Chapter 2. Functional Neuroanatomy: The Nervous System and Behavior
Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.
By Anna Vlasits A small corner of the neuroscience world was in a frenzy. It was mid-June and a scientific paper had just been published claiming that years worth of results were riddled with errors. The study had dug into the software used to analyze one kind of brain scan, called functional MRI. The software’s approach was wrong, the researchers wrote, calling into doubt “the validity of some 40,000 fMRI studies”—in other words, all of them. The reaction was swift. Twitter lit up with panicked neuroscientists. Bloggers and reporters rained down headlines citing “seriously flawed” “glitches” and “bugs.” Other scientists thundered out essays defending their studies. Finally, one of the authors of the paper, published in Proceedings of the National Academy of Sciences, stepped into the fray. In a blog post, Thomas Nichols wrote, “There is one number I regret: 40,000.” Their finding, Nichols went on to write, only affects a portion of all fMRI papers—or, some scientists think, possibly none at all. It wasn’t nearly as bad as the hype suggested. The brief kerfuffle could just be dismissed as a tempest in a teapot, science’s self-correcting mechanisms in action. But the study, and its response, heralds a new level of self-scrutiny for fMRI studies, which have been plagued for decades by accusations of shoddy science and pop-culture pandering. fMRI, in other words, is growing up, but not without some pains along the way. A bumpy start for brain scanning © 2016 Scientific American,
Keyword: Brain imaging
Link ID: 22513 - Posted: 08.04.2016
By Andy Coghlan Mysterious shrunken cells have been spotted in the human brain for the first time, and appear to be associated with Alzheimer’s disease. “We don’t know yet if they’re a cause or consequence,” says Marie-Ève Tremblay of Laval University in Québec, Canada, who presented her discovery at the Translational Neuroimmunology conference in Big Sky, Montana, last week. The cells appear to be withered forms of microglia – the cells that keep the brain tidy and free of infection, normally by pruning unwanted brain connections or destroying abnormal and infected brain cells. But the cells discovered by Tremblay appear much darker when viewed using an electron microscope, and they seem to be more destructive. “It took a long time for us to identify them,” says Tremblay, who adds that these shrunken microglia do not show up with the same staining chemicals that normally make microglia visible under the microscope. Compared with normal microglia, the dark cells appear to wrap much more tightly around neurons and the connections between them, called synapses. “It seems they’re hyperactive at synapses,” says Tremblay. Where these microglia are present, synapses often seem shrunken and in the process of being degraded. Tremblay first discovered these dark microglia in mice, finding that they increase in number as mice age, and appear to be linked to a number of things, including stress, the neurodegenerative condition Huntington’s disease and a mouse model of Alzheimer’s disease. “There were 10 times as many dark microglia in Alzheimer’s mice as in control mice,” says Tremblay. © Copyright Reed Business Information Ltd.
Every year, hundreds of human brains are delivered to a network of special research centres. Why do these "brain banks" exist and what do they do? Rachael Buchanan was given rare access. A neuroscientist once told me with great insistence that brains are beautiful. His words came back to me as I watched a technician at the Bristol brain bank carefully dissect one of the facility's freshly donated specimens. The intricate folds and switchbacks of its surface and its delicate branching structures, revealed by her cuts, were entrancing. They seem only faintly to echo the complexity and power that tissue had held in life. The brain being methodically portioned up for storage was one of around 40 donations the South West Dementia Brain Bank receives each year. This bank in Bristol is one of 10 centres that make up the Medical Research Council's Brain Bank Network. Between them annually they supply hundreds of samples of research tissue to scientists in the UK and abroad. One of the thousand brains already fixed and frozen in the store rooms at Bristol is that of Angela Carlson. Written into that 3lb (1.4kg) of dissected tissue are the experiences, memories and knowledge of a very adventurous woman, for her time. She spent her teens in the land army during World War Two, followed by stints as a cook and child minder in the USA, and in what was then Persia. Twice widowed and without children, she eventually settled in Dorset to be near her niece Susan Jonas. She died there from dementia, aged 89. © 2016 BBC
By BENEDICT CAREY Solving a hairy math problem might send a shudder of exultation along your spinal cord. But scientists have historically struggled to deconstruct the exact mental alchemy that occurs when the brain successfully leaps the gap from “Say what?” to “Aha!” Now, using an innovative combination of brain-imaging analyses, researchers have captured four fleeting stages of creative thinking in math. In a paper published in Psychological Science, a team led by John R. Anderson, a professor of psychology and computer science at Carnegie Mellon University, demonstrated a method for reconstructing how the brain moves from understanding a problem to solving it, including the time the brain spends in each stage. The imaging analysis found four stages in all: encoding (downloading), planning (strategizing), solving (performing the math), and responding (typing out an answer). “I’m very happy with the way the study worked out, and I think this precision is about the limit of what we can do” with the brain imaging tools available, said Dr. Anderson, who wrote the report with Aryn A. Pyke and Jon M. Fincham, both also at Carnegie Mellon. To capture these quicksilver mental operations, the team first taught 80 men and women how to interpret a set of math symbols and equations they had not seen before. The underlying math itself wasn’t difficult, mostly addition and subtraction, but manipulating the newly learned symbols required some thinking. The research team could vary the problems to burden specific stages of the thinking process — some were hard to encode, for instance, while others extended the length of the planning stage. The scientists used two techniques of M.R.I. data analysis to sort through what the participants’ brains were doing. One technique tracked the neural firing patterns during the solving of each problem; the other identified significant shifts from one kind of mental state to another. The subjects solved 88 problems each, and the research team analyzed the imaging data from those solved successfully. © 2016 The New York Times Company
By ERICA GOODE You are getting sleepy. Very sleepy. You will forget everything you read in this article. Hypnosis has become a common medical tool, used to reduce pain, help people stop smoking and cure them of phobias. But scientists have long argued about whether the hypnotic “trance” is a separate neurophysiological state or simply a product of a hypnotized person’s expectations. A study published on Thursday by Stanford researchers offers some evidence for the first explanation, finding that some parts of the brain function differently under hypnosis than during normal consciousness. The study was conducted with functional magnetic resonance imaging, a scanning method that measures blood flow in the brain. It found changes in activity in brain areas that are thought to be involved in focused attention, the monitoring and control of the body’s functioning, and the awareness and evaluation of a person’s internal and external environments. “I think we have pretty definitive evidence here that the brain is working differently when a person is in hypnosis,” said Dr. David Spiegel, a professor of psychiatry and behavioral sciences at Stanford who has studied the effectiveness of hypnosis. Functional imaging is a blunt instrument and the findings can be difficult to interpret, especially when a study is looking at activity levels in many brain areas. Still, Dr. Spiegel said, the findings might help explain the intense absorption, lack of self-consciousness and suggestibility that characterize the hypnotic state. © 2016 The New York Times Company
Laura Sanders Under duress, nerve cells get a little help from their friends. Brain cells called astrocytes send their own energy-producing mitochondria to struggling nerve cells. Those gifts may help the neurons rebound after injuries such as strokes, scientists propose in the July 28 Nature. It was known that astrocytes — star-shaped glial cells that, among other jobs, support neurons — take in and dispose of neurons’ discarded mitochondria. Now it turns out that mitochondria can move the other way, too. This astrocyte-to-neuron transfer is surprising, says neuroscientist Jarek Aronowski of the University of Texas Health Science Center at Houston. “Bottom line: It’s sort of shocking.” Study coauthor Eng Lo of Massachusetts General Hospital and Harvard Medical School cautions that the work is at a very early stage. But he hopes that a deeper understanding of this process might ultimately point out new ways to protect the brain from damage. Mitochondria produce the energy that powers cells in the body. Scientists have spotted the organelles moving into damaged cells in other parts of the body, including the lungs, heart and liver. The new study turns up signs of this mitochondrial generosity in the brain. Astrocytes produce mitochondria and shunt them out into the soup that surrounds cells, Lo and colleagues found. The researchers then put neurons into this mitochondria-rich broth. When starved of glucose and oxygen — a situation that approximates a stroke — the neurons took in the astrocyte-made organelles. |© Society for Science & the Public 2000 - 2016
By Emily Underwood If your car’s battery dies, you might call on roadside assistance—or a benevolent bystander—for a jump. When damaged neurons lose their “batteries,” energy-generating mitochondria, they call on a different class of brain cells, astrocytes, for a boost, a new study suggests. These cells respond by donating extra mitochondria to the floundering neurons. The finding, still preliminary, might lead to novel ways to help people recover from stroke or other brain injuries, scientists say. “This is a very interesting and important study because it describes a new mechanism whereby astrocytes may protect neurons,” says Reuven Stein, a neurobiologist at The Rabin Institute of Neurobiology in Tel Aviv, Israel, who was not involved in the study. To keep up with the energy-intensive work of transmitting information throughout the brain, neurons need a lot of mitochondria, the power plants that produce the molecular fuel—ATP—that keeps cells alive and working. Mitochondria must be replaced often in neurons, in a process of self-replication called fission—the organelles were originally microbes captured inside a cell as part of a symbiosis. But if mitochondria are damaged or if they can’t keep up with a cell’s needs, energy supplies can run out, killing the cell. In 2014, researchers published the first evidence that cells can transfer mitochondria in the brain—but it seemed more a matter of throwing out the trash. When neurons expel damaged mitochondria, astrocytes swallow them and break them down. Eng Lo and Kazuhide Hayakawa, both neuroscientsists at Massachusetts General Hospital in Charlestown, wondered whether the transfer could go the other way as well—perhaps astrocytes donated working mitochondria to neurons in distress. Research by other groups supported that idea: A 2012 study, for example, found that stem cells from bone marrow can donate mitochondria to lung cells after severe injury. © 2016 American Association for the Advancement of Science
By Jessica Boddy Ever wonder what it looks like when brain cells chat up a storm? Researchers have found a way to watch the conversation in action without ever cracking open a skull. This glimpse into the brain’s communication system could open new doors to diagnosing and treating disorders from epilepsy to Alzheimer’s disease. Being able to see where—and how—living brain cells are working is “the holy grail in neuroscience,” says Howard Federoff, a neurologist at Georgetown University in Washington, D.C., who was not involved with the work. “This is a possible new tool that could bring us closer to that.” Neurons, which are only slightly longer than the width of a human hair, are laid out in the brain like a series of tangled highways. Signals must travel down these highways, but there’s a catch: The cells don’t actually touch. They’re separated by tiny gaps called synapses, where messages, with the assistance of electricity, jump from neuron to neuron to reach their destinations. The number of functional synapses that fire in one area—a measure known as synaptic density—tends to be a good way to figure out how healthy the brain is. Higher synaptic density means more signals are being sent successfully. If there are significant interruptions in large sections of the neuron highway, many signals may never reach their destinations, leading to disorders like Huntington disease. The only way to look at synaptic density in the brain, however, is to biopsy nonliving brain tissue. That means there’s no way for researchers to investigate how diseases like Alzheimer’s progress—something that could hold secrets to diagnosis and treatment. © 2016 American Association for the Advancement of Science
Keyword: Brain imaging
Link ID: 22472 - Posted: 07.23.2016
Carl Zimmer The brain looks like a featureless expanse of folds and bulges, but it’s actually carved up into invisible territories. Each is specialized: Some groups of neurons become active when we recognize faces, others when we read, others when we raise our hands. On Wednesday, in what many experts are calling a milestone in neuroscience, researchers published a spectacular new map of the brain, detailing nearly 100 previously unknown regions — an unprecedented glimpse into the machinery of the human mind. Scientists will rely on this guide as they attempt to understand virtually every aspect of the brain, from how it develops in children and ages over decades, to how it can be corrupted by diseases like Alzheimer’s and schizophrenia. “It’s a step towards understanding why we’re we,” said David Kleinfeld, a neuroscientist at the University of California, San Diego, who was not involved in the research. Scientists created the map with advanced scanners and computers running artificial intelligence programs that “learned” to identify the brain’s hidden regions from vast amounts of data collected from hundreds of test subjects, a far more sophisticated and broader effort than had been previously attempted. While an important advance, the new atlas is hardly the final word on the brain’s workings. It may take decades for scientists to figure out what each region is doing, and more will be discovered in coming decades. “This map you should think of as version 1.0,” said Matthew F. Glasser, a neuroscientist at Washington University School of Medicine and lead author of the new research. “There may be a version 2.0 as the data get better and more eyes look at the data. We hope the map can evolve as the science progresses.” © 2016 The New York Times Company
Keyword: Brain imaging
Link ID: 22466 - Posted: 07.21.2016
Ian Sample Science editor When the German neurologist Korbinian Brodmann first sliced and mapped the human brain more than a century ago he identified 50 distinct regions in the crinkly surface called the cerebral cortex that governs much of what makes us human. Now researchers have updated the 100-year-old map in a scientific tour de force which reveals that the human brain has at least 180 different regions that are important for language, perception, consciousness, thought, attention and sensation. The landmark achievement hands neuroscientists their most comprehensive map of the cortex so far, one that is expected to supersede Brodmann’s as the standard researchers use to talk about the various areas of the brain. Scientists at Washington University in St Louis created the map by combining highly-detailed MRI scans from 210 healthy young adults who had agreed to take part in the Human Connectome Project, a massive effort that aims to understand how neurons in the brain are connected. Most previous maps of the human brain have been created by looking at only one aspect of the tissues, such as how the cells look under a microscope, or how active areas become when a person performs a certain task. But maps made in different ways do not always look the same, which casts doubt on where one part of the brain stops and another starts. Writing in the journal Nature, Matthew Glasser and others describe how they combined scans of brain structure, function and connectivity to produce the new map, which confirmed the existence of 83 known brain regions and added 97 new ones. Some scans were taken while patients simply rested in the machine, while others were recorded as they performed maths tasks, listened to stories, or categorised objects, for example by stating whether an image was of a tool or an animal. © 2016 Guardian News and Media Limited
Keyword: Brain imaging
Link ID: 22465 - Posted: 07.21.2016
NOBODY knows how the brain works. But researchers are trying to find out. One of the most eye-catching weapons in their arsenal is functional magnetic-resonance imaging (fMRI). In this, MRI scanners normally employed for diagnosis are used to study volunteers for the purposes of research. By watching people’s brains as they carry out certain tasks, neuroscientists hope to get some idea of which bits of the brain specialise in doing what. The results look impressive. Thousands of papers have been published, from workmanlike investigations of the role of certain brain regions in, say, recalling directions or reading the emotions of others, to spectacular treatises extolling the use of fMRI to detect lies, to work out what people are dreaming about or even to deduce whether someone truly believes in God. But the technology has its critics. Many worry that dramatic conclusions are being drawn from small samples (the faff involved in fMRI makes large studies hard). Others fret about over-interpreting the tiny changes the technique picks up. A deliberately provocative paper published in 2009, for example, found apparent activity in the brain of a dead salmon. Now, researchers in Sweden have added to the doubts. As they reported in the Proceedings of the National Academies of Science, a team led by Anders Eklund at Linkoping University has found that the computer programs used by fMRI researchers to interpret what is going on in their volunteers’ brains appear to be seriously flawed. © The Economist Newspaper Limited 2016
Keyword: Brain imaging
Link ID: 22444 - Posted: 07.15.2016
The most sophisticated, widely adopted, and important tool for looking at living brain activity actually does no such thing. Called functional magnetic resonance imaging, what it really does is scan for the magnetic signatures of oxygen-rich blood. Blood indicates that the brain is doing something, but it’s not a direct measure of brain activity. Which is to say, there’s room for error. That’s why neuroscientists use special statistics to filter out noise in their fMRIs, verifying that the shaded blobs they see pulsing across their computer screens actually relate to blood flowing through the brain. If those filters don’t work, an fMRI scan is about as useful at detecting neuronal activity as your dad’s “brain sucking alien” hand trick. And a new paper suggests that might actually be the case for thousands of fMRI studies over the past 15 years. The paper, published June 29 in the Proceedings of the National Academy of Science, threw 40,000 fMRI studies done over the past 15 years into question. But many neuroscientists—including the study’s whistleblowing authors—are now saying the negative attention is overblown. Neuroscience has long struggled over just how useful fMRI data is at showing brain function. “In the early days these fMRI signals were very small, buried in a huge amount of noise,” says Elizabeth Hillman, a biomedical engineer at the Zuckerman Institute at Columbia University. A lot of this noise is literal: noise from the scanner, noise from the electrical components, noise from the person’s body as it breathes and pumps blood.
Keyword: Brain imaging
Link ID: 22413 - Posted: 07.09.2016
Andrew Orlowski Special Report If the fMRI brain-scanning fad is well and truly over, then many fashionable intellectual ideas look like collateral damage, too. What might generously be called the “British intelligentsia” – our chattering classes – fell particularly hard for the promise that “new discoveries in brain science” had revealed a new understanding of human behaviour, which shed new light on emotions, personality and decision making. But all they were looking at was statistical quirks. There was no science to speak of, the results of the experiments were effectively meaningless, and couldn’t support the (often contradictory) conclusions being touted. The fMRI machine was a very expensive way of legitimising an anecdote. This is an academic scandal that’s been waiting to explode for years, for plenty of warning signs were there. In 2005, Ed Vul, now a psychology professor at UCSD, and Hal Pashler – then and now at UCSD – were puzzled by a claim being made in a talk by a neuroscience researcher. He was explaining study that purported to report a high correlation between a test subject’s brain activity and the speed with which they left the room after the study. “It seemed unbelievable to us that activity in this specific brain area could account for so much of the variance in walking speed,” explained Vul. “Especially so, because the fMRI activity was measured some two hours before the walking happened. So either activity in this area directly controlled motor action with a delay of two hours — something we found hard to believe — or there was something fishy going on.” IT © 1998–2016
Keyword: Brain imaging
Link ID: 22410 - Posted: 07.08.2016
It's no secret that passwords aren't impenetrable. Even outside of major incidents like the celebrity nude photo hack, or when millions of passwords get released online, like what happened to Twitter recently, many of us may still be at risk of having our data compromised due to password-related security flaws. According to a June 2015 survey from mobile identity company TeleSign, two in five people were notified in the preceding year that their personal information was compromised or that they had been hacked or had their password stolen. But a new technology developed by the BioSense lab at the University of California, Berkeley could make all of that a thing of the past. Over the course of three years, the lab's co-director, John Chuang, and his graduate students have been working on a technology called passthoughts, which would use a person's brainwaves to identify them, according to CNET. The team has found that a passthought — something like a song that someone could sing in their mind — isn't easily forgotten and can achieve a 99-per-cent authentication accuracy rate. The device used to capture passthoughts resembles a telephone headset. It relies on EEG technology, detecting electrical activity in your brain via electrodes strapped to your head. And although Chuang's team say the technology has improved greatly in recent years, the awkwardness of the device might hinder it from being widely adopted. ©2016 CBC/Radio-Canada.
Keyword: Brain imaging
Link ID: 22401 - Posted: 07.06.2016
Laura Sanders Busy nerve cells in the brain are hungry and beckon oxygen-rich blood to replenish themselves. But active nerve cells in newborn mouse brains can’t yet make this request, and their silence leaves them hungry, scientists report June 22 in the Journal of Neuroscience. Instead of being a dismal starvation diet, this lean time may actually spur the brain to develop properly. The new results, though, muddy the interpretation of the brain imaging technique called functional MRI when it is used on infants. Most people assume that all busy nerve cells, or neurons, signal nearby blood vessels to replenish themselves. But there were hints from fMRI studies of young children that their brains don’t always follow this rule. “The newborn brain is doing something weird,” says study coauthor Elizabeth Hillman of Columbia University. That weirdness, she suspected, might be explained by an immature communication system in young brains. To find out, she and her colleagues looked for neuron-blood connections in mice as they grew. “What we’re trying to do is create a road map for what we think you actually should see,” Hillman says. When 7-day-old mice were touched on their hind paws, a small group of neurons in the brain responded instantly, firing off messages in a flurry of activity. Despite this action, no fresh blood arrived, the team found. By 13 days, the nerve cell reaction got bigger, spreading across a wider stretch of the brain. Still the blood didn’t come. But by the time the mice reached adulthood, neural activity prompted an influx of blood. The results show that young mouse brains lack the ability to send blood to busy neurons, a skill that influences how the brain operates (SN: 11/14/15, p. 22). © Society for Science & the Public 2000 - 2016.
In a study of stroke patients, investigators confirmed through MRI brain scans that there was an association between the extent of disruption to the brain’s protective blood-brain barrier and the severity of bleeding following invasive stroke therapy. The results of the National Institutes of Health-funded study were published in Neurology. These findings are part of the Diffusion and Perfusion Imaging Evaluation for Understanding Stroke Evolution (DEFUSE)-2 Study, which was designed to see how MRIs can help determine which patients undergo endovascular therapy following ischemic stroke caused by a clot blocking blood flow to the brain. Endovascular treatment targets the ischemic clot itself, either removing it or breaking it up with a stent. The blood-brain barrier is a layer of cells that protects the brain from harmful molecules passing through the bloodstream. After stroke, the barrier is disrupted, becoming permeable and losing control over what gets into the brain. “The biggest impact of this research is that information from MRI scans routinely collected at a number of research hospitals and stroke centers can inform treating physicians on the risk of bleeding,” said Richard Leigh, M.D., a scientist at NIH’s National Institute of Neurological Disorders and Stroke (NINDS) and an author on the study. In this study, brain scans were collected from more than 100 patients before they underwent endovascular therapy, within 12 hours of stroke onset. Dr. Leigh and his team obtained the images from DEFUSE-2 investigators.
By Monique Brouillette The brain presents a unique challenge for medical treatment: it is locked away behind an impenetrable layer of tightly packed cells. Although the blood-brain barrier prevents harmful chemicals and bacteria from reaching our control center, it also blocks roughly 95 percent of medicine delivered orally or intravenously. As a result, doctors who treat patients with neurodegenerative diseases, such as Parkinson's, often have to inject drugs directly into the brain, an invasive approach that requires drilling into the skull. Some scientists have had minor successes getting intravenous drugs past the barrier with the help of ultrasound or in the form of nanoparticles, but those methods can target only small areas. Now neuroscientist Viviana Gradinaru and her colleagues at the California Institute of Technology show that a harmless virus can pass through the barricade and deliver treatment throughout the brain. Gradinaru's team turned to viruses because the infective agents are small and adept at entering cells and hijacking the DNA within. They also have protein shells that can hold beneficial deliveries, such as drugs or genetic therapies. To find a suitable virus to enter the brain, the researchers engineered a strain of an adeno-associated virus into millions of variants with slightly different shell structures. They then injected these variants into a mouse and, after a week, recovered the strains that made it into the brain. A virus named AAV-PHP.B most reliably crossed the barrier. © 2016 Scientific American,
Link ID: 22313 - Posted: 06.13.2016
By David Shultz We still may not know what causes consciousness in humans, but scientists are at least learning how to detect its presence. A new application of a common clinical test, the positron emission tomography (PET) scan, seems to be able to differentiate between minimally conscious brains and those in a vegetative state. The work could help doctors figure out which brain trauma patients are the most likely to recover—and even shed light on the nature of consciousness. “This is really cool what these guys did here,” says neuroscientist Nicholas Schiff at Cornell University, who was not involved in the study. “We’re going to make great use of it.” PET scans work by introducing a small amount of radionuclides into the body. These radioactive compounds act as a tracer and naturally emit subatomic particles called positrons over time, and the gamma rays indirectly produced by this process can be detected by imaging equipment. The most common PET scan uses fluorodeoxyglucose (FDG) as the tracer in order to show how glucose concentrations change in tissue over time—a proxy for metabolic activity. Compared with other imaging techniques, PET scans are relatively cheap and easy to perform, and are routinely used to survey for cancer, heart problems, and other diseases. In the new study, researchers used FDG-PET scans to analyze the resting cerebral metabolic rate—the amount of energy being used by the tissue—of 131 patients with a so-called disorder of consciousness and 28 healthy controls. Disorders of consciousness can refer to a wide range of problems, ranging from a full-blown coma to a minimally conscious state in which patients may experience brief periods where they can communicate and follow instructions. Between these two extremes, patients may be said to be in a vegetative state or exhibit unresponsive wakefulness, characterized by open eyes and basic reflexes, but no signs of awareness. Most disorders of consciousness result from head trauma, and where someone falls on the consciousness continuum is typically determined by the severity of the injury. © 2016 American Association for the Advancement of Science
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
Link ID: 22252 - Posted: 05.26.2016
By Emily Underwood One of the telltale signs of Alzheimer’s disease (AD) is sticky plaques of ß-amyloid protein, which form around neurons and are thought by a large number of scientists to bog down information processing and kill cells. For more than a decade, however, other researchers have fingered a second protein called tau, found inside brain cells, as a possible culprit. Now, a new imaging study of 10 people with mild AD suggests that tau deposits—not amyloid—are closely linked to symptoms such as memory loss and dementia. Although this evidence won’t itself resolve the amyloid-tau debate, the finding could spur more research into new, tau-targeting treatments and lead to better diagnostic tools, researchers say. Scientists have long used an imaging technique called positron emission tomography (PET) to visualize ß-amyloid deposits marked by radioactive chemical tags in the brains of people with AD. Combined with postmortem analyses of brain tissue, these studies have demonstrated that people with AD have far more ß-amyloid plaques in their brains than healthy people, at least as a general rule. But they have also revealed a puzzle: Roughly 30% of people without any signs of dementia have brains “chock-full” of ß-amyloid at autopsy, says neurologist Beau Ances at Washington University in St. Louis in Missouri. That mystery has inspired many in the AD field to ask whether a second misfolded protein, tau, is the real driver of the condition’s neurodegeneration and symptoms, or at least an important accomplice. Until recently, the only ways to test that hypothesis were to measure tau in brain tissue after a person died, or in a sample of cerebrospinal fluid (CSF) extracted from a living person by needle. But in the past several years, researchers have developed PET imaging agents that can harmlessly bind to tau in the living brain. The more tau deposits found in the temporal lobe, a brain region associated with memory, the more likely a person was to show deficits on a battery of memory and attention tests, the team reports today in Science Translational Medicine. © 2016 American Association for the Advancement of Science.