Posts tagged neuroscience
Articles and news from the latest research reports.
Electrical stimulation of brain area causes strange visual illusions
A new study shows that electrical stimulation of a small patch of the brain causes illusions that only affect the perception of faces. (Matt Cardy/Getty Images)
Ron Blackwell didn’t enter the hospital expecting to see his doctor’s face melt before his eyes. But that’s exactly what happened when researchers electrically stimulated a small part of his brain, according to a study published Tuesday in the Journal of Neuroscience.
The doctor’s face did not actually melt, of course. Instead, the researchers argue, the stimulation short-circuited a brain area called the fusiform gyrus. Previous studies have linked a part of that area to face processing by showing that it becomes active when people perceive faces. But it’s hard to know just how important the area is for facial processing unless you can actually change its activity level while someone views faces.
Blackwell, an epileptic, turned out to be the perfect test case. He was in Stanford’s hospital so that doctors — including the study author, Dr. Josef Parvizi — could study his epilepsy and decide whether they could perform surgery to remove the part of the brain responsible for his seizures. As part of that procedure, Parvizi laid down a strip of electrodes on the surface of the brain. That gave him the capacity to painlessly and harmlessly stimulate the part of the brain they covered, and one of those electrodes was right over the fusiform gyrus.
Along with collaborators led by Stanford psychologist Kalanit Grill-Spector, Parvizi stimulated the area to see whether it would affect Blackwell’s perception of the doctor’s face. When he performed a sham stimulation — counting down from three and pressing a button that did nothing — Blackwell reported no change.
But when Parvizi applied voltage, strange things suddenly began to happen to Blackwell’s face perception. “You just turned into somebody else,” Blackwell said in a video that was recorded as part of the experiment. “Your face metamorphosed. Your nose got saggy, went to the left. You almost looked like somebody I’d seen before, but somebody different. That was a trip.” As soon as the electricity was turned off, Blackwell’s visualization of Parvizi’s face returned to normal.
Later, Blackwell confirmed that it was only the doctor’s face that changed — his body and hands remained the same.
Though only a single case, the experiment provides strong confirmatory evidence that the fusiform gyrus is indeed directly involved in processing face perception, and that the area is specialized for doing so.
(Source: Los Angeles Times)
New hope for the blind from neuroscientists?
Scientists in the Texas Medical Center believe that there may be a way to use mental images to help some of the estimated 39 million people worldwide who are blind.
Scientists in the laboratories of Michael Beauchamp, Ph.D., an associate professor of neurobiology and anatomy at the The University of Texas Health Science Center at Houston (UTHealth) Medical School, and Daniel Yoshor, M.D., an associate professor of neurosurgery and neuroscience at Baylor College of Medicine, have discovered a neural mechanism for conscious perception that could use the brain’s image-generating ability.
“While much work remains to be done, the possibilities are exciting,” said Beauchamp, the study’s lead author. “If successful, we would in essence bypass eyes that no longer work and stimulate the brain to generate mental images. This type of device is known as a visual prosthetic.”
"Blue" Light Could Help Teenagers Combat Stress
Adolescents can be chronically sleep deprived because of their inability to fall asleep early in combination with fixed wakeup times on school days. According to the CDC, almost 70 percent of school children get insufficient sleep—less than 8 hours on school nights. This type of restricted sleep schedule has been linked with depression, behavior problems, poor performance at school, drug use, and automobile accidents. A new study from the Lighting Research Center (LRC) at Rensselaer Polytechnic Institute shows that exposure to morning short-wavelength “blue” light has the potential to help sleep-deprived adolescents prepare for the challenges of the day and deal with stress, more so than dim light.
The study was a collaboration between Associate Professor and Director of the LRC Light and Health Program Mariana Figueiro and LRC Director and Professor Mark S. Rea. Results of the study titled “Short-Wavelength Light Enhances Cortisol Awakening Response in Sleep-Restricted Adolescents,” were recently published in the open access International Journal of Endocrinology. The full text is available at http://www.hindawi.com/journals/ije/2012/301935/.
Aggressive Brain Tumors Can Originate From a Range of Nervous System Cells
Scientists have long believed that glioblastoma multiforme (GBM), the most aggressive type of primary brain tumor, begins in glial cells that make up supportive tissue in the brain or in neural stem cells. In a paper published October 18 in Science, however, researchers at the Salk Institute for Biological Studies have found that the tumors can originate from other types of differentiated cells in the nervous system, including cortical neurons.
GBM is one of the most devastating brain tumors that can affect humans. Despite progress in genetic analysis and classification, the prognosis of these tumors remains poor, with most patients dying within one to two years of diagnosis. The Salk researcher’s findings offer an explanation for the recurrence of GBM following treatment and suggest potential new targets to treat these deadly brain tumors.
"One of the reasons for the lack of clinical advances in GBMs has been the insufficient understanding of the underlying mechanisms by which these tumors originate and progress," says Inder Verma, a professor in Salk’s Laboratory of Genetics and the Irwin and Joan Jacobs Chair in Exemplary Life Science.
To better understand this process, Verma’s team harnessed the power of modified viruses, called lentiviruses, to disable powerful tumor suppressor genes that regulate the growth of cells and inhibit the development of tumors. With these tumor suppressors deactivated, cancerous cells are given free rein to grow out of control.
How Does the Brain Process Art?
New imaging techniques are mapping the locations of our aesthetic response
In Michelangelo’s Expulsion from Paradise, a fresco panel on the ceiling of the Sistine Chapel, the fallen-from-grace Adam wards off a sword-wielding angel, his eyes averted from the blade and his wrist bent back defensively. It is a gesture both wretched and beautiful. But what is it that triggers the viewer’s aesthetic response—the sense that we’re right there with him, fending off blows?
Recently, neuroscientists and an art historian asked ten subjects to examine the wrist detail from the painting, and—using a technique called transcranial magnetic stimulation (TMS)—monitored what happened in their brains. The researchers found that the image excited areas in the primary motor cortex that controlled the observers’ own wrists.
“Just the sight of the raised wrist causes an activation of the muscle,” reports David Freedberg, the Columbia University art history professor involved in the study. This connection explains why, for instance, viewers of Degas’ ballerinas sometimes report that they experience the sensation of dancing—the brain mirrors actions depicted on the canvas.
Freedberg’s study is part of the new but growing field of neuroaesthetics, which explores how the brain processes a work of art. The discipline emerged 12 years ago with publication of British neuroscientist Semir Zeki’s book, Inner Vision: An Exploration of Art and the Brain. Today, related studies depend on increasingly sophisticated brain-imaging techniques, including TMS and functional magnetic resonance imaging (fMRI), which maps blood flow and oxygenation in the brain. Scientists might monitor an observer’s reaction to a classical sculpture, then warp the sculpture’s body proportions and observe how the viewer’s response changes. Or they might probe what occurs when the brain contemplates a Chinese landscape painting versus an image of a simple, repetitive task.
Ulrich Kirk, a neuroscientist at the Virginia Tech Carilion Research Institute, is also interested in artworks’ contexts. Would a viewer respond the same way to a masterpiece enshrined in the Louvre if he beheld the same work displayed in a less exalted setting, such as a garage sale? In one experiment, Kirk showed subjects a series ofimages—some, he explained, were fine artwork; others were created by Photoshop. In reality, none were Photoshop-generated; Kirk found that different areas of viewers’ brains fired up when he declared an image to be “art.”
Kirk also hopes one day to plumb the brains of artists themselves. “You might be able to image creativity as it happens, by putting known artists in the fMRI,” he says.
Others, neuroscientists included, worry that neuroscience offers a reductionist perspective. Vilayanur Ramachandran, a neuroscientist at the University of California at San Diego, says that neuroaesthetics undoubtedly “enriches our understanding of human aesthetic experience.” However, he adds, “We have barely scratched the surface…the quintessence of art, and of genius, still eludes us—and may elude us forever.”
(Source: smithsonianmag.com)
About face: Study shows long-ignored segments of DNA play role in coordinating early stages of face development
The human face is a fantastically intricate thing. The billions of people on the planet have faces that are individually recognizable because each has subtle differences in its folds and curves. How is the face put together during development so that, out of billions of people, no two faces are exactly the same?
School of Medicine researcher Joanna Wysocka, PhD, and her colleagues have discovered key genetic elements that guide the earliest stages of the process.
Their research, published in the Sept. 13 issue of Cell Stem Cell, provides a resource for others studying facial development and could give insights to the cause of some facial birth defects. Because there is not enough genetic information in the body to define exactly where each cell will go, development of the face proceeds much like origami: genes provide instructions for folding, crimping, and movement of cells. As with origami, following a sequence of simple instructions can result in a complex, intricate object.
Wysocka focused on the first critical fold in the process of making an embryo, when the whole of the embryo is a flat sheet of cells that creases and closes over on itself to make a tube. Much of the tube eventually becomes the foundation of the brain and the spinal column, but one end sets the stage for the formation of the head and face. This process is driven by a small population of remarkable cells called neural crest cells.
"We were interested in identifying the portions of the human genome that are responsible for the behavior of the neural crest," Wysocka said.
What they discovered is that the modification of a collection of DNA sequences called “enhancers” can dial up or down the activity of the genes governing which cells eventually become the face. It’s almost as if they have discovered how the instructions for a piece of origami can be modified — slightly change how a fold is made and you may end up with something very different looking.
How fear skews our spatial perception
That snake heading towards you may be further away than it appears. Fear can skew our perception of approaching objects, causing us to underestimate the distance of a threatening one, finds a study published in Current Biology.
“Our results show that emotion and perception are not fully dissociable in the mind,” says Emory psychologist Stella Lourenco, co-author of the study. “Fear can alter even basic aspects of how we perceive the world around us. This has clear implications for understanding clinical phobias.”
Lourenco conducted the research with Matthew Longo, a psychologist at Birkbeck, University of London.
People generally have a well-developed sense for when objects heading towards them will make contact, including a split-second cushion for dodging or blocking the object, if necessary. The researchers set up an experiment to test the effect of fear on the accuracy of that skill.
New Dementia Diagnostic Exams and Gene Findings Bode Well for Treatment
The number of people affected by dementias continues to climb as baby boomers age, increasing the urgency to identify ways to prevent, diagnose and treat these neurodegenerative brain disorders.
Today it is possible to diagnose dementias more accurately than ever before, thanks to improvements in behavioral assessment tools, imaging techniques, gene testing and data collection and analysis, according to Bruce L. Miller, MD, a behavioral neurologist and professor of neurology at UCSF.
Miller, who came to UCSF in 1998 and directs the UCSF Memory and Aging Center, described recent advances during the lecture he gave at UCSF Mission Bay on Oct. 15 as part of receiving the Academic Senate’s 12th Annual Faculty Research Lectureship in Clinical Science.
The ability to diagnose different types of dementias accurately and to distinguish among the biological factors that cause them will become increasingly important as treatments become more promising and better targeted, Miller said.
Despite continued improvements in the tools available to physicians for diagnosing dementias, a common neurodegenerative disease known as frontotemporal dementia (FTD) remains understudied and is very often misdiagnosed, Miller said. For reasons that are in part historical, FTD still is thought of as a rare disease, a misconception that greatly contributes to its being underdiagnosed, he said. While Alzheimer’s disease is the most common dementia overall, among the population aged 65 and younger, FTD is just as common, according to Miller.
Biomarkers in Cerebrospinal Fluid Can Identify Patients with Alzheimer´s disease
Analysis of specific biomarkers in a cerebrospinal fluid sample can differentiate patients with Alzheimer’s disease from those with other types of dementia. The method, which is being studied by researchers at Sahlgrenska Academy, may eventually permit earlier detection of Alzheimer’s disease.
Due to the similarity of the symptoms, differentiating patients with Alzheimer’s from those with other types of dementia – or patients with Parkinson disease from those with other motor disorders – is often difficult.
Making a proper diagnosis is essential if proper treatment and medication are to commence at an early stage. A research team at Sahlgrenska Academy, University of Gothenburg, is developing a new method to differentiate patients with Alzheimer’s disease or Parkinson disease by analyzing a cerebrospinal fluid sample.
The study, led by Professor Kaj Blennow and conducted among 450 patients at Skåne University Hospital and Sahlgrenska University Hospital, involved testing five proteins that serve as biomarkers for the two diseases.
“Previous studies have shown that Alzheimer’s disease is associated with biochemical changes in specific proteins of the brain,” says Annika Öhrfelt, a researcher at Sahlgrenska Academy. “This study has found that the inclusion of a new protein can differentiate patients with Alzheimer’s disease from those with Lewy body dementia, Parkinson disease dementia and other types of dementia.”
Similarly, the biomarkers can differentiate patients with Parkinson disease from those with atypical Parkinsonian disorders.
“Additional studies are needed before the biomarkers can be used in clinical practice during the early stages of disease,” says Öhrfelt, “but these results represent an important step along the way.”
(Source: alphagalileo.org)
Clue to Alzheimer’s cause found in brain samples
Researchers at Washington University School of Medicine in St. Louis have found a key difference in the brains of people with Alzheimer’s disease and those who are cognitively normal but still have brain plaques that characterize this type of dementia.
“There is a very interesting group of people whose thinking and memory are normal, even late in life, yet their brains are full of amyloid beta plaques that appear to be identical to what’s seen in Alzheimer’s disease,” says David L. Brody, MD, PhD, associate professor of neurology. “How this can occur is a tantalizing clinical question. It makes it clear that we don’t understand exactly what causes dementia.”
Hard plaques made of a protein called amyloid beta are always present in the brain of a person diagnosed with Alzheimer’s disease, according to Brody. But the simple presence of plaques does not always result in impaired thinking and memory. In other words, the plaques are necessary – but not sufficient – to cause Alzheimer’s dementia.
The new study, available online in Annals of Neurology, still implicates amyloid beta in causing Alzheimer’s dementia, but not necessarily in the form of plaques. Instead, smaller molecules of amyloid beta dissolved in the brain fluid appear more closely correlated with whether a person develops symptoms of dementia. Called amyloid beta “oligomers,” they contain more than a single molecule of amyloid beta but not so many that they form a plaque.
Oligomers floating in brain fluid have long been suspected to have a role in Alzheimer’s disease. But they are difficult to measure. Most methods only detect their presence or absence, or very large quantities. Brody and his colleagues developed a sensitive method to count even small numbers of oligomers in brain fluid and used it to compare amounts in their samples.
The researchers examined samples of brain tissue and fluid from 33 deceased elderly subjects (ages 74 to 107). Ten subjects were normal – no plaques and no dementia. Fourteen had plaques, but no dementia. And nine had a diagnosis of Alzheimer’s disease – both plaques and dementia.
They found that cognitively normal patients with plaques and Alzheimer’s patients both had the same amount of plaque, but the Alzheimer’s patients had much higher oligomer levels.
But even oligomer levels did not completely distinguish the two groups. For example, some people with plaques but without dementia still had oligomers, even in similar quantity to some patients with Alzheimer’s disease. Where the two groups differed completely, according to Brody and his colleagues, was the ratio of oligomers to plaques. They measured more oligomers per plaque in patients with dementia, and fewer oligomers per plaque in the samples from cognitively normal people.
In people with plaques but no dementia, Brody speculates that the plaques could serve as a buffer, binding with free oligomers and keeping them tied down. And in dementia, perhaps the plaques have exceeded their capacity to capture the oligomers, leaving them free to float in the brain’s fluid, where they can damage or interfere with neurons.
Brody cautions that, due to the difficulty in getting samples, oligomer levels have never been measured in living people. Therefore, it’s possible these floating clumps of amyloid beta only form after death. Even so, he says, there is still a clear difference between the two groups.
“The plaques and oligomers appear to be in some kind of equilibrium,” Brody says. “What happens to shift the relationship between the oligomers and plaques? Like much Alzheimer’s research, this study raises more questions than it answers. But it’s an important next piece of the puzzle.”
(Source: news.wustl.edu)