By Abdul-Kareem Ahmed, M.D. “He wouldn’t want to live like this.” The cardiology team consulted us that Sunday evening. A patient was getting sleepy, and weak on one side. The man was 68 years old, not a healthy man, but a strong man. He had suffered a heart attack, again, and had been transferred from another hospital. Because he’d been far from a major medical center, where a wire might have been used to clear the blockage in his coronary arteries, he was treated with the next best method, a blood-thinner, and then sent to us. The drug, tenecteplase, is an enzyme that works by digesting clots. It effectively reverses the problem and is lifesaving for a majority of patients. But in a small minority of patients, it can also cause bleeding. Titrating the thickness of blood is precarious. If your blood is too thick you can clot. If it’s too thin you can bleed. The team had performed a rapid head CT. “He’s not going to make it,” my senior whispered as I scrolled through the fresh images. Our patient was bleeding into his brain, suffering a hemorrhagic stroke. Tenecteplase thinned his blood to save his heart, but it most likely had resulted in injury to his brain. I ran downstairs to examine him. He was big, and bald, and lying peacefully in his bed. With some encouragement, he gave me a grin, though lopsided. His pupils were different sizes, and half his body was paralyzed. But he was completely “there.” I was only one month into residency. Though I knew he was critical, and I knew our next decision would be difficult, I remained optimistic. © 2019 The New York Times Company

Keyword: Brain Injury/Concussion
Link ID: 25897 - Posted: 01.24.2019

David Cyranoski Japan has approved a stem-cell treatment for spinal-cord injuries. The event marks the first such therapy for this kind of injury to receive government approval for sale to patients. “This is an unprecedented revolution of science and medicine, which will open a new era of healthcare,” says oncologist Masanori Fukushima, head of the Translational Research Informatics Center, a Japanese government organization in Kobe that has been giving advice and support to the project for more than a decade. But independent researchers warn that the approval is premature. Ten specialists in stem-cell science or spinal-cord injuries, who were approached for comment by Nature and were not involved in the work or its commercialization, say that evidence that the treatment works is insufficient. Many of them say that the approval for the therapy, which is injected intravenously, was based on a small, poorly designed clinical trial. They say that the trial’s flaws — including that it was not double-blinded — make it difficult to assess the treatment’s long-term efficacy, because it is hard to rule out whether patients might have recovered naturally. And, although the cells used — known as mesenchymal stem cells (MSCs) — are thought to be safe, the infusion of stem cells into the blood has been connected with dangerous blood clots in the lungs. And all medical procedures carry risks, which makes them hard to justify unless they are proven to offer a benefit. © 2019 Springer Nature Publishing AG

Keyword: Regeneration; Stem Cells
Link ID: 25896 - Posted: 01.24.2019

/ By Courtenay Harris Bond When Anna Brennan was 15 years old, her mother abandoned her in the projects of northeast Philadelphia. Her aunt eventually took her in, but Brennan struggled with anxiety and depression. She also needed to support herself, so in ninth grade she dropped out of high school and went to work at an all-night diner downtown. At 20, she met her first husband, who also lived with mental illness and had substance use issues — and gave her a tooth-marked scar in her upper right shoulder. For years, Brennan waitressed seven days a week until she had her third child, Gemma, and her back pain started, forcing her to quit. “Our approach is: ‘Your urine is positive for substances. Let’s figure out how to make this work better for you.’” A physician prescribed painkillers, and Brennan became addicted. Her habit quickly turned from buying pills, which were expensive on the street, to snorting and then injecting heroin, which came cheap and pure. Twelve years into their marriage, Brennan’s husband committed suicide. Then she lost her house. Brennan’s two older kids went to stay with her sister, and Brennan hasn’t seen them in over a year. “I’m a drug addict,” Brennan says bluntly. “She won’t give them back.” Brennan started taking Suboxone, an opioid-replacement therapy that cut her cravings and kept her from experiencing withdrawal, two different times: in 2015 and then again from 2016 to 2018. During the second round, Brennan spent more than two years making trips to Prevention Point Philadelphia on Kensington Avenue. There, she met with her case manager and the doctor who prescribed her medication. Brennan seemed poised to be a success story. But she was weighed down by the stress of coping with a drug-addicted second husband, caring for her daughter Gemma, who is autistic; and despairing that she might never see her two older children again. Copyright 2019 Undark

Keyword: Drug Abuse
Link ID: 25895 - Posted: 01.24.2019

Jef Akst Levels of a protein called neurofilament light chain increase in the blood and spinal fluid of some Alzheimer’s patients 16 years before they develop symptoms, according to a study published today (January 21) in Nature Medicine. The results suggest that neurofilament light chain (NfL), which is part of the cytoskeleton of neurons and has previously been tied to brain damage in mice, could serve as a biomarker to noninvasively track the progression of the disease. “This is something that would be easy to incorporate into a screening test in a neurology clinic,” coauthor Brian Gordon, an assistant professor of radiology at Washington University, says in a press release. Gordon and his colleagues measured NfL in nearly 250 people carrying an Alzheimer’s-risk allele and more than 160 of their relatives who did not carry the variant. They found that those at risk of developing the disease had higher levels of the protein early on, and that NfL levels in both the blood and spinal fluid were on the rise well before the patients began to show signs of neurodegeneration, more than 16 years before disease onset. Examining a subset of the patients more closely, the team saw that the rate of increase in NfL correlated with the shrinkage of a brain region called the precuneus, and patients whose NfL levels were rising rapidly tested worse on cognitive tests. “It is not necessarily the absolute levels which tell you your neurodegeneration is ongoing, it is the rate of change,” coauthor Mathias Jucker, a professor of cellular neurology at the German Center for Neurodegenerative Diseases in Tübingen, tells The Guardian. © 1986 - 2019 The Scientist.

Keyword: Alzheimers
Link ID: 25894 - Posted: 01.24.2019

Bret Stetka As the story goes, nearly 80 years ago on the Faroe Islands - a stark North Atlantic archipelago 200 miles off the coast of Scotland — a neurologic epidemic may have washed, or rather convoyed, ashore. Before 1940 the incidence of multiple sclerosis on the Faroes was near, if not, zero, according to the tantalizing lore I recall from medical school. Yet in the years following British occupation of the islands during World War II, the rate of MS rose dramatically, leading many researchers to assume the outbreak was caused by some unknown germ transmitted by the foreign soldiers. We now know that MS is not infectious in the true sense of the word. It is not contagious in the way, say, the flu is. But infection does likely play a role in MS. As may be the case in Alzheimer's disease, it's looking more and more like MS strikes when infectious, genetic and immune factors gang up to eventually impair the function of neurons in the brain and spinal cord. Researchers are hoping to better understand this network of influences to develop more effective ways to treat MS, and perhaps prevent it in the first place. In the MS-free brain, electrical impulses zip down nerve fibers called axons causing the release of neurotransmitters. The wiring allows neurons to communicate with each other and generate biologic wonders like thought, sensation and movement. In many regions of the brain those axons are encased in an insulating jacket of protein and fat called myelin, which increases the speed that electrical nerve impulses travel. © 2019 npr

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 25893 - Posted: 01.22.2019

/ By Dave Levitan Scientific research on the effects of marijuana is rife with holes, thanks in large part to it still being categorized at the federal level alongside drugs such as heroin and LSD. Unfortunately, when research is scarce, it becomes easier to mislead people through cherry-picked data, sneaky word choice, and misinterpreted conclusions. On virtually every issue in his 272-page book, Adam Berenson commits one of the most common logical errors: He mixes up correlation and causation. Which brings us to Alex Berenson and Malcolm Gladwell, and what happens when tidy narratives outrun the science. Two weeks ago, Berenson, a former New York Times reporter and subsequent spy novelist, published a book with the ominous title “Tell Your Children: The Truth about Marijuana, Mental Illness, and Violence.” Gladwell, meanwhile, published a feature in the New Yorker, where he is a staff writer, drawing largely on Berenson’s book and questioning the supposed consensus that weed is among the safest drugs. Combined, these two works offer a master class in statistical malfeasance and a smorgasbord of logical fallacies and data-free fear-mongering that serve only to muddle an issue that, as experts point out, needs far more good-faith research. Berenson’s main argument is relatively simple. In his book, he claims, essentially, that the existing evidence really does contain solid answers, painting a truly alarming picture about marijuana: That it can and does cause psychosis and schizophrenia. He then makes the leap that since psychosis and schizophrenia can lead to violence, marijuana itself is causing violence to increase in the United States and elsewhere. Copyright 2019 Undark

Keyword: Drug Abuse; Schizophrenia
Link ID: 25892 - Posted: 01.22.2019

By James Gorman Carpenter ants follow trails. Just watch them wandering about on your wooden porch until they strike a trail of pheromones (chemicals ants use for communication) that another ant has laid down. Ants don’t have noses, so they wave their antennas around to pick up the trail, then off they go on the road to ruin. (Carpenter ants destroy houses.) Scientists know plenty about ants, including their ability to follow scent trails, but researchers at Harvard wanted to get a more detailed understanding of how exactly ants sniff, or taste, the pheromone-marked path. First, some basics: Ants use their antennas to pick up chemical cues left by other ants. And the chemical sense of ants, call it smell or taste or chemo-reception, enables them to follow straight trails, curved trails, even zigzags. To see how ants do it, the scientists mixed ink and ant pheromones and used the result to paint trails on paper. They set ants out on trails and recorded dozens of hours of ant movement. They analyzed the video and tried out different computer models of the ants’ behavior. What Ryan W. Dash and his adviser, Venkatesh N. Murthy, and other researchers found was that the ants had several strategies for path-following. The scientists published their results in the Journal of Experimental Biology. All the ants used their antennas to sweep the trail side to side. One strategy they used was probing. A probing ant moved slowly, keeping its antennas close together. The researchers termed another strategy exploratory: Ants still moved slowly, but they took winding paths moving away from and back to a trail. When they were locked into a pheromone trail, they moved along more quickly, keeping their antennas on either side of the path. They kept one antenna closer to the path, but which antenna varied from ant to ant. In other words, some were lefties and others were righties. © 2019 The New York Times Company

Keyword: Chemical Senses (Smell & Taste)
Link ID: 25891 - Posted: 01.22.2019

John Bergeron During the first weeks of the new year, resolutions are often accompanied by attempts to learn new behaviours that improve health. We hope that old bad habits will disappear and new healthy habits will become automatic. But how can our brain be reprogrammed to assure that a new health habit can be learned and retained? In 1949, Canadian psychologist Donald Hebb proposed the theory of Hebbian learning to explain how a learning task is transformed into a long-term memory. In this way, healthy habits become automatically retained after their continual repetition. Synapses transmit electrical signals. Svitlana Pavliuk Learning and memory are a consequence of how our brain cells (neurons) communicate with each other. When we learn, neurons communicate through molecular transmissions which hop across synapses producing a memory circuit. Known as long-term potentiation (LTP), the more often a learning task is repeated, the more often transmission continues and the stronger a memory circuit becomes. It is this unique ability of neurons to create and strengthen synaptic connections by repeated activation that leads to Hebbian learning. Understanding the brain requires investigation through different approaches and from a variety of specialities. The field of cognitive neuroscience initially developed through a small number of pioneers. Their experimental designs and observations led to the foundation for how we understand learning and memory today. © 2010–2019, The Conversation US, Inc.

Keyword: Learning & Memory
Link ID: 25890 - Posted: 01.22.2019

Alison Abbott Neuroscientists have for the first time discovered differences between the ‘software’ of humans and monkey brains, using a technique that tracks single neurons. They found that human brains trade off ‘robustness’ — a measure of how synchronized neuron signals are — for greater efficiency in information processing. The researchers hypothesize that the results might help to explain humans’ unique intelligence, as well as their susceptibility to psychiatric disorders. The findings were published in Cell1 on 17 January. Scientists say that this type of unusual study could help them to better translate research in animal models of psychiatric diseases into the clinic. The research exploited a rare set of data on the activity of single neurons collected deep in the brains of people with epilepsy who were undergoing neurosurgery to identify the origin of their condition. The technique is so difficult that only a handful of clinics around the world can participate in this type of research. The study also used similar, existing data from three monkeys and collected neuron information from two more. Over the decades, neuroscientists have discovered many subtle and significant differences in the anatomy — the hardware — of the brains of humans and other primates. But the latest study looked instead at differences in brain signals. © 2019 Springer Nature Publishing AG

Keyword: Schizophrenia; Epilepsy
Link ID: 25889 - Posted: 01.21.2019

By Scott Barry Kaufman Robert Plomin is a legend. For over 40 years he has been on the forefront of our understanding of the genetic and environmental influences on human behavior. Based on his groundbreaking work on twins, he showed that genes really do have a substantial influence on our psychological traits-- we are not born a lump of clay. Plomin coined the phrase "non-shared environment," and he was ranked as the 71st most "eminent psychologists of the 20th century." When I taught a course on human intelligence at NYU, I repeatedly cited his research and quoted his measured language and caution surrounding the interpretation of his findings. All of this makes it rather bewildering that, ever since his book Blueprint: How DNA Makes Us Who We Are came out, he has been spreading a lot of outdated misinformation in the media that is not supported by the latest science of genetics, including his own work. Also, many of his statements have been riddled with contradictions and logical non sequiturs, and some of his more exaggerated rhetoric is even potentially dangerous if actually applied to educational selection. Don't get me wrong: I am excited about the rapid progress scientists are making in using information about DNA to predict individual differences in intellectual functioning and personality. But I firmly believe we need to be more thoughtful in determining what relevance these rapidly emerging findings have for the actual individual human beings who are inhabited by the DNA.

Keyword: Development of the Brain; Genes & Behavior
Link ID: 25888 - Posted: 01.21.2019

By Perri Klass, M.D. Acute pain that calls out to warn you — “Hey, don’t walk on this broken leg!” — may be unpleasant, but it’s also protective. That acute pain is letting you know that a part of your body needs to heal, or in some other way needs extra attention, said Dr. Neil Schechter, the director of the chronic pain clinic at Boston Children’s Hospital. That’s very different, he said, from chronic pain that goes on over the course of months, whether abdominal pain or headache or musculoskeletal — it may persist and be incapacitating, because “the pain has become the disease.” That doesn’t mean the pain is any less painful for the person experiencing it. “There is really strong evidence supporting the psychological treatment for chronic pain, and that doesn’t imply that the pain itself is a psychological problem,” said Rachael Coakley, a psychologist who is the director of clinical innovation and outreach in pain medicine at Boston Children’s Hospital. Her book, “When Your Child Hurts,” is an excellent resource for parents. “When you’re a kid and you’ve had pain for a really long time, a lot of that is an experience of not having control over what’s happening in your body,” said Anna C. Wilson, a pediatric pain psychologist at Oregon Health and Science University. “Relaxation and other biobehavioral techniques help kids gain a sense of control.” She tells patients, “Your pain is absolutely real, and chronic pain in particular is a neurologic problem.” She recommended TED Talks by Dr. Elliot Krane, an anesthesiologist, and Lorimer Moseley, a neuroscience professor, to help explain chronic pain. Chronic pain develops, Dr. Schechter said, when there is an underlying biological vulnerability, either inherited or resulting from stressors like infections or procedures or traumas, and then a triggering event, such as a gastrointestinal infection or an injury. © 2019 The New York Times Company

Keyword: Pain & Touch; Development of the Brain
Link ID: 25887 - Posted: 01.21.2019

By David Grossman The brain remains famously remains one of the most mysterious parts of the human body. The challenges of neuroscience are among the most daunting in the medical field. Expansion microscopy is a crucial element of that study, a chemical technique that expands a small specimen to make it more observable at the molecular level. A new technique allows scientists to expand microscopy so instead of focusing a single sell, it can explore full neural circuits, at a speed around 1,000 times faster than before. A struggle in studying live cells is watching them without altering their actions. Scientists work around this problem by using thin sheets of light to illuminate cells with a piece of complex technology called a lattice light sheet microscope. By combining this microscope with expansion microscopy, scientists at the Howard Hughes Medical Institute (HHMI) were able to expand the possibility of how they could study insect brains. “I thought they were full of it,” says Eric Betzig, now an HHMI investigator at the University of California, Berkeley, in a press statement. "They" refers to Ruixuan Gao and Shoh Asano of MIT, who wanted to use Betzig's lab to attempt their combining of the two practices. While a complex procedure involving high-end scientific equipment, at its heart “the idea does sound a bit crude,” Gao says. “We’re stretching tissues apart." When the experiment was over, Betzig says, “I couldn’t believe the quality of the data I was seeing. You could have knocked me over with a feather.” ©2019 Hearst Magazine Media, Inc

Keyword: Brain imaging
Link ID: 25886 - Posted: 01.21.2019

By John Horgan In my freshman humanities class, I make students ponder the pros and cons of knowledge. We talk about Plato’s parable, in which people imprisoned in a cave mistake shadows projected on a wall for reality. I ask, Assuming we’re in the cave, how many of you want to escape? Most students dutifully raise their hands, because of course truth is good and ignorance is bad. Then I ask, What if the cave is comfy and the outside world nasty? I bring up The Matrix, in which humans live in a computer simulation, called the Matrix, constructed by evil machines. A band of rebels who have escaped this digital cave is trying to liberate other humans. A rebel named Cypher gives Agent Smith, nasty sentient software created by the machines, information to help him capture the rebels. Agent Smith asks Cypher what he wants for betraying his comrades, and Cypher says he doesn't want to live in reality any more. It’s ugly and stressful, and he hates being bossed around by the rebel leader. Cypher asks for a happy simulated life in the Matrix. Here is an excerpt from his dialogue with Agent Smith, which takes place in a virtual restaurant: Cypher: You know, I know this steak doesn't exist. I know that when I put it in my mouth, the Matrix is telling my brain that it is juicy and delicious. After nine years, you know what I realize? Ignorance is bliss. Agent Smith: Then we have a deal? Cypher: I don't want to remember nothing. Nothing. You understand? And I want to be rich. You know, someone important, like an actor. Agent Smith: Whatever you want.

Keyword: Alzheimers; Consciousness
Link ID: 25885 - Posted: 01.21.2019

Jonathan Lambert Pain is a complicated experience. Our skin and muscles sense it, just like they sense softness or warmth. But unlike other sensations, the experience of pain is distinctly unpleasant. Pain has to hurt for us to pay attention to it, and avoid hurting ourselves further. But for people in chronic pain, the pain has largely lost its purpose. It just hurts. While it has long been understood how nerves signal pain to the brain, scientists haven't known how the brain adds a layer of unpleasantness. Findings of a study published Thursday in Science offer an answer. A research team from Stanford University pinpointed the neurons in mouse brains that make pain hurt and were able to alter these neurons in a way that reduced the unpleasantness of pain without eliminating the sensation. The study lays the groundwork for future research into more targeted pain treatments. "This study is a major advance," says Irene Tracey, a pain neuroscientist at Oxford University who wasn't involved in the study. "It was a tour de force and a welcome addition to understanding this complex and major problem." Stanford neuroscientist Grégory Scherrer, who co-led the study, started the search for pain neurons in the amygdala — the slim, almond-shaped region scientists know regulates many emotions. The challenge for Scherrer was to sift through the tangle of neurons there and identify the ones associated with pain. © 2019 npr

Keyword: Pain & Touch
Link ID: 25884 - Posted: 01.19.2019

By David Blum Many of us have personally experienced or witnessed the impact of Parkinson’s disease (PD), a movement disorder that affects nearly 10 million people worldwide. This chronic, progressive neurodegenerative disorder leads to disability from motor impairments, such as tremors, rigidity, absence or slowness of movement and impaired balance, as well as from non-motor symptoms including sleep disruption, gastrointestinal issues, sexual dysfunction or loss of sense of smell or taste, to name a few. The ideal outcome of PD clinical research would be to find a cure. But researchers are also looking at novel ways to administer proven Parkinson’s medicines in order to help people living with the disease better control their symptoms and maintain their regular, daily activities. The brain cells that die from PD are responsible for producing dopamine, a neurotransmitter involved in complex behaviors including motor coordination, addiction and motivation. As a result, treatment typically includes the use of levodopa—a medication that is converted into dopamine in the brain and relieves PD symptoms. For the first few years after diagnosis, many individuals’ symptoms are well controlled by levodopa. The average age of onset is 60, but some people are diagnosed at 40 or even younger, potentially requiring treatment for decades. Over time, a patient’s response to levodopa changes, and the therapeutic window, or period when levodopa is effective, narrows, often leading to the prescription of additional levodopa or more frequent dosing of levodopa to manage symptoms. © 2019 Scientific American

Keyword: Parkinsons
Link ID: 25883 - Posted: 01.19.2019

Aimee Cunningham As public health officials tackle opioid addiction and overdoses, another class of prescription drugs has been contributing to a growing number of deaths across the United States. Benzodiazepines, such as Valium and Xanax, are commonly prescribed for anxiety and insomnia. The drugs are also highly addictive and can be fatal, especially when combined with alcohol or opioids. In the latest sign of the drug’s impact, the number of overdose deaths involving “benzos” rose from 0.54 per 100,000 in 1999 to 5.02 per 100,000 in 2017 among women aged 30 to 64, researchers report January 11 in the Morbidity and Mortality Weekly Report. That’s a spike of 830 percent, surpassed only by increases seen in overdose deaths involving synthetic opioids or heroin. Overall, there were 10,684 overdose deaths involving benzodiazepines in the United States in 2016, according to the National Institute on Drug Abuse. In 1999, the total was 1,135. Benzodiazepines have a sedating effect, and are particularly dangerous when used with other drugs that slow breathing, such as opioids and alcohol. In combination, the substances can “cause people to fall asleep and essentially never wake up again,” says Anna Lembke, an addiction psychiatrist at Stanford University School of Medicine. Benzos and opioids are often prescribed together, and opioids contribute to 75 percent of overdose deaths involving benzos. The rising number of deaths involving benzos hasn’t stopped the flow of prescriptions. The number of U.S. adults who filled a prescription for benzos rose from 8.1 million in 1996 to 13.5 million in 2013, a jump of 67 percent, a study in the American Journal of Public Health in 2016 found. The quantity of benzos acquired more than tripled over the same time. |© Society for Science & the Public 2000 - 2019.

Keyword: Drug Abuse; Stress
Link ID: 25882 - Posted: 01.19.2019

By Abby Goodnough WASHINGTON — A new study offers some of the strongest evidence yet of the connection between the marketing of opioids to doctors and the nation’s addiction epidemic. It found that counties where opioid manufacturers offered a large number of gifts and payments to doctors had more overdose deaths involving the drugs than counties where direct-to-physician marketing was less aggressive. The study, published Friday in JAMA Network Open, said the industry spent about $40 million promoting opioid medications to nearly 68,000 doctors from 2013 through 2015, including by paying for meals, trips and consulting fees. And it found that for every three additional payments that companies made to doctors per 100,000 people in a county, overdose deaths involving prescription opioids there a year later were 18 percent higher. Even as the opioid epidemic was killing more and more Americans, such marketing practices remained widespread. From 2013 through 2015, roughly 1 in 12 doctors received opioid-related marketing, according to the study, including 1 in 5 family practice doctors. The authors, from Boston Medical Center and New York University School of Medicine, found that counties where doctors received more industry marketing subsequently saw an increase in both the number of opioids prescribed and opioid-related overdose deaths. In response to the study, Dr. John Cullen, president of the American Academy of Family Physicians, said, “A limitation of the study, as acknowledged by the authors, is the many unknown variables that prevent drawing a direct causal link between pharmaceutical marketing and opioid-related deaths.” He added, “We’re very much aware of the critical and devastating impact of the opioid epidemic and work every day, with every patient interaction, to fight it. At the same time, we must protect the physician’s ability to provide adequate pain management.” © 2019 The New York Times Company

Keyword: Drug Abuse
Link ID: 25881 - Posted: 01.19.2019

By Diana Kwon o For the longest time the cerebellum, a dense, fist-size formation located at the base of the brain, never got much respect from neuroscientists. For about two centuries the scientific community believed the cerebellum (Latin for “little brain”), which contains approximately half of the brain’s neurons, was dedicated solely to the control of movement. In recent decades, however, the tide has started to turn, as researchers have revealed details of the structure’s role in cognition, emotional processing and social behavior. The longstanding interest in the cerebellum can be seen in the work of French physiologist Marie Jean Pierre Flourens—(1794–1867). Flourens removed the cerebella of pigeons and found the birds became unbalanced, although they could still move. Based on these observations, he concluded the cerebellum was responsible for coordinating movements. “[This] set the dogma that the cerebellum was involved in motor coordination,” says Kamran Khodakhah, a neuroscientist at Albert Einstein College of Medicine, adding: “For many years, we ignored the signs that suggested it was involved in other things.” One of the strongest pieces of evidence for the cerebellum’s broader repertoire emerged around two decades ago, when Jeremy Schmahmann, a neurologist at Massachusetts General Hospital, described cerebellar cognitive affective syndrome after discovering behavioral changes such as impairments in abstract reasoning and regulating emotion in individuals whose cerebella had been damaged. Since then this line of study has expanded. There has been human neuroimaging work showing the cerebellum is involved in cognitive processing and emotional control—and investigations in animals have revealed, among other things, that the structure is important for the normal development of social and cognitive capacities. Researchers have also linked altered cerebellar function to addiction, autism and schizophrenia.

Keyword: Drug Abuse; Emotions
Link ID: 25880 - Posted: 01.19.2019

Rachel Zamzow Patterns of brain activity in people with autism are unusually consistent over seconds—and even years, two new studies suggest. One study shows that patterns of connectivity remain stable in autistic adolescents, whereas they tend to change and specialize in controls. The other study found that connections remain fixed longer in people with autism than in controls. Both focused on so-called “functional connectivity,” the extent to which the activity of pairs of brain areas is synchronized. Together, the studies may help untangle seemingly contradictory findings on connectivity in autism: reports of both underconnectivity and overconnectivity in the brain. “Maybe the primary abnormality isn’t just that things are too weakly or strongly connected, that it has more to do with the timing of brain connections,” says Jeff Anderson, professor of radiology at the University of Utah, who led the second study. The studies also highlight the importance of measuring brain activity over varying time periods and at different ages. Researchers who home in on a single age may overlook differences that appear over time, says Mirella Dapretto, professor of psychiatry and biobehavioral sciences at the University of California, Los Angeles, and lead researcher on the adolescent study. “You miss some of the bigger picture.” Studying brain activity over time provides a rare window into the development of connectivity. © 1986 - 2019 The Scientist

Keyword: Autism; Development of the Brain
Link ID: 25879 - Posted: 01.19.2019

Laura Sanders Using laser light, ballooning tissue and innovative genetic tricks, scientists are starting to force brains to give up their secrets. By mixing and matching powerful advances in microscopy and cell biology, researchers have imaged intricate details of individual nerve cells in fruit flies and mice, and even controlled small groups of nerve cells in living mice. The techniques, published in two new studies, represent big steps forward for understanding how the brain operates, says molecular neuroscientist Hongkui Zeng of the Allen Institute for Brain Science in Seattle. “Without this kind of technology, we were only able to look at the soup level,” in which diverse nerve cells, or neurons, are grouped and analyzed together, she says. But the new studies show that nerve cells can be studied individually. That zoomed-in approach will begin to uncover the tremendous diversity that’s known to exist among cells, says Zeng, who was not involved in the research. “That is where the field is going. It’s very exciting to see that technologies are now enabling us to do that,” she says. These novel abilities came from multiple tools. At Howard Hughes Medical Institute’s Janelia Research Campus in Ashburn, Va., physicist Eric Betzig and his colleagues had developed a powerful microscope that can quickly peer deep into layers of brain tissue. Called a lattice light sheet microscope, the rig sweeps a thin sheet of laser light down through the brain, revealing cells’ structures. But like any microscope, it hits a wall when structures get really small, unable to resolve the most minute aspects of the scene. |© Society for Science & the Public 2000 - 2019.

Keyword: Brain imaging
Link ID: 25878 - Posted: 01.18.2019