Chapter 3. Neurophysiology: The Generation, Transmission, and Integration of Neural Signals

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By Sara Van Note On a recent Saturday morning, two-year-old Ryleigh and five-year-old Colton Arnett play with brightly colored play dough in the family room of their Albuquerque home. Colton narrates his creations with a gap-toothed smile. “I’m going to use a mold. I’m going to make a boat.” Ryleigh echoes him enthusiastically, “Mold! Boat!” An estimated 30,000 New Mexicans carry the mutation, and the numbers are increasing. Their mother, Lori Dunworth, remarks that Colton and his sister don’t usually play so well together. “Usually she’s a bit of a bully when it comes to toys.” Both Ryleigh and Colton receive speech therapy because of something that happened to Colton several years ago, when Dunworth and her husband, Toby Arnett, first noticed that Colton, who was two at the time, was making repeating clicking sounds while his face twitched on one side. After one episode lasted over 20 minutes, they called their doctor, who told them to take him to the hospital immediately. Colton had suffered a seizure, and scans would later reveal masses in his brain — lesions, it turned out, caused by abnormal blood vessels. “The original impact was devastating,” Arnett says. Colton was ultimately diagnosed with Cerebral Cavernous Malformations (CCM), a rare disease that can cause seizure, stroke, and death. He also tested positive for a genetic mutation that causes the disease, known as the Common Hispanic Mutation. Colton’s sister and his mom also have the mutation. Dunworth had no idea she was the carrier. “I’ve never had any symptoms, no seizures, no paralysis, no nothing,” she says. Copyright 2017 Undark

Keyword: Epilepsy; Genes & Behavior
Link ID: 24184 - Posted: 10.12.2017

By Dan Stark I used to tell people considering deep brain stimulation — which involves the surgical implantation of electrodes into the brain — that it gave the typical Parkinson’s sufferer perhaps 10 years of relief, during which the symptoms would be relatively minor. The bet — this is, after all, brain surgery that carries some risk of serious adverse results — would be that sometime during that decade, researchers would come up with a real solution. In other words, DBS was a way to buy time. Still, 10 years is no small period, particularly for those who have no other hope. My experience is typical. I had DBS just under 12 years ago. Things went so well that I became a huge fan of the procedure. But DBS works on only some Parkinson’s symptoms. (Drooling, for example, is not affected.) For slightly more than a decade, DBS performed wonders on me, eliminating the shakes that had accompanied my attempts to beat back Parkinson’s symptoms with medicine alone. But because DBS masks the symptoms while not affecting the underlying disease, in the end it will fail the Parkinson’s patient. For me, the failure was in the form of a one-two punch. The first blow was self-inflicted. In April, one of the batteries powering my neural implants died. That was my fault; one should monitor the batteries and replace them in advance. Because I hadn’t, I got a taste of what life would be like without the stimulators. © 1996-2017 The Washington Post

Keyword: Parkinsons
Link ID: 24132 - Posted: 10.02.2017

By John Horgan “The Forgotten Era of Brain Chips,” published in Scientific American in October 2005, has provoked as much interest as anything I’ve ever written. It focuses on Jose Manuel Rodriguez Delgado, a pioneer in brain-stimulation research. I keep hearing from journalists and others wanting more information on Delgado, whom I interviewed in 2005 and who died in 2011. Delgado fascinates conspiracy theorists, too. An article on Infowars.com describes him as a “madman” who believed that “no human being has an inherent right to his own personality.” Given widespread interest in and misinformation about Delgado, whose work prefigures current research on brain implants (see “Further Reading”), I’m posting an edited version of my 2005 article. --John Horgan Once among the world’s most acclaimed scientists, Jose Manuel Rodriguez Delgado has become an urban legend, whose career is shrouded in misinformation. Delgado pioneered that most unnerving of technologies, the brain chip, which manipulates the mind by electrically stimulating neural tissue with implanted electrodes. Long a McGuffin of science fictions, from The Terminal Man to The Matrix, brain chips are now being tested as treatments for epilepsy, Parkinson’s disease, paralysis, depression, and other disorders. In part because it was relatively unencumbered by ethical regulations, Delgado’s research rivaled and even surpassed much of what is being done today. In 1965, The New York Times reported on its front page that he had stopped a charging bull in its tracks by sending a radio signal to a device implanted in its brain. He also implanted radio-equipped electrode arrays, which he called “stimoceivers,” in dogs, cats, monkeys, chimpanzees, gibbons, and humans. With the push of a button, he could evoke smiles, snarls, bliss, terror, hunger, garrulousness, lust, and other responses. © 2017 Scientific American,

Keyword: Aggression
Link ID: 24131 - Posted: 10.02.2017

Mariah Quintanilla Kenneth Catania knows just how much it hurts to be zapped by an electric eel. For the first time, the biologist at Vanderbilt University in Nashville has measured the strength of a defensive electrical attack on a real-life potential predator — himself. Catania placed his arm in a tank with a 40-centimeter-long electric eel (relatively small as eels go) and determined, in amperes, the electrical current that flowed into him when the eel struck. At its peak, the current reached 40 to 50 milliamperes in his arm, he reports online September 14 in Current Biology. This zap was painful enough to cause him to jerk his hand from the tank during each trial. “If you’ve ever been on a farm and touched an electric fence, it’s pretty similar to that,” he says. This is Catania’s latest study in a body of research analyzing the intricacies of an electric eel’s behavior. The way electric eels have been described by biologists in the past has been fairly primitive, says Jason Gallant, a biologist who heads the Michigan State University Electric Fish Lab in East Lansing who was not involved in the study. Catania’s work reveals that “what the electric eel is doing is taking the electric ability that it has and using that to its absolute advantage in a very sophisticated, deliberate way,” he says. Electric eels use electric current to navigate, communicate and hunt for small prey. But when faced with a large land-based predator, eels will launch themselves from the water and electrify the animal with a touch of the head. |© Society for Science & the Public 2000 - 2017.

Keyword: Aggression
Link ID: 24068 - Posted: 09.15.2017

By Giorgia Guglielmi The trillions of bacteria that live in our intestines, known collectively as the gut microbiome, have been linked to maladies from eye disease to rheumatoid arthritis. Now, two new studies have added another disease: multiple sclerosis (MS), an autoimmune disorder that strips away nerve cells’ protective covers, leading to muscle weakness, blindness, and even death. What’s more, the studies suggest how our gut microbes make the immune system turn against nerve cells—a finding that could lead to treatments, like drugs based on microbial byproducts, that might improve the course of the disease. MS affects 2.5 million people worldwide, but little is known about what causes the disease, which progressively disrupts information flow from and within the brain. Most researchers think it starts when genetically predisposed people encounter an as-yet-unknown environmental trigger. Previous studies have identified particular bacteria present in increased amounts in the guts of MS patients. But the new papers “took it to the next level” in trying to understand how these bacteria affect the immune system, says Francisco Quintana, a neuroimmunologist at Brigham and Women’s Hospital in Boston not involved with the work. “These are going to be landmark studies.” In the first paper, a team of researchers led by Sergio Baranzini, a human geneticist at the University of California, San Francisco, analyzed the microbiomes of 71 people with MS and 71 healthy individuals, aged 19 to 71. They found that two bacterial groups, Acinetobacter and Akkermansia, were four times more abundant in MS patients than in individuals with no disease. Another group, Parabacteroides, was four times as abundant in healthy people. © 2017 American Association for the Advancement of Science

Keyword: Multiple Sclerosis
Link ID: 24059 - Posted: 09.13.2017

By Mo Costandi Voluntary movements are one of the brain’s main “outputs,” yet science still knows very little about how networks of neurons plan, initiate and execute them. Now, researchers from Columbia University and the Champalimaud Center for the Unknown in Lisbon, Portugal, say they have discovered an “activity map” that the brain uses to guide animals’ movements. The findings, published Wednesday in Neuron, could advance our understanding of how the brain learns new movements—and of what goes wrong in related disorders such as Parkinson's disease. Movements are controlled and coordinated by multiple brain structures including the primary motor cortex. Located at the back of the frontal lobe, it contains cells whose long fibers extend down through the spinal cord, where they contact “secondary” motor neurons that signal the body muscles. A set of deep brain structures called the basal ganglia are also critical for movement, as evidenced by their degeneration in conditions such as Parkinson’s. One component of the basal ganglia, called the striatum, receives information about possible actions from the motor cortex and is thought to be involved in selecting, preparing and executing the appropriate commands before they are sent to the body. Earlier research had shown that signals leave the striatum along one of two distinct pathways: one that facilitates movement, and another that suppresses it. A number of more recent studies show that both pathways are active during motion, however, suggesting that they do not act by simply sending “stop” and “go” signals. And although it has long been suspected that different groups of neurons in the striatum represent distinct actions, exactly how they might do so has remained unclear. © 2017 Scientific American

Keyword: Parkinsons; Brain imaging
Link ID: 24016 - Posted: 08.31.2017

By Meredith Wadman Luca Rossi tried to hang himself in a bedroom in Perugia, Italy, in 2012. Suspended by his belt from a wardrobe, he had begun to choke when his fiancée unexpectedly walked in. He struggled to safety, defeated even in this intended last act. The 35-year-old physician had everything to live for: a medical career, plans for a family, and supportive parents. But Rossi* was addicted to crack cocaine. He had begun his habit not long after medical school, confidently assuming that he could control the drug. Now, it owned him. Once ebullient and passionate, he no longer smiled or cried. He knew he might be endangering his patients, but even that didn’t matter. He was indifferent to all except obtaining his next fix. “It pushes you to suicide because it fills you with your own emptiness,” he says. In the first months after his near suicide, Rossi didn’t drop his $3500-a-month habit. Early in 2013, he learned that his fiancée was pregnant. Frightened by impending fatherhood, he smoked even more. He didn’t—couldn’t—stop. Then, in April 2013, Rossi’s father, a chemist, happened upon a local newspaper article describing work just published in Nature. Neuroscientists led by Antonello Bonci and Billy Chen at the National Institute on Drug Abuse (NIDA) in Baltimore, Maryland, had studied rats trained to seek cocaine compulsively—animals so powerfully addicted that they tolerated repeated electric shocks to their feet to get their fixes. The rats had also been genetically engineered so that their neurons could be controlled with light. When the researchers stimulated the animals’ brains in an area that regulates impulse control, the rats essentially kicked their habit. “They would almost instantaneously stop searching for cocaine,” Bonci says. © 2017 American Association for the Advancement of Science

Keyword: Brain imaging; Drug Abuse
Link ID: 24013 - Posted: 08.30.2017

Kerri Smith Marta Zlatic owns what could be the most tedious film collection ever. In her laboratory at the Janelia Research Campus in Ashburn, Virginia, the neuroscientist has stored more than 20,000 hours of black-and-white video featuring fruit-fly (Drosophila) larvae. The stars of these films are doing mundane maggoty things, such as wriggling and crawling about, but the footage is helping to answer one of the biggest questions in modern neuroscience: how the circuitry of the brain creates behaviour. It's a major goal across the field: to work out how neurons wire up, how signals move through the networks and how these signals work together to pilot an animal around, to make decisions or — in humans — to express emotions and create consciousness. Even under the most humdrum conditions — “normal lighting; no sensory cues; they're not hungry”, says Zlatic — her fly larvae can be made to perform 30 different actions, including retracting or turning their heads, or rolling. The actions are generated by a brain comprising just 15,000 neurons. That is nothing compared with the 86 billion in a human brain, which is one of the reasons Zlatic and her teammates like the maggots so much. “At the moment, really, the Drosophila larva is the sweet spot,” says Albert Cardona, Zlatic's collaborator and husband, who is also at Janelia. “If you can get the wiring diagram, you have an excellent starting point for seeing how the central nervous system works.” © 2017 Macmillan Publishers Limited

Keyword: Brain imaging
Link ID: 23944 - Posted: 08.10.2017

Michael Viney I first saw them by night, or rather by flashlight aimed beside the dinghy as we fished a mile beyond Brighton’s pier. A whole shoal of them appeared beneath the boat, waving their arms, their button eyes glistening. We were not fishing for squid – too foreign a taste for England in those days. But this early glimpse left me fascinated with their kind, not least their giant, still greatly mysterious relative with eyes the size of hubcaps. The Brighton squids were the regular, long-fin Doryteuthis of inshore waters, not the huge, deep-water Architeuthis dux, snared this summer as trawler by-catch on the Porcupine Bank. The Cú na Mara (a nice echo) landed two separate specimens at Dingle a few weeks apart. Expiring on they way up, each was around 6m long, counting in the tentacles. They brought to seven the number landed in 350 years, including a remarkable three in 1995 alone. Two of those were trawled from the Porcupine Bank by a Marine Institute survey vessel. Dr Kevin Flannery, the Dingle marine biologist, would now like the institute to send its remote cameras for a proper look around. Meanwhile, the second squid, as dead as the first but in better shape, will soon be on display in the Dingle Oceanworld aquarium. What could seem strangest is that giant squid are soft-bodied molluscs, like limpets or winkles. Abandoning external shells to work on jet propulsion, they have developed genes and nerves of special interest to science. © 2017 THE IRISH TIMES

Keyword: Miscellaneous
Link ID: 23923 - Posted: 08.07.2017

Brandie Jefferson It wasn't long ago that there were no treatments for multiple sclerosis. In the 1970s, some doctors used chemotherapy to treat the degenerative neurological disease. Since then, more than a dozen drugs have been developed or approved, including infusions, oral medications and self-administered shots. None of these are a magic bullet for a disease that can be disabling and deadly. But now there is a new drug, Ocrevus, that looks like a game-changer. It uses a novel approach to blocking the inflammation that drives the disease and looks as if it's spectacularly effective. It also costs $65,000 a year. I have MS. Should I take Ocrevus? That, I discovered, is not a simple question to answer. But because I'm an MS patient and a science journalist, I was determined to try to figure it out. In March, the FDA approved Ocrevus (ocrelizumab) for the treatment of relapsing-remitting multiple sclerosis, the most common form of the disease. People with RRMS tend to have flare-ups when their symptoms worsen, followed by periods of remission and, in some cases, a full or partial recovery. In two clinical trials sponsored by the drug's eventual manufacturer, F. Hoffmann-La Roche, RRMS patients who were given ocrelizumab had about 50 percent fewer relapses and up to 95 percent fewer new lesions on the brain and spinal cord than those who were given Rebif, a common therapy. MS is an autoimmune disease, meaning the body attacks itself. The body's nerve endings and the fatty tissue that coats them, called myelin, bear the brunt of the immune system's attacks. As a result, the central nervous system has difficulty communicating with the nerves, leading to a disease that manifests itself in different ways, such as pain, fatigue, disability and slurred speech. © 2017 npr

Keyword: Multiple Sclerosis
Link ID: 23838 - Posted: 07.14.2017

By Matthew Hutson Artificial neural networks, computer algorithms that take inspiration from the human brain, have demonstrated fancy feats such as detecting lies, recognizing faces, and predicting heart attacks. But most computers can’t run them efficiently. Now, a team of engineers has designed a computer chip that uses beams of light to mimic neurons. Such “optical neural networks” could make any application of so-called deep learning—from virtual assistants to language translators—many times faster and more efficient. “It works brilliantly,” says Daniel Brunner, a physicist at the FEMTO-ST Institute in Besançon, France, who was not involved in the work. “But I think the really interesting things are yet to come.” Most computers work by using a series of transistors, gates that allow electricity to pass or not pass. But decades ago, physicists realized that light might make certain processes more efficient—for example, building neural networks. That’s because light waves can travel and interact in parallel, allowing them to perform lots of functions simultaneously. Scientists have used optical equipment to build simple neural nets, but these setups required tabletops full of sensitive mirrors and lenses. For years, photonic processing was dismissed as impractical. Now, researchers at the Massachusetts Institute of Technology (MIT) in Cambridge have managed to condense much of that equipment to a microchip just a few millimeters across. © 2017 American Association for the Advancement of Science

Keyword: Robotics
Link ID: 23758 - Posted: 06.21.2017

By Neuroskeptic A high-profile paper in Cell reports on a new brain stimulation method that’s got many neuroscientists excited. The new technique, called temporal interference (TI) stimulation, is said to be able to reach structures deep inside the brain, using nothing more than scalp electrodes. Currently, the only way to stimulate deep brain structures is by implanting electrodes (wires) into the brain – which is an expensive and potentially dangerous surgical procedure. TI promises to make deep brain stimulation an everyday, non-invasive tool. But will it really work? The paper comes from Nir Grossman et al. from the lab of Edward S. Boyden at MIT. Their technique is based around applying two electrical fields to the subject’s head. Each field is applied using two scalp electrodes. It is the interaction between the two fields that creates brain stimulation. Both fields oscillate at slightly different frequencies, for instance 2 kHz and 2.01 kHz. Where these fields overlap, a pattern of interference is created which oscillates with an ‘envelope’ at a much lower frequency, say 10 Hz. The frequency of the two fields is too high to have any effect on neural activity, but the interference pattern does have an effect. Crucially, while the electric fields are strongest close to the electrodes, the interference pattern is most intense at a remote point – which could be deep in the brain.

Keyword: Brain imaging; Parkinsons
Link ID: 23740 - Posted: 06.14.2017

In a pair of studies, scientists at the National Institutes of Health explored how the human brain stores and retrieves memories. One study suggests that the brain etches each memory into unique firing patterns of individual neurons. Meanwhile, the second study suggests that the brain replays memories faster than they are stored. The studies were led by Kareem Zaghloul, M.D., Ph.D., a neurosurgeon-researcher at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS). Persons with drug resistant epilepsy in protocols studying surgical resection of their seizure focus at the NIH’s Clinical Center enrolled in this study. To help locate the source of the seizures, Dr. Zaghloul’s team surgically implanted a grid of electrodes into the patients’ brains and monitored electrical activity for several days. “The primary goal of these recordings is to understand how to stop the seizures. However, it’s also a powerful opportunity to learn how the brain works,” said Dr. Zaghloul. For both studies, the researchers monitored brain electrical activity while testing the patients’ memories. The patients were shown hundreds of pairs of words, like “pencil and bishop” or “orange and navy,” and later were shown one of the words and asked to remember its pair. In one study, published in the Journal of Neuroscience, the patients correctly remembered 38 percent of the word pairs they were shown. Electrical recordings showed that the brain waves the patients experienced when they correctly stored and remembered a word pair often occurred in the temporal lobe and prefrontal cortex regions. Nevertheless, the researchers showed that the waves that appeared when recalling the words happened faster than the waves that were present when they initially stored them as memories.

Keyword: Learning & Memory; Epilepsy
Link ID: 23704 - Posted: 06.03.2017

Mo Costandi Since 1997, more than 100,000 Parkinson’s Disease patients have been treated with deep brain stimulation (DBS), a surgical technique that involves the implantation of ultra-thin wire electrodes. The implanted device, sometimes referred to as a ‘brain pacemaker’, delivers electrical pulses to a structure called the subthalamic nucleus, located near the centre of the brain, and effectively alleviates many of the physical symptoms of the disease, such as tremor, muscle rigidity, and slowed movements. DBS is generally safe but, like any surgical procedure, comes with some risks. First and foremost, it is highly invasive, requiring small holes to be drilled in the patient’s skull, through which the electrodes are inserted. Potential complications of this include infection, stroke, and bleeding on the brain. The electrodes, which are implanted for long periods of time, sometimes move out of place; they can also cause swelling at the implantation site; and the wire connecting them to the battery, typically placed under the skin of the chest, can erode, all of which require additional surgical procedures. Now, researchers at the Massachusetts Institute of Technology have a developed a new method that can stimulate cells deep inside the brain non-invasively, using multiple electric fields applied from outside the organ. In a study published today in the journal Neuron, they show that the method can selectively stimulate deep brain structures in live mice, without affecting the activity of cells in the overlying regions, and also that it can be easily adjusted to evoke movements by stimulation of the motor cortex. © 2017 Guardian News and Media Limited o

Keyword: Parkinsons
Link ID: 23700 - Posted: 06.02.2017

By Gary Stix In April, DARPA announced contracts for a program to develop practical methods to help someone learn more quickly. In the ensuing press coverage, the endeavor drew immediate comparisons to the The Matrix—in which Neo, the Keanu Reeves character, has his brain reprogrammed so that he instantly masters Kung Fu. DARPA is known for setting ambitious goals for its technology development programs. But it is not requiring contractors for the $50 million, four-year effort to find a way to let a special forces soldier upload neural codes to instantaneously execute a flawless Wushu butterfly kick. The agency did award contracts, though, to find some means of zapping nerves in the peripheral nervous system outside the brain to speed the rate at which a foreign language can be learned by as much as 30 percent, a still not-too-shabby goal. Sending an electrical current into the vagus nerve in the neck from a surgically implanted device is already approved for treating epilepsy and depression. The DARPA program, in tacit acknowledgement that mandatory surgery might be unacceptable for students contemplating an accelerated Mandarin class, wants to develop a non-invasive device to stimulate a peripheral nerve, perhaps in the ear. The goal is to hasten, not just the learning of foreign languages, but also to facilitate pattern recognition tasks such as combing through surveillance imagery. © 2017 Scientific American,

Keyword: Learning & Memory
Link ID: 23699 - Posted: 06.02.2017

A cannabis compound has been proven for the first time to reduce the frequency of seizures in people with a rare, severe form of epilepsy, according to the results of a randomized trial. For years, parents have pointed to anecdotal benefits of cannabidiol (CBD), a compound in the marijuana plant that does not produce a high, saying it reduces seizures in treatment-resistant epilepsy. Now doctors have performed a randomized trial to show cause and effect, with the findings published in Wednesday's issue of the New England Journal of Medicine. To conduct the study, the researchers focused on Dravet syndrome, a rare form of epilepsy that begins in infancy and is linked to a particular mutation that often resists combinations of up to 10 conventional seizure medications. They enrolled 120 patients who ranged in age from 2.5 to 18 years. Sixty-one patients were randomly assigned to cannabidiol, and the 59 others to placebo. Neither the researchers nor the families knew who received the medication to prevent bias. All continued to take their existing medications. "The message is that cannabidiol does work in reducing convulsing seizures in children with Dravet syndrome," said lead author Dr. Orrin Devinksy, who is director of NYU's Langone Comprehensive Epilepsy Center. For those in the cannabinoid group, the median number of convulsive seizures per month dropped from 12.4 per month before treatment, to 5.9 seizures, the researchers reported. The placebo group, in comparison, only saw their convulsive seizures fall from 14.9 per month, to 14.1. ©2017 CBC/Radio-Canada.

Keyword: Epilepsy; Drug Abuse
Link ID: 23659 - Posted: 05.25.2017

By Esther Landhuis On the heels of one failed drug trial after another, a recent study suggests people with early Alzheimer’s disease could reap modest benefits from a device that uses magnetic fields to produce small electric currents in the brain. Alzheimer’s is a degenerative brain disorder that afflicts more than 46 million people worldwide. At present there are no treatments that stop or slow its progression, although several approved drugs offer temporary relief from memory loss and other cognitive symptoms by preventing the breakdown of chemical messengers among nerve cells. The new study tested a regimen that combines computerized cognitive training with a procedure known as repetitive transcranial magnetic stimulation (rTMS). The U.S. Food and Drug Administration has cleared rTMS devices for some migraine sufferers as well as for people with depression who have not responded to antidepressant medications. Last month at the 13th International Conference on Alzheimer’s and Parkinson’s Diseases in Vienna, Israel-based Neuronix reported results of a phase III clinical trial of its therapy system, known as neuroAD, in Alzheimer’s patients. More than 99 percent of Alzheimer’s drug trials have failed. The last time a phase III trial for a wholly new treatment succeeded (not just a combination of two already approved drugs) was about 15 years ago. The recent study did not test a drug but rather a device, which usually has an easier time gaining FDA clearance. NeuroAD has been approved for use in Europe and the U.K., where six weeks of therapy costs about $6,700. The system is not commercially available in the U.S., but based on the latest results the company submitted an application for FDA clearance last fall. © 2017 Scientific American

Keyword: Alzheimers
Link ID: 23635 - Posted: 05.19.2017

Jon Hamilton Tiny, 3-D clusters of human brain cells grown in a petri dish are providing hints about the origins of disorders like autism and epilepsy. An experiment using these cell clusters — which are only about the size of the head of a pin — found that a genetic mutation associated with both autism and epilepsy kept developing cells from migrating normally from one cluster of brain cells to another, researchers report in the journal Nature. "They were sort of left behind," says Dr. Sergiu Pasca, an assistant professor of psychiatry and behavioral sciences at Stanford. And that type of delay could be enough to disrupt the precise timing required for an actual brain to develop normally, he says. The clusters — often called minibrains, organoids or spheroids — are created by transforming skin cells from a person into neural stem cells. These stem cells can then grow into structures like those found in the brain and even form networks of communicating cells. Brain organoids cannot grow beyond a few millimeters in size or perform the functions of a complete brain. But they give scientists a way to study how parts of the brain develop during pregnancy. "One can really understand both a process of normal human brain development, which we frankly don't understand very well, [and] also what goes wrong in the brain of patients affected by diseases," says Paola Arlotta, a professor of stem cell and regenerative biology at Harvard who was not involved in the cell migration study. Arlotta is an author of a second paper in Nature about creating a wide variety of brain cells in brain organoids. © 2017 npr

Keyword: Development of the Brain; Autism
Link ID: 23545 - Posted: 04.27.2017

By KAREN BARROW The World Health Organization estimates that more than 50 million people worldwide have some form of epilepsy, a neurological disorder that is characterized by recurring episodes of seizure. While seizures come in various forms, those with epilepsy cope with similar issues: social stigma, complex treatment options and a feeling of powerlessness. Here, eight men, women and children discuss what it’s like to live with epilepsy. Denise L. Pease, an assistant comptroller for New York City, began having complex partial seizures after a car accident in which she suffered a traumatic brain injury. But because Ms. Pease lives alone, it wasn’t until a relative saw her having a tonic-clonic seizure, what used to be known as a grand mal seizure, that she realized she had developed epilepsy. Tonic-clonic seizures typically involve the whole body and can be very dramatic. Ms. Pease began to notice that she would get a strange taste in her mouth before a seizure, so whenever that happened she made sure she was seated in a safe location and waited for the seizure to pass. This sensation of an oncoming seizure, called an aura, is common among people with epilepsy. After eight years of trying different medications to control her epilepsy, Ms. Pease is happy to be back at work and no longer lives in fear of an imminent seizure. Ms. Pease is hopeful that she will soon be able to drive, and she continues to plan for her future. “When you have epilepsy, you have to be your own advocate,” she said. Sallie Gallagher’s son, Michael, started having complex partial seizures at age 4. This type of seizure doesn’t cause the full-body twitching associated with tonic-clonic seizure, but it can cause a person to start to act strangely or be completely unaware of his surroundings. © 2017 The New York Times Company

Keyword: Epilepsy
Link ID: 23544 - Posted: 04.27.2017

By BENEDICT CAREY Well-timed pulses from electrodes implanted in the brain can enhance memory in some people, scientists reported on Thursday, in the most rigorous demonstration to date of how a pacemaker-like approach might help reduce symptoms of dementia, head injuries and other conditions. The report is the result of decades of work decoding brain signals, helped along in recent years by large Department of Defense grants intended to develop novel treatments for people with traumatic brain injuries, a signature wound of the Iraq and Afghanistan wars. The research, led by a team at the University of Pennsylvania, is published in the journal Current Biology. Previous attempts to stimulate human memory with implanted electrodes had produced mixed results: Some experiments seemed to sharpen memory, but others muddled it. The new paper resolves this confusion by demonstrating that the timing of the stimulation is crucial. Zapping memory areas when they are functioning poorly improves the brain’s encoding of new information. But doing so when those areas are operating well — as they do for stretches of the day in most everyone, including those with deficits — impairs the process. “We all have good days and bad days, times when we’re foggy, or when we’re sharp,” said Michael Kahana, who with Youssef Ezzyat led the research team. “We found that jostling the system when it’s in a low-functioning state can jump it to a high-functioning one.” Researchers cautioned that implantation is a delicate procedure and that the reported improvements may not apply broadly. The study was of epilepsy patients; scientists still have much work to do to determine whether this approach has the same potential in people with other conditions, and if so how best to apply it. But in establishing the importance of timing, the field seems to have turned a corner, experts said. © 2017 The New York Times Company

Keyword: Learning & Memory; Epilepsy
Link ID: 23520 - Posted: 04.21.2017