Chapter 2. Cells and Structures: The Anatomy of the Nervous System
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By ABIGAIL ZUGER, M.D. In history’s long parade of pushy mothers and miserably obedient children, no episode beats Dr. Frank H. Netter’s for a happy ending. Both parties got the last laugh. Netter was born to immigrant parents in New York in 1906. He was an artist from the time he could grab a pencil, doodling through high school, winning a scholarship to art school, and enunciating intentions of making his living as an illustrator. Then his mother stepped in, and with an iron hand, deflected him to medicine. Frank’s siblings and cousins all had respectable careers, she informed him, and he would, too. To his credit, he lasted quite a while: through medical school, hospital training and almost an entire year as a qualified doctor. But he continued drawing the whole time, making sketches in his lecture notes to clarify abstruse medical concepts for himself, then doing the same for classmates and even professors. Then, fatefully, his work attracted the notice of advertising departments at pharmaceutical companies. In the midst of the Depression, he demanded and received $7,500 for a series of five drawings, many times what he might expect to earn from a full year of medical practice. He put down his scalpel for good. Thanks to a five-decade exclusive contract with Ciba (now Novartis), he ultimately became possibly the best-known medical illustrator in the world, creating thousands of watercolor plates depicting every aspect of 20th-century medicine. His illustrations were virtually never used to market specific products, but distributed free of charge to doctors as a public service, and collected into popular textbooks. © 2014 The New York Times Company
Keyword: Brain imaging
Link ID: 19197 - Posted: 02.04.2014
by Aviva Rutkin "He moistened his lips uneasily." It sounds like a cheap romance novel, but this line is actually lifted from quite a different type of prose: a neuroscience study. Along with other sentences, including "Have you got enough blankets?" and "And what eyes they were", it was used to build the first map of how the brain processes the building blocks of speech – distinct units of sound known as phonemes. The map reveals that the brain devotes distinct areas to processing different types of phonemes. It might one day help efforts to read off what someone is hearing from a brain scan. "If you could see the brain of someone who is listening to speech, there is a rapid activation of different areas, each responding specifically to a particular feature the speaker is producing," says Nima Mesgarani, an electrical engineer at Columbia University in New York City. Snakes on a brain To build the map, Mesgarani's team turned to a group of volunteers who already had electrodes implanted in their brains as part of an unrelated treatment for epilepsy. The invasive electrodes sit directly on the surface of the brain, providing a unique and detailed view of neural activity. The researchers got the volunteers to listen to hundreds of snippets of speech taken from a database designed to provide an efficient way to cycle through a wide variety of phonemes, while monitoring the signals from the electrodes. As well as those already mentioned, sentences ran the gamut from "It had gone like clockwork" to "Junior, what on Earth's the matter with you?" to "Nobody likes snakes". © Copyright Reed Business Information Ltd.
By Jennifer Ouellette It was a brisk October day in a Greenwich Village café when New York University neuroscientist David Poeppel crushed my dream of writing the definitive book on the science of the self. I had naively thought I could take a light-hearted romp through genotyping, brain scans, and a few personality tests and explain how a fully conscious unique individual emerges from the genetic primordial ooze. Instead, I found myself scrambling to navigate bumpy empirical ground that was constantly shifting beneath my feet. How could a humble science writer possibly make sense of something so elusively complex when the world’s most brilliant thinkers are still grappling with this marvelous integration that makes us us? “You can’t. Why should you?” Poeppel asked bluntly when I poured out my woes. “We work for years and years on seemingly simple problems, so why should a very complicated problem yield an intuition? It’s not going to happen that way. You’re not going to find the answer.” Well, he was right. Darn it. But while I might not have found the Ultimate Answer to the source of the self, it proved to be an exciting journey and I learned some fascinating things along the way. 1. Genes are deterministic but they are not destiny. Except for earwax consistency. My earwax is my destiny. We tend to think of our genome as following a “one gene for one trait” model, but the real story is far more complicated. True, there is one gene that codes for a protein that determines whether you will have wet or dry earwax, but most genes serve many more than one function and do not act alone. Height is a simple trait that is almost entirely hereditary, but there is no single gene helpfully labeled height. Rather, there are several genes interacting with one another that determine how tall we will be. Ditto for eye color. It’s even more complicated for personality traits, health risk factors, and behaviors, where traits are influenced, to varying degrees, by parenting, peer pressure, cultural influences, unique life experiences, and even the hormones churning around us as we develop in the womb.
Alison Abbott By slicing up and reconstructing the brain of Henry Gustav Molaison, researchers have confirmed predictions about a patient that has already contributed more than most to neuroscience. No big scientific surprises emerge from the anatomical analysis, which was carried out by Jacopo Annese of the Brain Observatory at the University of California, San Diego, and his colleagues, and published today in Nature Communications1. But it has confirmed scientists’ deductions about the parts of the brain involved in learning and memory. “The confirmation is surely important,” says Richard Morris, who studies learning and memory at the University of Edinburgh, UK. “The patient is a classic case, and so the paper will be extensively cited.” Molaison, known in the scientific literature as patient H.M., lost his ability to store new memories in 1953 after surgeon William Scoville removed part of his brain — including a large swathe of the hippocampus — to treat his epilepsy. That provided the first conclusive evidence that the hippocampus is fundamental for memory. H.M. was studied extensively by cognitive neuroscientists during his life. After H.M. died in 2008, Annese set out to discover exactly what Scoville had excised. The surgeon had made sketches during the operation, and brain-imaging studies in the 1990s confirmed that the lesion corresponded to the sketches, although was slightly smaller. But whereas brain imaging is relatively low-resolution, Annese and his colleagues were able to carry out an analysis at the micrometre scale. © 2014 Nature Publishing Group
by Helen Thomson The brain that made the greatest contribution to neuroscience and to our understanding of memory has become a gift that keeps on giving. A 3D reconstruction of the brain of Henry Molaison, whose surgery to cure him of epilepsy left him with no short-term memory, will allow scientists to continue to garner insights into the brain for years to come. "Patient HM" became arguably the most famous person in neuroscience after he had several areas of his brain removed in 1953. His resulting amnesia and willingness to be tested have given us unprecedented insights into where memories are formed and stored in the brain. On his death in 2008, HM was revealed to the world as Henry Molaison. Now, a post-mortem examination of his brain, and a new kind of virtual 3D reconstruction, have been published. As a child, Molaison had major epileptic seizures. Anti-epileptic drugs failed, so he sought help from neurosurgeon William Scoville at Hartford Hospital in Connecticut. When Molaison was 27 years old, Scoville removed portions of his medial temporal lobes, which included an area called the hippocampus on both sides of his brain. As a result, Molaison's epilepsy became manageable, but he could not form any new memories, a condition known as anterograde amnesia. He also had difficulty recollecting his long-term past – partial retrograde amnesia.
Keyword: Learning & Memory
Link ID: 19172 - Posted: 01.27.2014
By Gary Stix The blood-brain barrier is the Berlin Wall of human anatomy and physiology Its closely packed cells shield neurons and the like from toxins and pathogens, while letting pass glucose and other essential chemicals for brain metabolism (caffeine?). For years, pharmaceutical companies and academic researchers have engaged in halting efforts to traverse this imposing blockade in order to deliver some of the big molecules that might potentially help slow the progression of devastating neurological diseases. Like would-be refugees from the former East Germany, many medications get snagged by border guards during the crossing—a molecular security force that either impedes or digests any invader. There have been many attempts to secure safe passage—deploying chemicals that make brain-barrier “endothelial” cells shrivel up, or wielding tiny catheters or minute bubbles that slip through minuscule breaches. Success has been mixed at best—none of these molecular cargo carriers have made their way as far as human trials. Roche, the Swiss-based drugmaker, reported in the Jan. 8 Neuron a bit of progress toward overcoming the lingering technical impediments. The study described a new technique that tricks one of the BBB’s natural checkpoints to let through an elaborately engineered drug that attacks the amyloid-beta protein fragments that may be the primary culprit inflicting the damage wrought by Alzheimer’s. The subterfuge involves the transferrin receptor, a docking site used to transport iron into the brain. Roche took a fragment of an antibody that binds the transferrin receptor and latched it onto another antibody that, once on the other side of the BBB, attaches to and then removes amyloid. © 2014 Scientific American
Link ID: 19121 - Posted: 01.13.2014
By JAMES GORMAN ST. LOUIS — Deanna Barch talks fast, as if she doesn’t want to waste any time getting to the task at hand, which is substantial. She is one of the researchers here at Washington University working on the first interactive wiring diagram of the living, working human brain. To build this diagram she and her colleagues are doing brain scans and cognitive, psychological, physical and genetic assessments of 1,200 volunteers. They are more than a third of the way through collecting information. Then comes the processing of data, incorporating it into a three-dimensional, interactive map of the healthy human brain showing structure and function, with detail to one and a half cubic millimeters, or less than 0.0001 cubic inches. Dr. Barch is explaining the dimensions of the task, and the reasons for undertaking it, as she stands in a small room, where multiple monitors are set in front of a window that looks onto an adjoining room with an M.R.I. machine, in the psychology building. She asks a research assistant to bring up an image. “It’s all there,” she says, reassuring a reporter who has just emerged from the machine, and whose brain is on display. And so it is, as far as the parts are concerned: cortex, amygdala, hippocampus and all the other regions and subregions, where memories, fear, speech and calculation occur. But this is just a first go-round. It is a static image, in black and white. There are hours of scans and tests yet to do, though the reporter is doing only a demonstration and not completing the full routine. Each of the 1,200 subjects whose brain data will form the final database will spend a good 10 hours over two days being scanned and doing other tests. The scientists and technicians will then spend at least another 10 hours analyzing and storing each person’s data to build something that neuroscience does not yet have: a baseline database for structure and activity in a healthy brain that can be cross-referenced with personality traits, cognitive skills and genetics. And it will be online, in an interactive map available to all. © 2014 The New York Times Company
Keyword: Brain imaging
Link ID: 19106 - Posted: 01.07.2014
By JAMES GORMAN St. Louis — I knew I wouldn’t find my “self” in a brain scan. I also knew as I headed into the noisy torpedo tube of a souped-up M.R.I. machine at Washington University in St. Louis that unless there was something terribly wrong (“Igor, look! His head is filled with Bitcoins!”), I would receive no news of the particulars of how my brain was arranged. Even if I had been one of the 1,200 volunteers in the part of the Human Connectome Project being conducted there, I wouldn’t have gotten a report of my own personal connectome and what it meant. Once the 10 hours of scans and tests are finished, and 10 hours more of processing and analysis done, the data for each of the volunteers — all anonymous — becomes part of a database to help scientists develop tools so that one day such an individual report might be possible. Besides, I was just going through a portion of the process, to see what it was like. Even so, I do have this sense of myself as an individual, different from others in ways good, bad and inconsequential, and the pretty reasonable feeling that whatever a “self” is, it lies behind my eyes and between my ears. That’s where I feel that “I” live. So I couldn’t shake the sense that there would be something special in seeing my brain, even if I couldn’t actually spot where all the song lyrics I’ve memorized are stored, or locate my fondness for cooking and singing and my deep disappointment that I can’t carry a tune (though I can follow a recipe). So I climbed into the M.R.I. machine. I tried to hold my head perfectly still as I stared at a spot marked by a cross, tried to corral my fading memory to perform well on tests, curled my toes and moved my fingers so that muscle motion could be mapped, and wondered at the extraordinary noises M.R.I. machines make. © 2014 The New York Times Company
After nearly a year of meetings and public debate, the National Institutes of Health (NIH) today announced how it intends to spend its share of funding for the Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative, a $110 million U.S. effort to jump-start the development of new technologies that can map the brain’s vast and intricate neural circuits in action. In short, it’s looking for big ideas, such as taking a census of all the cells in the brain, even if there’s little data so far on how to accomplish them. The agency is calling for grant applications in six “high-priority” research areas drawn from a September report by its 15-member scientific advisory committee for the project. The agency is committing to spend roughly $40 million per year for 3 years on these areas, says Story Landis, director of the National Institute of Neurological Disorders and Stroke. “We hope that there will be additional funds that will become available, but obviously that depends upon what our budget is,” she says. The six funding streams center almost exclusively on proof-of-concept testing and development of new technologies and novel approaches for tasks considered fundamental to understanding how neurons work together to produce behavior in the brain; for example, classifying different types of brain cells, and determining how they contribute to specific neural circuits. NIH’s focus on innovation means that most grant applicants will not have to supply preliminary data for their proposals—a departure from “business as usual” that will likely startle many scientists and reviewers but is necessary to give truly innovative ideas a fair shot, Landis says. Only one call for funding, aimed at optimizing existing technologies for recording and manipulating large numbers of neurons that “aren’t ready for prime time,” will require such background, she says. © 2013 American Association for the Advancement of Science.
Keyword: Brain imaging
Link ID: 19047 - Posted: 12.18.2013
A study in mice shows how a breakdown of the brain’s blood vessels may amplify or cause problems associated with Alzheimer’s disease. The results published in Nature Communications suggest that blood vessel cells called pericytes may provide novel targets for treatments and diagnoses. “This study helps show how the brain’s vascular system may contribute to the development of Alzheimer’s disease,” said study leader Berislav V. Zlokovic, M.D. Ph.D., director of the Zilkha Neurogenetic Institute at the Keck School of Medicine of the University of Southern California, Los Angeles. The study was co-funded by the National Institute of Neurological Diseases and Stroke (NINDS) and the National Institute on Aging (NIA), parts of the National Institutes of Health. Alzheimer’s disease is the leading cause of dementia. It is an age-related disease that gradually erodes a person’s memory, thinking, and ability to perform everyday tasks. Brains from Alzheimer’s patients typically have abnormally high levels of plaques made up of accumulations of beta-amyloid protein next to brain cells, tau protein that clumps together to form neurofibrillary tangles inside neurons, and extensive neuron loss. Vascular dementias, the second leading cause of dementia, are a diverse group of brain disorders caused by a range of blood vessel problems. Brains from Alzheimer’s patients often show evidence of vascular disease, including ischemic stroke, small hemorrhages, and diffuse white matter disease, plus a buildup of beta-amyloid protein in vessel walls. Furthermore, previous studies suggest that APOE4, a genetic risk factor for Alzheimer’s disease, is linked to brain blood vessel health and integrity.
Link ID: 19033 - Posted: 12.14.2013
By Ingfei Chen The way doctors diagnose Alzheimer's disease may be starting to change. Traditionally clinicians have relied on tests of memory and reasoning skills and reports of social withdrawal to identify patients with Alzheimer's. Such assessments can, in expert hands, be fairly conclusive—but they are not infallible. Around one in five people who are told they have the neurodegenerative disorder actually have other forms of dementia or, sometimes, another problem altogether, such as depression. To know for certain that someone has Alzheimer's, doctors must remove small pieces of the brain, examine the cells under a microscope and count the number of protein clumps called amyloid plaques. An unusually high number of plaques is a key indicator of Alzheimer's. Because such a procedure risks further impairing a patient's mental abilities, it is almost always performed posthumously. In the past 10 years, however, scientists have developed sophisticated brain scans that can estimate the amount of plaque in the brain while people are still alive. In the laboratory, these scans have been very useful in studying the earliest stages of Alzheimer's, before overt symptoms appear. The results are reliable enough that last year the Food and Drug Administration approved one such test called Amyvid to help evaluate patients with memory deficits or other cognitive difficulties. Despite the FDA's approval, lingering doubts about the exact role of amyloid in Alzheimer's and ambivalence about the practical value of information provided by the scan have fueled debate about when to order an Amyvid test. Not everyone who has an excessive amount of amyloid plaque develops Alzheimer's, and at the moment, there is generally no way to predict whom the unlucky ones will be. Recent studies have shown that roughly one third of older citizens in good mental health have moderate to high levels of plaque, with no noticeable ill effects. And raising the specter of the disorder in the absence of symptoms may upset more people than it helps because no effective treatments exist—at least not yet. © 2013 Scientific American
Helen Shen Dyslexia may be caused by impaired connections between auditory and speech centres of the brain, according to a study published today in Science1. The research could help to resolve conflicting theories about the root causes of the disorder, and lead to targeted interventions. When people learn to read, their brains make connections between written symbols and components of spoken words. But people with dyslexia seem to have difficulty identifying and manipulating the speech sounds to be linked to written symbols. Researchers have long debated whether the underlying representations of these sounds are disrupted in the dyslexic brain, or whether they are intact but language-processing centres are simply unable to access them properly. A team led by Bart Boets, a clinical psychologist at the Catholic University of Leuven in Belgium, analysed brain scans and found that phonetic representations of language remain intact in adults with dyslexia, but may be less accessible than in controls because of deficits in brain connectivity. "The authors took a really inventive and thoughtful approach," says John Gabrieli, a neuroscientist at the Massachusetts Institute of Technology in Cambridge, Massachusetts. "They got a pretty clear answer." Communication channels Boets and his team used a technique called multivoxel pattern analysis to study fine-scale brain signals as people listened to a battery of linguistic fragments such as 'ba' and 'da'. To the researchers' surprise, neural activity in the primary and secondary auditory cortices of participants with dyslexia showed consistently distinct signals for different sounds. © 2013 Nature Publishing Group
By Neuroskeptic This morning, the world woke up to the news that Scientists discover the difference between male and female brains Britain’s Independent today actually made that their front page. They went on to discuss “the hardwired difference that could explain why men are ‘better at map reading’”. The rest of the world’s media were no less excited. Well. I don’t have time to get into criticizing the media or decrying gender stereotypes, so let’s just stick to the science. The study in question, published in PNAS, is called Sex differences in the structural connectome of the human brain. The authors used diffusion tensor imaging (DTI) to estimate the integrity of the white matter tracts going in various directions at each point in the brain. In a large sample of 428 males and 521 females aged from 8 to 22, they report sex differences in the pattern of white matter connectivity. In general, the female brains were ‘more connected’ than the male, except in the cerebellum: here’s the plot for a summary measure, the Participation Coefficient. I have two issues with this: Head Motion. A perennial Neuroskeptic favorite, this one. A paper just last week showed convincingly that even modest amounts of head movement during the MRI scan causes changes in DTI. Various commentators on Twitter and elsewhere swiftly pointed out that it’s not implausible that men and women might move different amounts on average, so that might account for at least some of these results.
Ian Sample, science correspondent Scientists have drawn on nearly 1,000 brain scans to confirm what many had surely concluded long ago: that stark differences exist in the wiring of male and female brains. Maps of neural circuitry showed that on average women's brains were highly connected across the left and right hemispheres, in contrast to men's brains, where the connections were typically stronger between the front and back regions. Ragini Verma, a researcher at the University of Pennsylvania, said the greatest surprise was how much the findings supported old stereotypes, with men's brains apparently wired more for perception and co-ordinated actions, and women's for social skills and memory, making them better equipped for multitasking. "If you look at functional studies, the left of the brain is more for logical thinking, the right of the brain is for more intuitive thinking. So if there's a task that involves doing both of those things, it would seem that women are hardwired to do those better," Verma said. "Women are better at intuitive thinking. Women are better at remembering things. When you talk, women are more emotionally involved – they will listen more." She added: "I was surprised that it matched a lot of the stereotypes that we think we have in our heads. If I wanted to go to a chef or a hairstylist, they are mainly men." The findings come from one of the largest studies to look at how brains are wired in healthy males and females. The maps give scientists a more complete picture of what counts as normal for each sex at various ages. Armed with the maps, they hope to learn more about whether abnormalities in brain connectivity affect brain disorders such as schizophrenia and depression. © 2013 Guardian News and Media Limited
At the Society for Neuroscience meeting earlier this month in San Diego, California, Science sat down with Geoffrey Ling, deputy director of the Defense Sciences Office at the Defense Advanced Research Projects Agency (DARPA), to discuss the agency’s plans for the Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative, a neuroscience research effort put forth by President Barack Obama earlier this year. So far, DARPA has released two calls for grant applications, with at least one more likely: The first, called SUBNETS (Systems-Based Neurotechnology for Emerging Therapies), asks researchers to develop novel, wireless devices, such as deep brain stimulators, that can cure neurological disorders such as posttraumatic stress (PTS), major depression, and chronic pain. The second, RAM (Restoring Active Memory), calls for a separate wireless device that repairs brain damage and restores memory loss. Below is an extended version of a Q&A that appears in the 29 November issue of Science. Q: Why did DARPA get involved in the BRAIN project? G.L.: It’s really focused on our injured warfighters, but it has a use for civilians who have stress disorders and civilians who also have memory disorders from dementia and the like. But at the end of the day, it is still meeting [President Obama’s] directive. Of all the things he could have chosen—global warming, alternative fuels—he chose this, so in my mind the neuroscience community should be as excited as all get-up. Q: Why does SUBNETS focus on deep brain stimulation (DBS)? G.L.: We’ve opened the possibility of using DBS but we haven’t exclusively said that. We’re challenging people to go after neuropsychiatric disorders like PTS [and] depression. We’re challenging the community to come up with something in 5 years that’s clinically feasible. DBS is an area that has really been traditionally underfunded, so we thought what the heck, let’s give it a go—in this new BRAIN Initiative the whole idea is to go after the things that there aren’t 400 R01 grants for—and let’s be bold, and boy, if it works, fabulous. © 2013 American Association for the Advancement of Science
By Dwayne Godwin and Jorge Cham Dwayne Godwin is a neuroscientist at the Wake Forest University School of Medicine. His Twitter handle is @brainyacts. Jorge Cham draws the comic strip Piled Higher and Deeper at www.phdcomics.com. © 2013 Scientific American
Keyword: Brain imaging
Link ID: 18980 - Posted: 11.30.2013
By Neuroskeptic Claims that children with autism have abnormal brain white matter connections may just reflect the fact that they move about more during their MRI scans. So say a team of Harvard and MIT neuroscientists, including Nancy “Voodoo Correlations” Kanwisher, in a new paper: Spurious group differences due to head motion in a diffusion MRI study. Essentially, the authors show how head movement during a diffusion tensor imaging (DTI) scan causes apparant differences in the integrity of white matter tracts, like these ones: In comparisons of two randomized groups of healthy children – in whom no white matter differences ought to appear – spurious effects were seen whenever one group moved more than the other: As for autism, the authors found that kids with autism moved more, on average, than controls, and that matching the two groups by motion reduced the magnitude of the group differences in white matter (though many remained significant). Technically, the motion-related differences manifested as increases in RD and reductions in FA; these were localized: The pathways that exhibited the most substantial motion-induced group differences in our data were the corpus callosum and the cingulum bundle. Perhaps this is related to their proximity to non-brain voxels (such as the ventricles) … deeper brain areas appear to be more affected than more superﬁcial ones, thus distance from the head coils may also be a factor. The good news is that there’s a simple fix: entering the motion parameters, extracted from the DTI data itself, as a covariate in the analysis. The authors show that this is extremely effective. The bad news is that most researchers don’t do this.
Peter Hildebrand Neuroscience is a rapidly growing field, but one that is usually thought to be too complex and expensive for average Americans to participate in directly. Now, an explosion of cheap scientific devices and online tutorials are on the verge of changing that. This change could have exciting implications for our future understanding of the brain. From 1995 to 2005, the amount of money spent on neuroscience research doubled. A lot of that research used medical devices, like MRI and CT Scan machines, and drugs that everyday citizens don’t have access to. Even in colleges, experience with powerful research equipment is reserved for upperclassmen and graduate students. The lowlier castes can work with models or dissect animal brains, but as scientist and engineer Greg Gage points out in this TED video, the brain isn’t like the heart or the lungs. You can’t tell how it works just by looking at it. Gage is calling for “neuro-revolution,” in which scientists and inventors come together to put the tools for learning neuroscience into the hands of the public. He may be onto something too, because those tools are looking more accessible than ever before. One of the most well publicized examples of this punk rock revolution has been Gage’s own “SpikerBox,” which he co-developed with Tim Marzullo. Roughly the size of your fist, the SpikerBox is a small collection of electronic components bolted between two squares of orange plastic. Coming out of one end are two pins that you can use to record the electrical activity of nerve cells in, say, a recently severed cockroach leg. There’s also a port that allows you to attach the box to a smartphone or tablet, and watch the spikes of activity as the neurons are stimulated. © 2013 Salon Media Group, Inc.
Keyword: Brain imaging
Link ID: 18976 - Posted: 11.26.2013
Ian Sample, science correspondent in San Diego Criminal courts in the United States are facing a surge in the number of defendants arguing that their brains were to blame for their crimes and relying on questionable scans and other controversial, unproven neuroscience, a legal expert who has advised the president has warned. Nita Farahany, a professor of law who sits on Barack Obama's bioethics advisory panel, told a Society for Neuroscience meeting in San Diego that those on trial were mounting ever more sophisticated defences that drew on neurological evidence in an effort to show they were not fully responsible for murderous or other criminal actions. Lawyers typically drew on brain scans and neuropsychological tests to reduce defendants' sentences, but in a substantial number of cases the evidence was used to try to clear defendants of all culpability. "What is novel is the use by criminal defendants to say, essentially, that my brain made me do it," Farahany said following an analysis of more than 1,500 judicial opinions from 2005 to 2012. The rise of so-called neurolaw cases has caused serious concerns in the country where brain science first appeared in murder cases. The supreme court has begun a review of how such evidence can be used in criminal cases. But legal and scientific experts nevertheless foresee the trend spreading to other countries, including the UK, and Farahany said she was expanding her work abroad. The survey even found cases where defendants had used neuroscience to argue that their confessions should be struck out because they were not competent to provide them. "When people introduce this evidence for competency, it has actually been relatively successful," Farahany said. © 2013 Guardian News and Media Limited
Kenneth S. Kosik Twenty years of research and more than US$1-billion worth of clinical trials have failed to yield an effective drug treatment for Alzheimer's disease. Most neuroscientists, clinicians and drug developers now agree that people at risk of the condition will probably need to receive medication before the onset of any cognitive symptoms. Yet a major stumbling block for early intervention is the absence of tools that can reveal the first expression of the insidious disease. So far, researchers have tended to focus on macroscopic changes associated with the disease, such as the build up of insoluble plaques of protein in certain areas of the brain, or on individual genes or molecular pathways that seem to be involved in disease progression. I contend that detecting the first disruptions to brain circuitry, and tracking the anatomical and physiological damage underlying the steady cognitive decline that is symptomatic of Alzheimer's, will require tools that operate at the 'mesoscopic' scale: techniques that probe the activity of thousands or millions of networked neurons. Although such tools are yet to be realized, several existing technologies indicate that they are within reach. Charted territory All the current approaches that are used to diagnose Alzheimer's are crude and unreliable. Take the classic biomarkers of the disease: a build up of plaques of the protein β-amyloid in a person's cerebral cortex, for instance, or elevated levels of the tau protein and dampened levels of β-amyloid in their cerebrospinal fluid. Although such markers are predictive of the disease, the interval between their appearance and the onset of cognitive problems is hugely variable, ranging from months to decades. © 2013 Nature Publishing Group