integration of human cells into recipient tissues and allows scientists to grow human organs in pigs.

    However, this is a different approach to the recent high-profile breakthroughs in the United States, where genetically modified pig kidneys and even a heart have been placed inside humans, the report said.

     

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  • Asteroid sample returned to Earth…

    A capsule containing a sample from a distant asteroid has been successfully returned to Earth and will soon be available for study, thanks to a Japanese Space Agency (JAXA) mission called Hayabusa2.

    The Hayabusa2 spacecraft visited asteroid Ryugu and collected a sample before bringing it back to Earth as part of a mission that has lasted six years so far. The sample was placed in a capsule and sent down to Earth, and the spacecraft will now carry on its mission by visiting another asteroid.

    As the capsule entered the atmosphere, it could be seen streaking across the sky in a fireball which was visible in many parts of the world. It was even visible from the International Space Station, where JAXA astronaut Soichi Noguchi spotted it pass him by.

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  • Brain scientists haven’t been able to find major differences between women’s and men’s brains, despite over a century of searching

    Are there innate differences between female and male brains?
    SebastianKaulitzki/Science Photo Library via Getty Images

    Ari Berkowitz, University of Oklahoma

    People have searched for sex differences in human brains since at least the 19th century, when scientist Samuel George Morton poured seeds and lead shot into human skulls to measure their volumes. Gustave Le Bon found men’s brains are usually larger than women’s, which prompted Alexander Bains and George Romanes to argue this size difference makes men smarter. But John Stuart Mill pointed out, by this criterion, elephants and whales should be smarter than people.

    So focus shifted to the relative sizes of brain regions. Phrenologists suggested the part of the cerebrum above the eyes, called the frontal lobe, is most important for intelligence and is proportionally larger in men, while the parietal lobe, just behind the frontal lobe, is proportionally larger in women. Later, neuroanatomists argued instead the parietal lobe is more important for intelligence and men’s are actually larger.

    In the 20th and 21st centuries, researchers looked for distinctively female or male characteristics in smaller brain subdivisions. As a behavioral neurobiologist and author, I think this search is misguided because human brains are so varied.

    Anatomical brain differences

    The largest and most consistent brain sex difference has been found in the hypothalamus, a small structure that regulates reproductive physiology and behavior. At least one hypothalamic subdivision is larger in male rodents and humans.

    But the goal for many researchers was to identify brain causes of supposed sex differences in thinking – not just reproductive physiology – and so attention turned to the large human cerebrum, which is responsible for intelligence.

    Within the cerebrum, no region has received more attention in both race and sex difference research than the corpus callosum, a thick band of nerve fibers that carries signals between the two cerebral hemispheres.

    In the 20th and 21st centuries, some researchers found the whole corpus callosum is proportionally larger in women on average while others found only certain parts are bigger. This difference drew popular attention and was suggested to cause cognitive sex differences.

    But smaller brains have a proportionally larger corpus callosum regardless of the owner’s sex, and studies of this structure’s size differences have been inconsistent. The story is similar for other cerebral measures, which is why trying to explain supposed cognitive sex differences through brain anatomy has not been very fruitful.

    Female and male traits typically overlap

    Chart showing that male traits in blue and female traits in pink overlap quite a bit.
    A chart showing how measurements that often differ between sexes, like height, substantially overlap.
    Ari Berkowitz, CC BY

    Even when a brain region shows a sex difference on average, there is typically considerable overlap between the male and female distributions. If a trait’s measurement is in the overlapping region, one cannot predict the person’s sex with confidence. For example, think about height. I am 5’7″. Does that tell you my sex? And brain regions typically show much smaller average sex differences than height does.

    Neuroscientist Daphna Joel and her colleagues examined MRIs of over 1,400 brains, measuring the 10 human brain regions with the largest average sex differences. They assessed whether each measurement in each person was toward the female end of the spectrum, toward the male end or intermediate. They found that only 3% to 6% of people were consistently “female” or “male” for all structures. Everyone else was a mosaic.

    Prenatal hormones

    When brain sex differences do occur, what causes them?

    A 1959 study first demonstrated that an injection of testosterone into a pregnant rodent causes her female offspring to display male sexual behaviors as adults. The authors inferred that prenatal testosterone (normally secreted by the fetal testes) permanently “organizes” the brain. Many later studies showed this to be essentially correct, though oversimplified for nonhumans.

    Researchers cannot ethically alter human prenatal hormone levels, so they rely on “accidental experiments” in which prenatal hormone levels or responses to them were unusual, such as with intersex people. But hormonal and environmental effects are entangled in these studies, and findings of brain sex differences have been inconsistent, leaving scientists without clear conclusions for humans.

    Genes cause some brain sex differences

    A zebra finch showing male plumage on one side and female plumage on the other side.
    A half male, half female zebra finch, 2003.
    Copyright 2003 National Academy of Sciences, CC BY-NC

    While prenatal hormones probably cause most brain sex differences in nonhumans, there are some cases where the cause is directly genetic.

    This was dramatically shown by a zebra finch with a strange anomaly – it was male on its right side and female on its left. A singing-related brain structure was enlarged (as in typical males) only on the right, though the two sides experienced the same hormonal environment. Thus, its brain asymmetry was not caused by hormones, but by genes directly. Since then, direct effects of genes on brain sex differences have also been found in mice.

    Learning changes the brain

    Many people assume human brain sex differences are innate, but this assumption is misguided.

    Humans learn quickly in childhood and continue learning – alas, more slowly – as adults. From remembering facts or conversations to improving musical or athletic skills, learning alters connections between nerve cells called synapses. These changes are numerous and frequent but typically microscopic – less than one hundredth of the width of a human hair.

    Man studying massive maps of London
    Some London taxi drivers do not use GPS – they know the city by heart, a learning process that takes three to four years on average.
    Carl Court/AFP via Getty Images

    Studies of an unusual profession, however, show learning can change adult brains dramatically. London taxi drivers are required to memorize “the Knowledge” – the complex routes, roads and landmarks of their city. Researchers discovered this learning physically altered a driver’s hippocampus, a brain region critical for navigation. London taxi drivers’ posterior hippocampi were found to be larger than nondrivers by millimeters – more than 1,000 times the size of synapses.

    [Deep knowledge, daily. Sign up for The Conversation’s newsletter.]

    So it’s not realistic to assume any human brain sex differences are innate. They may also result from learning. People live in a fundamentally gendered culture, in which parenting, education, expectations and opportunities differ based on sex, from birth through adulthood, which inevitably changes the brain.

    Ultimately, any sex differences in brain structures are most likely due to a complex and interacting combination of genes, hormones and learning.The Conversation

    Ari Berkowitz, Presidential Professor of Biology; Director, Cellular & Behavioral Neurobiology Graduate Program, University of Oklahoma

    This article is republished from The Conversation under a Creative Commons license. Read the original article.

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  • How gene editing a person’s brain cells could be used to curb the opioid epidemic

    CRISPR/Cas is a tool for editing genes.
    STEVEN MCDOWELL/SCIENCE PHOTO LIBRARY / Getty Images

    Craig W. Stevens, Oklahoma State University

    Even as the COVID-19 pandemic cripples the economy and kills hundreds of people each day, there is another epidemic that continues to kill tens of thousands of people each year through opioid drug overdose.

    Opioid analgesic drugs, like morphine and oxycodone, are the classic double-edged swords. They are the very best drugs to stop severe pain but also the class of drugs most likely to kill the person taking them.
    In a recent journal article, I outlined how a combination of state-of-the-art molecular techniques, such as CRISPR gene editing and brain microinjection methods, could be used to blunt one edge of the sword and make opioid drugs safer.

    I am a pharmacologist interested in the way opioid drugs such as morphine and fentanyl can blunt pain. I became fascinated in biology at the time when endorphins – natural opioids made by our bodies – were discovered. I have been intrigued by the way opioid drugs work and their targets in the brain, the opioid receptors, for the last 30 years. In my paper, I propose a way to prevent opioid overdoses by modifying an opioid user’s brain cells using advanced technology.

    Opioid receptors stop breathing

    Opioids kill by stopping a person from breathing (respiratory depression). They do so by acting on a specific set of respiratory nerves, or neurons, found in the lower part of the brain that contain opioid receptors. Opioid receptors are proteins that bind morphine, heroin and other opioid drugs. The binding of an opioid to its receptor triggers a reaction in neurons that reduces their activity. Opioid receptors on pain neurons mediate the pain-killing, or analgesic, effects of opioids. When opioids bind to opioid receptors on respiratory neurons, they slow breathing or, in the case of an opioid overdose, stop it entirely.

    Respiratory neurons are located in the brainstem, the tail-end part of the brain that continues into the spine as the spinal cord. Animal studies show that opioid receptors on respiratory neurons are responsible for opioid-induced respiratory depression – the cause of opioid overdose. Genetically altered mice born without opioid receptors do not die from large doses of morphine unlike mice with these receptors present.

    The brainstem is the the red part protruding from the bottom of the brain.
    MedicalRF.com / Getty Images

    Unlike laboratory mice, humans cannot be altered when embryos to remove all opioid receptors from the brain and elsewhere. Nor would it be a good idea. Humans need opioid receptors to serve as the targets for our natural opioid substances, the endorphins, which are released into the brain during times of high stress and pain.

    Also, a total opioid receptor knockout in humans would leave that person unresponsive to the beneficial pain-killing effects of opioids. In my journal article, I argue that what is needed is a selective receptor removal of the opioid receptors on respiratory neurons. Having reviewed the available technology, I believe this can be done by combining CRISPR gene editing and a new neurosurgical microinjection technique.

    CRISPR to the rescue: Destroying opioid receptors

    CRISPR, which is an acronym for clustered regularly interspaced short palindromic repeats, is a gene editing method that was discovered in the genome of bacteria. Bacteria get infected by viruses too and CRISPR is a strategy that bacteria evolved to cut-up the viral genes and kill invading pathogens.

    The CRISPR method allows researchers to target specific genes expressed in cell lines, tissues, or whole organisms, to be cut-up and removed – knocked out – or otherwise altered. There is a commercially available CRISPR kit which knocks out human opioid receptors produced in cells that are grown in cell cultures in the lab. While this CRISPR kit is formulated for in vitro use, similar conditional opioid receptor knock-out techniques have been demonstrated in live mice.

    To knockout opioid receptors in human respiratory neurons, a sterile solution containing CRISPR gene-editing molecules would be prepared in the laboratory. Besides the gene-editing components, the solution contains chemical reagents that allow the gene-editing machinery to enter the respiratory neurons and make their way into the nucleus and into the neuron’s genome.

    How does one get the CRISPR opioid receptor knockout solution into a person’s respiratory neurons?

    Enter the intracranial microinjection instrument (IMI) developed by Miles Cunningham and his colleagues at Harvard. The IMI allows for computer-controlled delivery of small volumes of solution at specific places in the brain by using an extremely thin tube – about twice the diameter of a human hair – that can enter the brain at the base of the skull and thread through brain tissue without damage.

    The computer can direct the robotic placement of the tube as it is fed images of the brain taken before the procedure using MRI. But even better, the IMI also has a recording wire embedded in the tube that allows measurement of neuronal activity to identify the right group of nerve cells.

    Because the brain itself feels no pain, the procedure could be done in a conscious patient using only local anesthetics to numb the skin. Respiratory neurons drive the breathing muscles by firing action potentials which are measured by the recording wire in the tube. When the activity of the respiratory neurons matches the breathing movements by the patients, the proper location of the tube is confirmed and the CRISPR solution injected.

    The call for drastic action

    Opioid receptors on neurons in the brain have a half-life of about 45 minutes. Over a period of several hours, the opioid receptors on respiratory neurons would degrade and the CRISPR gene-editing machinery embedded in the genome would prevent new opioid receptors from appearing. If this works, the patient would be protected from opioid overdose within 24 hours. Because the respiratory neurons do not replenish, the CRISPR opioid receptor knockout should last for life.

    With no opioid receptors on respiratory neurons, the opioid user cannot die from opioid overdose. After proper backing from National Institute on Drug Abuse and leading research and health care institutions, I believe CRISPR treatment could enter clinical trials in between five to 10 years. The total cost of opioid-involved overdose deaths is about US$430 billion per year. CRISPR treatment of only 10% of high-risk opioid users in one year would save thousands of lives and $43 billion.

    [Deep knowledge, daily. Sign up for The Conversation’s newsletter.]

    Intracranial microinjection of CRISPR solutions might seem drastic. But drastic actions that are needed to save human lives from opioid overdoses. A large segment of the opioid overdose victims are chronic pain patients. It may be possible that chronic pain patients in a terminal phase of their lives and in hospice care would volunteer in phase I clinical trials for the CRISPR opioid receptor knockout treatment I propose here.

    Making the opioid user impervious to death by opioids is a permanent solution to a horrendous problem that has resisted efforts by prevention, treatment and pharmacological means. Steady and well-funded work to prove the CRISPR method, first with preclinical animal models then in clinical trials, is a moonshot for the present generation of biomedical scientists.The Conversation

    Craig W. Stevens, Professor of Pharmacology, Oklahoma State University

    This article is republished from The Conversation under a Creative Commons license. Read the original article.

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