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By Tina Hesman Saey One particular retrovirus — embedded in the DNA of jawed vertebrates — helps turn on production of a protein needed to insulate nerve fibers, researchers report February 15 in Cell. Such insulation, called myelin, may have helped make speedy thoughts and complex brains possible. The retrovirus trick was so handy, in fact, that it showed up many times in the evolution of vertebrates with jaws, the team found. Retroviruses — also known as jumping genes or retrotransposons — are RNA viruses that make DNA copies of themselves to embed in a host’s DNA. Scientists once thought of remnants of ancient viruses as genetic garbage, but that impression is changing, says neuroscientist Jason Shepherd, who was not involved in the study. “We’re finding more and more that these retrotransposons and retroviruses have influenced the evolution of life on the planet,” says Shepherd, of the University of Utah Spencer Fox Eccles School of Medicine in Salt Lake City. Remains of retroviruses were already known to have aided the evolution of the placenta, the immune system and other important milestones in human evolution (SN: 5/16/17). Now, they’re implicated in helping to produce myelin. Myelin is a coating of fat and protein that encases long nerve fibers known as axons. The coating works a bit like the insulation around an electrical wire: Nerves sheathed in myelin can send electrical signals faster than uninsulated nerves can. © Society for Science & the Public 2000–2024.

Related chapters from BN: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 13: Memory and Learning
Link ID: 29154 - Posted: 02.20.2024

By Simon Makin Our thoughts and feelings arise from networks of neurons, brain cells that send signals using chemicals called neurotransmitters. But neurons aren't alone. They're supported by other cells called glia (Greek for “glue”), which were once thought to hold nerve tissue together. Today glia are known to help regulate metabolism, protect neurons and clean up cellular waste—critical but unglamorous roles. Now, however, neuroscientists have discovered a type of “hybrid” glia that sends signals using glutamate, the brain's most common neurotransmitter. These findings, published in Nature, breach the rigid divide between signaling neurons and supportive glia. “I hope it's a boost for the field to move forward, to maybe begin studying why certain [brain] circuits have this input and others don't,” says study co-author Andrea Volterra, a neuroscientist at the University of Lausanne in Switzerland. Around 30 years ago researchers began reporting that star-shaped glia called astrocytes could communicate with neurons. The idea was controversial, and further research produced contradictory results. To resolve the debate, Volterra and his team analyzed existing data from mouse brains. These data were gathered using a technique called single-cell RNA sequencing, which lets researchers catalog individual cells' molecular profiles instead of averaging them in a bulk tissue sample. Of nine types of astrocytes they found in the hippocampus—a key memory region—one had the cellular machinery required to send glutamate signals. The small numbers of these cells, present only in certain regions, may explain why earlier research missed them. “It's quite convincing,” says neuroscientist Nicola Hamilton-Whitaker of King's College London, who was not involved in the study. “The reason some people may not have seen these specialized functions is they were studying different astrocytes.” © 2023 SCIENTIFIC AMERICAN,

Related chapters from BN: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 2: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 29025 - Posted: 11.26.2023

By Meghan Rosen In endurance athletes, some brain power may come from an unexpected source. Marathon runners appear to rely on myelin, the fatty tissue bundled around nerve fibers, for energy during a race, scientists report October 10 in a paper posted at bioRxiv.org. In the day or two following a marathon, this tissue seems to dwindle drastically, brain scans of runners reveal. Two weeks after the race, the brain fat bounces back to nearly prerace levels. The find suggests that the athletes burn so much energy running that they need to tap into a new fuel supply to keep the brain operating smoothly. “This is definitely an intriguing observation,” says Mustapha Bouhrara, a neuroimaging scientist at the National Institute on Aging in Baltimore. “It is quite plausible that myelin lipids are used as fuel in extended exercise.” If what the study authors are seeing is real, he says, the work could have therapeutic implications. Understanding how runners’ myelin recovers so rapidly might offer clues for developing potential treatments — like for people who’ve lost myelin due to aging or neurodegenerative disease. Much of the human brain contains myelin, tissue that sheathes nerve fibers and acts as an insulator, like rubber coating an electrical wire. That insulation lets electrical messages zip from nerve cell to nerve cell, allowing high-speed communication that’s crucial for brain function. The fatty tissue seems to be a straightforward material with a straightforward job, but there’s likely more to it than that, says Klaus-Armin Nave, a neurobiologist at the Max Planck Institute for Multidisciplinary Sciences in Göttingen, Germany. “For the longest time, it was thought that myelin sheathes were assembled, inert structures of insulation that don’t change much after they’re made,” he says. Today, there’s evidence that myelin is a dynamic structure, growing and shrinking in size and abundance depending on cellular conditions. The idea is called myelin plasticity. “It’s hotly researched,” Nave says. © Society for Science & the Public 2000–2023.

Related chapters from BN: Chapter 10: Vision: From Eye to Brain; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 7: Vision: From Eye to Brain; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 28983 - Posted: 11.01.2023

By Laura Dattaro A brain is nothing if not communicative. Neurons are the chatterboxes of this conversational organ, and they speak with one another by exchanging pulses of electricity using chemical messengers called neurotransmitters. By repeating this process billions of times per second, a brain converts clusters of chemicals into coordinated actions, memories and thoughts. Researchers study how the brain works by eavesdropping on that chemical conversation. But neurons talk so loudly and often that if there are other, quieter voices, it might be hard to hear them. For most of the 20th century, neuroscientists largely agreed that neurons are the only brain cells that propagate electrical signals. All the other brain cells, called glia, were thought to serve purely supportive roles. Then, in 1990, a curious phenomenon emerged: Researchers observed an astrocyte, a subtype of glial cell, responding to glutamate, the main neurotransmitter that generates electrical activity. In the decades since, research teams have come up with conflicting evidence, some reporting that astrocytes signal, and others retorting that they definitely do not. The disagreement played out at conferences and in review after review of the evidence. The two sides seemed irreconcilable. A new paper published in Nature in September presents the best proof yet that astrocytes can signal, gathered over eight years by a team co-led by Andrea Volterra, visiting faculty at the Wyss Center for Bio and Neuro Engineering in Geneva, Switzerland. The study includes two key pieces of evidence: images of glutamate flowing from astrocytes, and genetic data suggesting that these cells, dubbed glutamatergic astrocytes, have the cellular machinery to use glutamate the way neurons do. The paper also helps explain the decades of contradictory findings. Because only some astrocytes can perform this signaling, both sides of the controversy are, in a sense, right: A researcher’s results depend on which astrocytes they sampled. All Rights Reserved © 2023

Related chapters from BN: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 4: Development of the Brain
Link ID: 28972 - Posted: 10.25.2023

Sruthi S. Balakrishnan For nearly two decades, academic and industry researchers working to find ways to slow the progression of Alzheimer’s disease have focused chiefly on the amyloid-β plaques that accumulate among neurons. Dozens of clinical trials have tested drugs designed to remove or reduce these plaques, but successes have been few. Aducanumab, Biogen’s amyloid-attacking antibody drug (brand name Aduhelm) that was approved earlier this year following a long drought in new treatments for Alzheimer’s disease (AD), has been mired in controversy after scientists raised questions about the drug’s efficacy. This lack of progress has prompted many research groups to look instead at non-neuronal cells in the brain, and in particular, at immune cells known as microglia. Vital in both developing and mature brains, these cells help shape neurons, control how they communicate, keep an eye out for pathogenic intruders, and mediate neuroinflammation. This last role has emerged as particularly important as researchers uncover evidence that inflammation is linked to many neurological diseases—including AD—as well as to other conditions associated with aging. Many scientists have been waiting for the pharmaceutical industry to take notice of this link. “We knew all this ten years before, the rest of the world just didn’t pay attention to it,” says Jean Harry, a neurotoxicologist at the National Institute of Environmental Health Sciences in Durham, North Carolina. Key players in driving change have been recent genome-wide association studies (GWAS), which have pointed to AD–associated mutations in genes that are highly expressed in microglia, strengthening the evidence for links between these cells and the disease. “You can’t ignore it anymore,” says Bobbi Fleiss, a microglial neurobiologist at RMIT University in Melbourne, Australia. © 1986–2021 The Scientist.

Related chapters from BN: Chapter 15: Emotions, Aggression, and Stress; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress; Chapter 13: Memory and Learning
Link ID: 28019 - Posted: 10.02.2021

By Sundas Hashmi It was the afternoon of Jan. 31. I was preparing for a dinner party and adding final touches to my cheese platter when everything suddenly went dark. I woke up feeling baffled in a hospital bed. My husband filled me in: Apparently, I had suffered a massive seizure a few hours before our guests were to arrive at our Manhattan apartment. Our children’s nanny found me and I was rushed to the hospital. That had been three days earlier. My husband and I were both mystified: I was 37 years old and had always been in excellent health. In due course, a surgeon dropped by and told me I had a glioma, a type of brain tumor. It was relatively huge but operable. I felt sick to my stomach. Two weeks later, I was getting wheeled to the operating theater. I wouldn’t know the pathology until much later. I said my goodbyes to everyone — most importantly to my children, Sofia, 6, and Nyle, 2 — and prepared to die. But right before the surgery, in a very drugged state, I asked the surgeon to please get photos of me and my brother from my husband. I wanted the surgeon to see them. My brother had died two decades earlier from a different kind of brain tumor — a glioblastoma. I was 15 at the time, and he was 18. He died within two years of being diagnosed. Those two years were the worst period of my life. Doctors in my home country of Pakistan refused to take him, saying his case was fatal. So, my parents gathered their savings and flew him to Britain, where he was able to get a biopsy (his tumor was in an inoperable location) and radiation. Afterward, we had to ask people for donations so he could get the gamma knife treatment in Singapore that my parents felt confident would save him. In the end, nothing worked, and he died, taking 18 years of memories with him. © 2020 The New York Times Company

Related chapters from BN: Chapter 1: Introduction: Scope and Outlook; Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System
Related chapters from MM:Chapter 1: Cells and Structures: The Anatomy of the Nervous System; Chapter 2: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 27536 - Posted: 10.21.2020

Katarina Zimmer Long believed to be simple, pathogen-eating immune cells, macrophages have a far more extensive list of job duties. They appear to have specialized functions across body tissues, help repair damaged tissue, play a key role in regulating inflammation and pain, and participate in other roles scientists are just beginning to reveal. Now, a group of researchers in the Netherlands has identified a mechanism by which macrophages may help resolve inflammatory pain in mice. In a study recently posted as a preprint to bioRxiv, they report that the immune cells shuttle mitochondria to sensory neurons that innervate inflamed tissue, and that this helps resolve pain. The researchers speculate that the mechanism could replenish functional mitochondria in neurons during chronic inflammatory conditions, which is associated with dysfunctional mitochondria. “I think the transfer of mitochondria is quite convincing,” Jan Van den Bossche, an immunologist at Amsterdam University Medical Center who wasn’t involved in the research, writes to The Scientist in an email. If the findings can be replicated, “this could have [implications for] many diseases with chronic inflammation and pain,” he adds. The research is the result of a five-year project that began when Niels Eijkelkamp, a neuroimmunologist at the University Medical Center Utrecht, and his colleagues started investigating how inflammatory pain resolves, “so we could understand what causes chronic pain,” he says. © 1986–2020 The Scientist

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 11: Emotions, Aggression, and Stress
Link ID: 27097 - Posted: 03.06.2020

Elena Renken The sting of a paper cut or the throb of a dog bite is perceived through the skin, where cells react to mechanical forces and send an electrical message to the brain. These signals were believed to originate in the naked endings of neurons that extend into the skin. But a few months ago, scientists came to the surprising realization that some of the cells essential for sensing this type of pain aren’t neurons at all. It’s a previously overlooked type of specialized glial cell that intertwines with nerve endings to form a mesh in the outer layers of the skin. The information the glial cells send to neurons is what initiates the “ouch”: When researchers stimulated only the glial cells, mice pulled back their paws or guarded them while licking or shaking — responses specific to pain. This discovery is only one of many recent findings showing that glia, the motley collection of cells in the nervous system that aren’t neurons, are far more important than researchers expected. Glia were long presumed to be housekeepers that only nourished, protected and swept up after the neurons, whose more obvious role of channeling electric signals through the brain and body kept them in the spotlight for centuries. But over the last couple of decades, research into glia has increased dramatically. “In the human brain, glial cells are as abundant as neurons are. Yet we know orders of magnitude less about what they do than we know about the neurons,” said Shai Shaham, a professor of cell biology at the Rockefeller University who focuses on glia. As more scientists turn their attention to glia, findings have been piling up to reveal a family of diverse cells that are unexpectedly crucial to vital processes. All Rights Reserved © 2020

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 11: Emotions, Aggression, and Stress
Link ID: 27002 - Posted: 01.28.2020

By Donna Jackson Nakazawa More than a decade ago, I was diagnosed with a string of autoimmune diseases, one after another, including a bone marrow disorder, thyroiditis, and then Guillain-Barré syndrome, which left me paralyzed while raising two young children. I recovered from Guillain-Barré only to relapse, becoming paralyzed again. My immune system was repeatedly and mistakenly attacking my body, causing the nerves in my arms, legs, and those I needed to swallow to stop communicating with my brain, leaving me confined to — and raising my children from — bed. As I slowly began to recover and learn to walk again, I noticed that along with residual physical losses I had experienced shifts in my mood and clarity of mind. Although I’d always been an optimistic person, I felt a bleak unshakable dread, which didn’t feel like the “old me.” I also noticed cognitive glitches. Names, words, and facts were hard to bring to mind. I can still recall cutting up slices of watermelon, putting them in a bowl, and staring down at them thinking, “What is this again?” I knew the word but couldn’t remember it. I covered my lapse by bringing the bowl to the table and waiting for my children to call out, “Yay! Watermelon!” And I thought, “Yes. Of course. Watermelon.” As a science journalist whose niche spans neuroscience, immunology, and human emotion, I knew at the time that it didn’t make scientific sense that inflammation in the body could be connected to — much less cause — illness in the brain. At that time, scientific dogma held that the brain was the only organ in the body not ruled by the immune system. The brain was considered to be “immune privileged.” © 2020 STAT

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 4: Development of the Brain
Link ID: 26971 - Posted: 01.20.2020

Heidi Ledford Tumour cells can plug into — and feed off — the brain’s complex network of neurons, according to a trio of studies. This nefarious ability could explain the mysterious behaviour of certain tumours, and point to new ways of treating cancer. The studies1,2,3, published on 18 September in Nature, describe this startling capability in brain cancers called gliomas, as well as in some breast cancers that spread to the brain. The findings bolster a growing realization among doctors and scientists that the nervous system plays an important role in the growth of cancers, says Michelle Monje, a paediatric neuro-oncologist at Stanford University in California and lead author of one of the studies1. Even so, finding cancer cells that behave like neurons was a surprise. “It’s unsettling,” Monje says. “We don’t think of cancer as forming an electrically active tissue like the brain.” Feeding off the brain Frank Winkler, a neurologist at Heidelberg University in Germany and a lead author on another of the Nature studies2, stumbled on the phenomenon in 2014 while studying communication networks established by cells in some brain tumours. He and his team discovered synapses, structures that neurons use to communicate with one another, in the tumours. It was “crazy stuff”, Winkler says. “Our first reaction was, ‘This is just difficult to believe.’” The researchers assumed that the tumour synapses would be a random occurrence. But as Winkler and his colleagues report in their latest study, they found synapses in glioma samples taken from cancer cells grown in culture, human glioma tumours transplanted into mice and glioma samples taken from ten people.

Related chapters from BN: Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System
Related chapters from MM:Chapter 1: Cells and Structures: The Anatomy of the Nervous System
Link ID: 26625 - Posted: 09.19.2019

By Kenneth Miller A model of Ben Barres’ brain sits on the windowsill behind his desk at Stanford University School of Medicine. To a casual observer, there’s nothing remarkable about the plastic lump, 3-D-printed from an MRI scan. Almost lost in the jumble of papers, coffee mugs, plaques and trophies that fill the neurobiologist’s office, it offers no hint about what Barres’ actual gray matter has helped to accomplish: a transformation of our understanding of brains in general, and how they can go wrong. Barres is a pioneer in the study of glia. This class of cells makes up 90 percent of the human brain, but gets far less attention than neurons, the nerve cells that transmit our thoughts and sensations at lightning speed. Glia were long regarded mainly as a maintenance crew, performing such unglamorous tasks as ferrying nutrients and mopping up waste, and occasionally mounting a defense when the brain faced injury or infection. Over the past two decades, however, Barres’ research has revealed that they actually play central roles in sculpting the developing brain, and in guiding neurons’ behavior at every stage of life. “He has made one shocking, revolutionary discovery after another,” says biologist Martin Raff, emeritus professor at University College London, whose own work helped pave the way for those advances. Recently, Barres and his collaborators have made some discoveries that may revolutionize the treatment of neurodegenerative ailments, from glaucoma and multiple sclerosis to Alzheimer’s disease and stroke. What drives such disorders, their findings suggest, is a process in which glia turn from nurturing neurons to destroying them. Human trials of a drug designed to block that change are just beginning.

Related chapters from BN: Chapter 17: Learning and Memory; Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 1: Cells and Structures: The Anatomy of the Nervous System
Link ID: 26258 - Posted: 05.22.2019

By Ashley Yeager At first glance, neurons and muscle cells are the stars of gross motor function. Muscle movement results from coordination between nerve and muscle cells: when an action potential arrives at the presynaptic neuron terminal, calcium ions flow, causing proteins to fuse with the cell membrane and release some of the neuron’s contents, including acetylcholine, into the cleft between the neuron and muscle cell. Acetylcholine binds to receptors on the muscle cell, sending calcium ions into it and causing it to contract. But there’s also a third kind of cell at neuromuscular junctions, a terminal/perisynaptic Schwann cell (TPSC). These cells are known to aid in synapse formation and in the repair of injured peripheral motor axons, but their possible role in synaptic communications has been largely ignored. Problems with synaptic communication can underlie muscle fatigue, notes neuroscientist Thomas Gould of the University of Nevada, Reno, in an email to The Scientist. “Because these cells are activated by synaptic activity, we wondered what the role of this activation was.” To investigate, he and his colleagues stimulated motor neurons from neonatal mouse diaphragm tissue producing a calcium indicator, and found that TPSCs released calcium ions from the endoplasmic reticulum into the cytosol and could take in potassium ions from the synaptic cleft between neurons and muscle cells. However, TPSCs lacking the protein purinergic 2Y1 receptor (P2Y1R) didn’t release calcium or appear to take in potassium ions. © 1986-2018 The Scientist

Related chapters from BN: Chapter 11: Motor Control and Plasticity; Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 1: Cells and Structures: The Anatomy of the Nervous System
Link ID: 24964 - Posted: 05.12.2018

By NEIL GENZLINGER Ben Barres, a neuroscientist who did groundbreaking work on brain cells known as glia and their possible relation to diseases like Parkinson’s, and who was an outspoken advocate of equal opportunity for women in the sciences, died on Wednesday at his home in Palo Alto, Calif. He was 63. In announcing the death, Stanford University, where Dr. Barres was a professor, said he had had pancreatic cancer. Dr. Barres was transgender, having transitioned from female to male in 1997, when he was in his 40s and well into his career. That gave him a distinctive outlook on the difficulties that women and members of minorities face in academia. and especially in the sciences. An article he wrote for the journal Nature in 2006 titled “Does Gender Matter?” took on some prominent scholars who had argued that women were not advancing in the sciences because of innate differences in their aptitude. “I am suspicious when those who are at an advantage proclaim that a disadvantaged group of people is innately less able,” he wrote. “Historically, claims that disadvantaged groups are innately inferior have been based on junk science and intolerance.” The article cited studies documenting obstacles facing women, but it also drew on Dr. Barres’s personal experiences. He recounted dismissive treatment he had received when he was a woman and how that had changed when he became a man. “By far,” he wrote, “the main difference that I have noticed is that people who don’t know I am transgendered treat me with much more respect: I can even complete a whole sentence without being interrupted by a man.” Dr. Barres (pronounced BARE-ess) was born on Sept. 13, 1954, in West Orange, N.J., with the given name Barbara. “I knew from a very young age — 5 or 6 — that I wanted to be a scientist, that there was something fun about it and I would enjoy doing it,” he told The New York Times in 2006. “I decided I would go to M.I.T. when I was 12 or 13.” © 2017 The New York Times Company

Related chapters from BN: Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 1: Cells and Structures: The Anatomy of the Nervous System; Chapter 8: Hormones and Sex
Link ID: 24472 - Posted: 12.30.2017

Acclaimed Stanford neuroscientist Ben Barres, MD, PhD, died on Dec. 27, 20 months after being diagnosed with pancreatic cancer. He was 63. Barres’ path-breaking discoveries of the crucial roles played by glial cells — the unsung majority of brain cells, which aren’t nerve cells — revolutionized the field of neuroscience. Barres was incontestably visionary yet, ironically, face-blind — he suffered from prosopagnosia, an inability to distinguish faces, and relied on voices or visual cues such as hats and hairstyles to identify even people he knew well. And there were many of them. A professor of neurobiology, of developmental biology and of neurology, Barres was widely praised as a stellar and passionate scientist whose methodologic rigor was matched only by his energy and enthusiasm. He was devoted to his scholarly pursuits and to his trainees, advocating unrelentingly on their behalf. He especially championed the cause of women in academia, with whom he empathized; he was transgender. “Ben was a remarkable person. He will be remembered as a brilliant scientist who transformed our understanding of glial cells and as a tireless advocate who promoted equity and diversity at every turn,” said Marc Tessier-Lavigne, PhD, president of Stanford University. “He was also a beloved mentor to students and trainees, a dear friend to many in our community and a champion for the fundamental dignity of us all.”

Related chapters from BN: Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System
Related chapters from MM:Chapter 1: Cells and Structures: The Anatomy of the Nervous System
Link ID: 24461 - Posted: 12.28.2017

By Shawna Williams THE PAPER P. Réu et al., “The lifespan and turnover of microglia in the human brain,” Cell Rep, 20:779-84, 2017. A RENEWABLE RESOURCE? Evidence has emerged that some of the brain’s cells can be renewed in adulthood, but it is difficult to study the turnover of cells in the human brain. When it comes to microglia, immune cells that ward off infection in the central nervous system, it’s been unclear how “the maintenance of their numbers is controlled and to what extent they are exchanged,” says stem cell researcher Jonas Frisén of the Karolinska Institute in Sweden. NUCLEAR SIGNATURE Frisén and colleagues used brain tissue from autopsies, together with the known changes in concentrations of carbon-14 in the atmosphere over time, to estimate how frequently microglia are renewed. They also analyzed microglia from the donated brains of two patients who had received a labeled nucleoside as part of a cancer treatment trial in the 1990s. SLOW CHURN Microglia, which populate the brain as blood cell progenitors during fetal development, were replaced at a median rate of 28 percent per year; on average, the cells were 4.2 years old. For Marie-Ève Tremblay, a neuroscientist at the Université Laval in Québec City who was not involved in the study, what stands out is the range of microglia ages found—from brand-new to more than 20 years old. “That’s quite striking!” she writes in an email to The Scientist. © 1986-2017 The Scientist

Related chapters from BN: Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 1: Cells and Structures: The Anatomy of the Nervous System; Chapter 4: Development of the Brain
Link ID: 24159 - Posted: 10.07.2017

Laurel Hamers Zika’s damaging neurological effects might someday be enlisted for good — to treat brain cancer. In human cells and in mice, the virus infected and killed the stem cells that become a glioblastoma, an aggressive brain tumor, but left healthy brain cells alone. Jeremy Rich, a regenerative medicine scientist at the University of California, San Diego, and colleagues report the findings online September 5 in the Journal of Experimental Medicine. Previous studies had shown that Zika kills stem cells that generate nerve cells in developing brains (SN: 4/2/16, p. 26). Because of similarities between those neural precursor cells and stem cells that turn into glioblastomas, Rich’s team suspected the virus might also target the cells that cause the notoriously deadly type of cancer. In the United States, about 12,000 people are expected to be diagnosed with glioblastoma in 2017. (It’s the type of cancer U.S. Senator John McCain was found to have in July.) Even with treatment, most patients live only about a year after diagnosis, and tumors frequently recur. In cultures of human cells, Zika infected glioblastoma stem cells and halted their growth, Rich and colleagues report. The virus also infected full-blown glioblastoma cells but at a lower rate, and didn’t infect normal brain tissues. Zika-infected mice with glioblastoma either saw their tumors shrink or their tumor growth slow compared with uninfected mice. The virus-infected mice lived longer, too. In one trial, almost half of the mice survived more than six weeks after being infected with Zika, while all of the uninfected mice died within two weeks of receiving a placebo. |© Society for Science & the Public 2000 - 2017. A

Related chapters from BN: Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 1: Cells and Structures: The Anatomy of the Nervous System; Chapter 4: Development of the Brain
Link ID: 24039 - Posted: 09.06.2017

Jon Hamilton Doctors use words like "aggressive" and "highly malignant" to describe the type of brain cancer discovered in Arizona Sen. John McCain. The cancer is a glioblastoma, the Mayo Clinic said in a statement Wednesday. It was diagnosed after doctors surgically removed a blood clot from above McCain's left eye. Doctors who were not involved in his care say the procedure likely removed much of the tumor as well. Glioblastomas, which are the most common malignant brain tumor, tend to be deadly. Each year in the U.S., about 12,000 people are diagnosed with the tumor. Most die within two years, though some survive more than a decade. "It's frustrating," says Nader Sanai, director of neurosurgical oncology at the Barrow Neurological Institute in Phoenix. Only "a very small number" of patients beat the disease, he says. And the odds are especially poor for older patients like McCain, who is 80. "The older you are, the worse your prognosis is," Sanai says, in part because older patients often aren't strong enough to tolerate aggressive radiation and chemotherapy. Arizona Sen. John McCain on Capitol Hill in April 2017, three months before he was diagnosed with brain cancer. © 2017 npr

Related chapters from BN: Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System
Related chapters from MM:Chapter 1: Cells and Structures: The Anatomy of the Nervous System
Link ID: 23857 - Posted: 07.21.2017

By Teal Burrell In neuroscience, neurons get all the glory. Or rather, they used to. Researchers are beginning to discover the importance of something outside the neurons—a structure called the perineuronal net. This net might reveal how memories are stored and how various diseases ravage the brain. The realization of important roles for structures outside neurons serves as a reminder that the brain is a lot more complicated than we thought. Or, it’s exactly as complicated as neuroscientists thought it was 130 years ago. In 1882, Italian physician and scientist Camillo Golgi described a structure that enveloped cells in the brain in a thin layer. He later named it the pericellular net. His word choice was deliberate; he carefully avoided the word “neuron” since he was engaged in a battle with another neuroscience luminary, Santiago Ramón y Cajal, over whether the nervous system was a continuous meshwork of cells that were fused together—Golgi’s take—or a collection of discrete cells, called neurons—Ramón y Cajal’s view. Ramón y Cajal wasn’t having it. He argued Golgi was wrong about the existence of such a net, blaming the findings on Golgi’s eponymous staining technique, which, incidentally, is still used today. Ramón y Cajal’s influence was enough to shut down the debate. While some Golgi supporters labored in vain to prove the nets existed, their findings never took hold. Instead, over the next century, neuroscientists focused exclusively on neurons, the discrete cells of the nervous system that relay information between one another, giving rise to movements, perceptions, and emotions. (The two adversaries would begrudgingly share a Nobel Prize in 1906 for their work describing the nervous system.) © 1996-2016 WGBH Educational Foundation

Related chapters from BN: Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System
Related chapters from MM:Chapter 1: Cells and Structures: The Anatomy of the Nervous System
Link ID: 22252 - Posted: 05.26.2016

By Amina Zafar, Tragically Hip frontman ​Gord Downie's resilience and openness about his terminal glioblastoma and his plans to tour could help to reduce stigma and improve awareness, some cancer experts say. Tuesday's news revealed that the singer has an aggressive form of cancer that originated in his brain. An MRI scan last week showed the tumour has responded well to surgery, radiation and chemotherapy, doctors said. "I was quickly impressed by Gord's resilience and courage," Downie's neuro-oncologist, Dr. James Perry of Sunnybrook Health Sciences Centre, told a news conference. Perry said it's daunting for many of his patients to reveal the diagnosis to their family, children and co-workers. "The news today, while sad, also creates for us in brain tumour research an unprecedented opportunity to create awareness and to create an opportunity for fundraising for research that's desperately needed to improve the odds for all people with this disease," Perry said. Dr. James Perry, head of neurology at Toronto's Sunnybrook Health Sciences Centre, calls Gord Downie's sad news an unprecedented opportunity to fundraise for brain tumour research. (Aaron Vincent Elkaim/Canadian Press) "Gord's courage in coming forward with his diagnosis will be a beacon for all patients with glioblastoma in Canada. They will see a survivor continuing with his craft despite its many challenges." ©2016 CBC/Radio-Canada.

Related chapters from BN: Chapter 1: Introduction: Scope and Outlook; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 20: ; Chapter 14: Attention and Higher Cognition
Link ID: 22251 - Posted: 05.26.2016

By Diana Kwon Microglia, the immune cells of the brain, have long been the underdogs of the glia world, passed over for other, flashier cousins, such as astrocytes. Although microglia are best known for being the brain’s primary defenders, scientists now realize that they play a role in the developing brain and may also be implicated in developmental and neurodegenerative disorders. The change in attitude is clear, as evidenced by the buzz around this topic at this year’s Society for Neuroscience (SfN) conference, which took place from October 17 to 21 in Chicago, where scientists discussed their role in both health and disease. Activated in the diseased brain, microglia find injured neurons and strip away the synapses, the connections between them. These cells make up around 10 percent of all the cells in the brain and appear during early development. For decades scientists focused on them as immune cells and thought that they were quiet and passive in the absence of an outside invader. That all changed in 2005, when experimenters found that microglia were actually the fastest-moving structures in a healthy adult brain. Later discoveries revealed that their branches were reaching out to surrounding neurons and contacting synapses. These findings suggested that these cellular scavengers were involved in functions beyond disease. The discovery that microglia were active in the healthy brain jump-started the exploration into their underlying mechanisms: Why do these cells hang around synapses? And what are they doing? © 2015 Scientific American

Related chapters from BN: Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 1: Cells and Structures: The Anatomy of the Nervous System; Chapter 11: Emotions, Aggression, and Stress
Link ID: 21566 - Posted: 10.26.2015