Posts tagged brain

June 12, 2012

Financial loss can lead to irrational behavior. Now, research by Weizmann Institute scientists reveals that the effects of loss go even deeper: Loss can compromise our early perception and interfere with our grasp of the true situation. The findings, which recently appeared in the Journal of Neuroscience, may also have implications for our understanding of the neurological mechanisms underlying post-traumatic stress disorder.

The experiment was conducted by Dr. Rony Paz and research student Offir Laufer of the Neurobiology Department. Subjects underwent a learning process based on classic conditioning and involving money. They were asked to listen to a series of tones composed of three different notes. After hearing one note, they were told they had earned a certain sum; after a second note, they were informed that they had lost some of their money; and a third note was followed by the message that their bankroll would remain the same. According to the findings, when a note was tied to gain, or at least to no loss, the subjects improved over time in a learned task – distinguishing that note from other, similar notes. But when they heard the “lose money” note, they actually got worse at telling one from the other.

Functional MRI (fMRI) scans of the brain areas involved in the learning process revealed an emotional aspect: The amygdala, which is tied to emotions and reward, was strongly involved. The researchers also noted activity in another area in the front of the brain, which functions to moderate the emotional response. Subjects who exhibited stronger activity in this area showed less of a drop in their abilities to distinguish between tones.

Paz: “The evolutionary origins of that blurring of our ability to discriminate are positive: If the best response to the growl of a lion is to run quickly, it would be counterproductive to distinguish between different pitches of growl. Any similar sound should make us flee without thinking. Unfortunately, that same blurring mechanism can be activated today in stress-inducing situations that are not life-threatening – like losing money – and this can harm us.”

That harm may even be quite serious: For instance, it may be involved in post-traumatic stress disorder. If sufferers are unable to distinguish between a stimulus that should cause a panic response and similar, but non-threatening, stimuli, they may experience strong emotional reactions in inappropriate situations.

This perceptional blurring may even expand over time to encompass a larger range of stimuli. Paz intends to investigate this possibility in future research.

Provided by Weizmann Institute of Science

Source: medicalxpress.com

June 12, 2012

You pick up your cell phone and dial the new number of a friend. Ten numbers. One. Number. At. A. Time. Because you haven’t actually typed the number before, your brain handles each button press separately, as a sequence of distinct movements.

This image shows identified brain regions linked to the parsing (left) and concatenation (right) processes involved in motor chunking. Trials with greater parsing showed increased activation of the left prefrontal and parietal cortex and trials with greater concatenation showed increased activation of the putamen. Credit: Photo by Nicholas Wymbs

After dialing the number a few more times, you find yourself typing it out as a series of three successive bursts of movement: the area code, the first three numbers, the last four numbers. Those three separate chunks allow you to type the number faster, and with greater precision. Eventually, dialed often enough, the number is stored in your brain as one chunk. Who needs speed dial?

"You can think about a chunk as a rhythm," said Nicholas Wymbs, a postdoctoral researcher in UC Santa Barbara’s Department of Psychological and Brain Sciences, and the lead author of a new study on motor chunking in the journal Neuron, published by Cell Press. “We highlight the two-part process that seems to occur when we are chunking. This is demonstrated by the rhythm we use when typing the phone number: rapid bursts of finger movements that are interspersed by pauses.”

The rhythm is the human brain taking information and processing it in an efficient way, according to Wymbs. “On one level, the brain is going to try to divide up, or parse, long sequences of movement,” he said. “This parsing process functions to group or cluster movements in the most efficient way possible.”

But it is also in our brain’s best interest to assemble single or short strings of movements into longer, integrated sequences so that a complex behavior can be made with as little effort as possible. “The motor system in the brain wants to output movement in the most computational, low-cost way as possible,” Wymbs said. “With this integrative process, it’s going to try to bind as many individual motor movements into a fluid, uniform movement as it possibly can.”

This diagram illustrates how the subjects in the experiment used their left hands to respond to the “notes” on a button box. Credit: Illustration by Nicholas Wymbs

The two processes are at odds with each other, and it’s how the brain reconciles this struggle during motor learning that intrigues Wymbs and the study’s other authors, including Scott Grafton, professor of psychology and director of the UCSB Brain Imaging Center. “What we are interested in is functional plasticity of the brain –– how the brain changes when we learn actions, or motor sequences as we refer to them in this paper,” Wymbs said.

The study was conducted using human subjects in the Magnetic Resonance Imaging (MRI) scanner in the Brain Imaging Center. The experiment involved three days of training with people performing and practicing three separate motor sequences for up to 200 trials each during the collection of functional MRI data. The subjects were all right-handed but they were asked to learn the sequences using the four fingers of their left hands. Participants practiced the sequences during the operation of the MRI scanner by tapping out responses with a button box that looked like a set of piano keys, with long, rectangular buttons.

"People would see a static image shown on a video screen that detailed the sequence to be typed out," Wymbs said. "They’re lying down inside the scanner and they see this image above their eyes. Interestingly, some people reported that the images looked like something out of (the video game) Guitar Hero, and, indeed, it does look a bit like guitar tablature. They would have to type out the ‘notes’ from left to right, as you normally would when reading music.

"After practicing a sequence for 200 trials, they would get pretty good at it," Wymbs added. "After awhile, the note patterns become familiar. At the start of the training, it would take someone about four and a half seconds to complete each sequence of 12 button presses. By the end of the experiment, the average participant could produce the same sequence in under three seconds."

The researchers’ goal was to look at which areas of the brain support the two-part process of chunking. “We feel that the motor process, or the concatenation process as we refer to it in the paper, tends to take over as you continue to practice and continue to learn the sequences,” Wymbs said. “That’s the one that’s tied to the motor output system –– the thing that’s actually accomplishing what we set out to do.”

With the experience of repeating a motor sequence, such as typing out a phone number, speaking, typing on a computer, or even texting, it becomes more automatic. “With automaticity comes the recruitment of core motor output regions,” Wymbs said.

The scientists discovered that the putamen –– a brain region that is critically important to movement –– supports the concatenation process of motor chunking, with robust connectivity to parts of the brain that are intimately tied to the output of skilled motor behavior. On the other hand, they found that cortical regions in the left hemisphere respond more during the parsing process of motor chunking. “These regions have been linked to the manipulation of motor information, which is something that we probably do more of when we just begin to learn the sequences as chunks,” Wymbs said.

"Initially, when you’re doing one of these 12-element sequences, you want to pause,” Wymbs added. “That would evoke more of the parsing mechanism. But then, over time, as you learn a sequence so that it becomes more automatic, and the concatenation process takes over and it wants to put all of these individual elements into a single fluid behavior.”

According to Wymbs, the findings could have implications for the study and diagnosis of Parkinson’s and other diseases of the motor system that involve action. “We show here that there are two potentially competing systems that lead to the isolation of different systems that both work to allow us to process things efficiently when we’re learning,” Wymbs said.

Provided by University of California - Santa Barbara

Source: medicalxpress.com

June 11, 2012

Researchers at the Martinos Center for Biomedical Imaging at Massachusetts General Hospital have identified a portion of the brain responsible for determining how far away a sound originates, a process that does not rely solely on how loud the sound is. The investigators’ report, which will appear in the early edition of Proceeding of the National Academy of Sciences, is receiving early online release this week.

This is an image of human cerebral cortex, digitally “inflated” to smooth out normal folds and ridges, showing in red the portion of auditory cortex that responds to the distance from which sounds arrive. Credit: Jyrki Ahveninen, Ph.D., Martinos Center for Biomedical Imaging, Massachusetts General Hospital

"Although sounds get louder when the source approaches us, humans are able to discriminate between loud sounds that come from far away and softer sound from a closer source, suggesting that our brains use distance cues independent of loudness," says Jyrki Ahveninen, PhD, of the Martinos Center, senior author of the PNAS report. "Using functional MRI we found a group of neurons in the auditory cortex sensitive to the distance of sound sources and different from those that process changes in loudness. In addition to providing basic scientific information, our results could help future studies of hearing disorders.”

The human brain has distinct areas for processing sensory information – signals responsible for vision, hearing, taste etc. Studies of the visual cortex, located at the back of the brain, have produced detailed maps of areas handling particular portions of the visual field. But understanding of the auditory cortex, located on the side of the head above and behind the ear, is quite limited. While it is known that the portion of the auditory cortex extending toward the back of the head determines where a sound comes from, exactly how the brain translates complex auditory signals to determine both the location and distance from which a sound originates is not yet known.

In their search for auditory neurons that process sound distance, the research team faced some particular challenges. In research laboratories that study hearing, sounds must be delivered to study participants through headphones, which means the acoustical “space” in which a sound is generated must be simulated. This must be done with exquisite accuracy, since environmental aspects causing sound to reverberate probably contribute to distance perception. Since the MRI equipment itself generates a loud noise, the researchers scanned participants’ brains once every 12 seconds to measure responses to sounds presented during intervening quiet periods.

In the first experiment, study participants – 12 adults with normal hearing – listened to a series of paired sounds of varying degrees of loudness and at simulated distances ranging from 15 to 100 cm and were asked to indicate whether the second sound was closer or farther away than the first. Although the differences in loudness varied randomly, participants were quite accurate in distinguishing the simulated distances of the sounds. Acoustical analysis of the particular sound cues presented indicated that the reverberations produced by a sound, which are more pronounced in a closed environment and for sounds traveling farther, may be more important distance cues than are the differences between sounds perceived by a participant’s two ears.

After the first experiment confirmed the accuracy of the simulated acoustical environment, functional MR images taken while participants listened to another series of paired sounds recorded how activity in the auditory cortex changed in response to sounds of varying loudness and direction as well as during sound of constant levels and silence. The images produced identified a small area that appears to be sensitive to cues indicating distance but not loudness. As far as the investigators know, this is the first time neurons sensitive to sound-source distances have been discovered.

"The identified area is located near other auditory cortical areas that process spatial information," says corresponding author Norbert Kopco, PhD. "This is consistent with a general model of perceptual processing in the brain, suggesting that in hearing, as in vision and other senses, spatial information is processed separately from information about the object’s identity or characteristics such as the musical pitch of sound. Our study also illustrates how important it is to combine expertise from different fields – in our case imaging/physiology, psychology, and computational neuroscience – to advance our understanding of such a complex system as the human brain.”

Provided by Massachusetts General Hospital

Source: medicalxpress.com

ScienceDaily (June 11, 2012) — In a pair of related studies, scientists from the Florida campus of The Scripps Research Institute have identified several proteins that help regulate cells’ response to light — and the development of night blindness, a rare disease that abolishes the ability to see in dim light.

In the new studies, published recently in the journals Proceedings of the National Academy of Sciences (PNAS) and The Journal of Cell Biology, Scripps Florida scientists were able to show that a family of proteins known as Regulator of G protein Signaling (RGS) proteins plays an essential role in vision in a dim-light environment.

"We were looking at the fundamental mechanisms that shape our light sensation," said Kirill Martemyanov, a Scripps Research associate professor who led the studies. "In the process, we discovered a pair of molecules that are indispensible for our vision and possibly play critical roles in the brain."

In the PNAS study, Martemyanov and his colleagues identified a pair of regulator proteins known as RGS7 and RGS11 that are present specifically in the main relay neurons of the retina called the ON-bipolar cells. “The ON-bipolar cells provide an essential link between the retinal light detectors — photoreceptors and the neurons that send visual information to the brain,” explained Martemyanov. “Stimulation with light excites these neurons by opening the channel that is normally kept shut by the G proteins in the dark. RGS7 and RGS11 facilitate the G protein inactivation, thus promoting the opening of the channel and allowing the ON-bipolar cells to transmit the light signal. It really takes a combined effort of two RGS proteins to help the light overcome the barrier for propagating the excitation that makes our dim vision possible.”

In the Journal of Cell Biology study, Martemyanov and his colleagues unraveled another key aspect of the RGS7/RGS11 regulatory response — they identified a previously unknown pair of orphan G protein-coupled receptors (GPCRs) that interact with these RGS proteins and dictate their biological function.

GPCRs are a large family of more than 700 proteins, which sit in the cell membrane and sense various molecules outside the cell, including odors, hormones, neurotransmitters, and light. After binding these molecules, GPCRs trigger the appropriate response inside the cell. However, for many GPCRs the activating molecules have not yet been identified and these are called “orphan” receptors.

The Martemyanov group has found that two orphan GPCRs — GPR158 and GPR179 — recruit RGS proteins and thus help serve as brakes for the conventional GPCR signaling rather than play an active signaling role.

In the case of retinal ON-bipolar cells, GPR179 is required for the correct localization of RGS7 and RGS11. Their mistargeting in animal models lacking GPR179 or human patients with mutations in the GPR179 gene may account for their night blindness, according to the new study. Intriguingly, in the brain GPR158 appears to play a similar role in localizing RGS proteins, but instead of contributing to vision, it helps RGS proteins regulate the m-opioid receptor, a GPCRs that mediates pleasurable and pain-killing effects of opioids.

"We are really in the very beginning of unraveling this new biology and understanding the role of discovered orphan GPR158/179 in regulation of neurotransmitter signaling in the brain and retina," Martemyanov said. "The hope is that better understanding of these new molecules will lead to the design of better treatments for addictive disorders, pain, and blindness."

Source: Science Daily

ScienceDaily (June 11, 2012) — Researchers at the University of Missouri have demonstrated the effectiveness of a potential new therapy for stroke patients in an article published in the journal Molecular Neurodegeneration. Created to target a specific enzyme known to affect important brain functions, the new compound being studied at MU is designed to stop the spread of brain bleeds and protect brain cells from further damage in the crucial hours after a stroke.

In a model of induced stroke in mice, MU researchers have shown the success of a treatment in stopping further bleeding in the brain after a stroke (above). The outlined area shows the stroke damage. (Credit: Image courtesy of University of Missouri School of Medicine)

Stroke is a leading cause of death in the U.S. with more than 800,000 deaths occurring each year from stroke and other cardiac events. Other than surgery, existing emergency treatments for stroke victims such as the use of a tissue plasminogen activator (tPA) must be administered within hours of the stroke onset because of the risk for brain hemorrhaging. The injectable medication can only be used to treat the most common type of stroke that occurs when blood clots block blood flow to the brain, called ischemic stroke.

"For a stroke victim, time is a matter of life and death. While we are still in the research phase for this type of compound, we believe it could be combined with tPA in the future to buy ischemic stroke patients a longer window of time to receive emergency treatment," said Zezong Gu, MD, PhD, the article’s corresponding author and assistant professor of pathology and anatomical sciences at the MU School of Medicine. The new compound being studied also has potential for use in patients experiencing hemorrhagic stroke, which is a less common type of stroke caused by bleeding within the brain, Gu said.

MU researchers collaborated with a team at the University of Notre Dame to study the effects of the new compound, a thiirane class of gelatinase selective inhibitors, on the function of a type of matrix metalloproteinase (MMP) enzyme, particularly MMP-9. MMP-9 is part of a group of more than 20 enzymes or MMPs that are known to contribute to many key pathological events in the brain after stroke, traumatic brain injury and other neurodegenerative events.

In 2005, Gu served as a lead author on a research paper published in the Journal of Neuroscience that identified MMP-9 as a promising target for development of therapeutic drugs for stroke patients. Since then, his lab at MU medical school’s Center for Translational Neuroscience has been studying the function of MMP enzymes and how to inhibit the harmful effects of MMP-9.

"MMPs play a role in the structure of blood vessels in the brain and are also needed in the interactions between cells during development and tissue remodeling," Gu said. "Unregulated, the activity of these enzymes contributes to neurological disorders and stroke. With this compound, we’ve now confirmed a potential method to rescue the blood vessels from the damaging effects of MMP-9 and protect neurons at the same time."

MU researchers successfully used a model of ischemic stroke in mice and studied the effects of the MMP-9 inhibitor compound on brain activity after a stroke.

"Our lab at the Center for Translational Neuroscience is one of only a few in the United States that has successfully induced a blood clot in the brains of mice," said Jiankun Cui, MD, the article’s lead author and assistant professor of pathology and anatomical sciences at the MU School of Medicine. "To be able to study the effectiveness of this potential new treatment under these conditions provides us with a highly unique set of data showing this compound can disrupt key harmful pathological events that occur after a stroke."

Source: Science Daily

ScienceDaily (June 11, 2012) — Out of control competitive aggression could be a result of a lagging neurotransmitter called dopamine, say researchers presenting a study at the Society of Nuclear Medicine’s 2012 Annual Meeting. During a computer game against a putative cheating adversary, participants who had a lower capacity to synthesize this neurotransmitter in the brain were more distracted from their basic motivation to earn money and were more likely to act out with aggression.

Out of control competitive aggression could be a result of a lagging neurotransmitter called dopamine, say researchers. During a computer game against a putative cheating adversary, participants who had a lower capacity to synthesize this neurotransmitter in the brain were more distracted from their basic motivation to earn money and were more likely to act out with aggression. (Credit: © lassedesignen / Fotolia)

For many people, anger is an almost automatic response to life’s challenges. In clinical psychiatry, scientists look at not only the impact of aggressive behavior on the individual, their loved ones and the community but also the triggers in the brain that lead to aggressive response. The neurobiology of aggression is not well understood, but scientists are aware of a relationship between the neurotransmitter serotonin and certain aggressive behaviors. The objective of this study was to explore whether higher levels of another brain chemical called dopamine, involved in pleasure and reward, increased aggressive response in its subjects. To scientists’ surprise, it was not as they first theorized.

"The results of this study were astonishingly opposite of what was previously hypothesized," says Ingo Vernaleken, M.D., lead author of the study and research scientist for the department of psychiatry at RWTH Aachen University in Aachen, Germany. "Subjects with more functional dopaminergic reward-systems were not more aggressive in competitive situations and could concentrate even more on the game. Subjects with lower dopaminergic capacity were more likely to be distracted by the cheating behavior."

In this study, 18 healthy adults in their twenties were tested for aggression using the psychological behavioral task known as the point subtraction aggression paradigm (PSAP). Participants were asked to play a computer game that required them to press a bar multiple times with the incentive of winning money, but they were also told that an adversary in the next room who is able to cheat may steal some of their winnings. What the paranoid participants did not know was that there was no adversary. The computer program is designed to perform randomized deductions of the subjects’ monetary reward to simulate the cheating competitor.The participant had three choices to react: punish the cheater, shield against the adversary by repeatedly pressing a defense button, or continue playing the game in order to maximize their ability to win cash, which indicated resilience.

"The PSAP focuses on aggressive reaction within a competitive situation," says Vernaleken. "Aggression and its neurobiological mechanisms in humans have been only moderately investigated in the past. Furthermore, most of the previous studies mainly covered the more reactive part of aggression, which merely reflects impulsive behavior and appears to be associated merely with the serotonin system. This investigation focuses on the association with the dopaminergic reward-system, which reflects goal-directed aggression."

Subjects’ brains were imaged using positron emission tomography, which provides a range of information about physiological functions inside the body, depending on the imaging probe used. In this investigation, F-18 FDOPA, a biomarker that lights up enzymes’ ability to synthesize this transmitter, was used and the uptake of this drug in the brain was analyzed to gauge the correlation between the participants’ dopamine synthesis capacity and aggressive behavior.

Results of the study showed a significant impact on aggressive response in areas in the brain where dopamine synthesis was present, especially in the basal ganglia, which among other functions include the motivation center. Minimized aggression was associated with higher dopamine levels in both the midbrain and the striatum, which plays a role in planning and executive function. People with greater capacity for dopamine synthesis were more invested in the monetary reward aspect of the PSAP, instead of acting in defense or with aggression against their perceived adversary, whereas subjects with lower capacities had a higher vulnerability to act either aggressive, defensive or both.

"Thus, we think that a well-functioning reward system causes more resilience against provocation," says Vernaleken. "However, we cannot exclude that in a situation where the subject would directly profit from aggressive behavior, in absence of alternatives, the correlation might be the other way around."

Further research is required to explore the link between dopamine and a range of aggressive behavior. More insight into these relationships could potentially lead to new psychological therapies and drug treatments to moderate or prevent aggressive response.

Source: Science Daily

ScienceDaily (June 11, 2012) — An arsenal of Alzheimer’s research revealed at the Society of Nuclear Medicine’s 59th Annual Meeting indicates that beta-amyloid plaque in the brain not only is involved in the pathology of Alzheimer’s disease but may also precede even mild cognitive decline. These and other studies advance molecular imaging for the early detection of beta-amyloid, for which one product is now approved in the United States , as a major push forward in the race for better treatments.

"Diagnosis of Alzheimer’s disease can now be made when the patient first presents symptoms and still has largely preserved mental function," says Christopher Rowe, M.D., a lead investigator for the Australian Imaging, Biomarkers and Lifestyle study of aging (AIBL) and professor of nuclear medicine at Austin Hospital in Melbourne, Australia. "Previously there was an average delay of three years between consulting a doctor over memory concerns and the diagnosis of Alzheimer’s, as the diagnosis required the presence of dementia. When used as an adjunct to other diagnostic measures, molecular imaging can help lead to earlier diagnosis. This may give the patient several years to prepare for dementia while they still have control over their destiny."

According to the World Health Organization, Alzheimer’s disease affects an estimated 18 million people worldwide, and incidence of the disease is expected to double by the year 2025 to 34 million. The National Institute on Aging estimates that as many as 50 percent of Americans aged 85 or older are affected.

Alzheimer’s disease is a chronic and currently incurable neurodegenerative disease. Beta-amyloid burden can begin to build in the brain several years, if not more than a decade, before an individual shows any sign of dementia. Those who go on to develop Alzheimer’s disease not only lose their ability to remember their loved ones but also have difficulty with essential bodily functions such as breathing and swallowing in the late stages of disease.

In one study, researchers used a molecular imaging technique called positron emission tomography (PET), which images physiological patterns in the body. PET was combined with an imaging agent called F-18 florbetaben, which binds to amyloid in the brain. This and other PET agents are drawn to targets in the body and emit a positron signal that is picked up by a scanner. Here molecular imaging was performed in conjunction with clinical and neuropsychological testing in order to better understand the long-term effects of beta amyloid plaques in the brains of older individuals with mild cognitive impairment. Those of the 45 subjects in the study who showed high levels of imaging agent binding during imaging and atrophy of the hippocampus, the memory center, had an 80 percent chance of developing Alzheimer’s disease within two years, researchers said.

"Molecular imaging is proving to be an essential part of Alzheimer’s disease detection," says Rowe. "This and other amyloid imaging techniques will have an increasing role in the earlier and more accurate diagnosis of neurodegenerative conditions such as Alzheimer’s disease due to their ability to measure the actual underlying disease process."

Another AIBL study included 194 healthy participants, 92 people with mild cognitive impairment and 70 subjects with Alzheimer’s disease, and used another imaging agent called C-11 PiB (Pittsburgh compound B) with PET to gauge amyloid burden in the brain. Researchers showed that, in this study group, widespread amyloid plaque build-up preceded cognitive impairment, and those with extensive amyloid burden were at higher risk of cognitive decline.

This and another study mark two of the first studies of their kind focusing on beta amyloid in healthy subjects. In the other study, 137 adults with normal cognitive function aged 30 to 89 years were imaged using PET with F-18 florbetapir, now FDA-approved for the detection of beta amyloid plaques, as well as functional magnetic resonance imaging in order to explore how amyloid build-up affects connections in specific areas of the brain involved in cognition, namely the default mode and salience networks, which are responsible for different states of wakeful rest and alertness. Those with increased amyloid burden in these neural networks were prone to impaired cognitive performance.

"The effect of beta amyloid in healthy aging is of great interest since this protein is strongly associated with Alzheimer’s disease and may be predictive of the transition from mild cognitive impairment to Alzheimer’s disease," says Michael Devous, Sr., Ph.D., director of neuroimaging at the Alzheimer’s Disease Center at UT Southwestern Medical Center in Dallas, Texas. "Less is known about its impact on cognition in otherwise healthy aging individuals. In addition, brain connectivity in these areas is thought to be sensitive to early changes in brain function caused both by aging itself and by disease processes such as Alzheimer’s disease."

Another study assessed the PET imaging agent C-11 PiB for its ability to detect amyloid plaque in comparison to another imaging agent, 18-F fluorodeoxyglucose (F-18 FDG). The latter acts like glucose, the brain’s primary energy source, to map out the metabolic functioning of the brain. Results of the study showed C-11 PiB amyloid imaging to be a better means of evaluating amyloid patterns in the brain than F-18 FDG imaging. In addition, of the 100 healthy participants, 15 percent were shown to have some amyloid build-up when molecular imaging was performed.

"We are using state-of-the-art, noninvasive PET and MRI technologies to look at some of the earliest developments of Alzheimer’s disease onset in the brains of normal middle-aged people," says Guofan Xu, M.D., Ph.D., lead author of the study and research scientist at the department of nuclear medicine and radiology at the University of Wisconsin located in Madison. "With this we can evaluate whether pathological changes associated with Alzheimer’s disease are happening many years before onset of significant clinical symptoms."

No treatments are currently available to cure or prevent Alzheimer’s disease. With advances in molecular imaging to detect beta amyloid plaques, researchers have an important new tool that may bring the medical community one step closer to making therapies and vaccines a reality for the disease.

Source: Science Daily

June 11, 2012

Scientists studying the Chinese mindfulness meditation known as integrative body-mind training (IBMT) say they’ve confirmed and expanded their findings on changes in structural efficiency of white matter in the brain that can be related to positive behavioral changes in subjects practicing the technique regularly for a month.

In a paper appearing this week in the online Early Edition of the Proceedings of the National Academy of Sciences, scientists Yi-Yuan Tang and Michael Posner report improved mood changes coincided with increased axonal density — more brain-signaling connections — and an expansion of myelin, the protective fatty tissue that surrounds the axons, in the brain’s anterior cingulate region.

Deficits in activation of the anterior cingulate cortex have been associated with attention deficit disorder, dementia, depression, schizophrenia and many other disorders.

IBMT was adapted from traditional Chinese medicine in the 1990s in China, where it is practiced by thousands of people. It differs from other forms of meditation because it depends heavily on the inducement of a high degree of awareness and balance of the body, mind and environment. The meditative state is facilitated through training and trainer-group dynamics, harmony and resonance.

In 2010, research led by Tang, a visiting research professor at the University of Oregon, and Michael I. Posner, professor of psychology at the UO, first reported positive structural changes in brain connectivity, based on functional magnetic resonance imaging, that correlated to behavioral regulation. The study was done in the UO’s Robert and Beverly Lewis Center for Neuroimaging with 45 participating UO undergraduate students.

The new findings came from additional scrutiny of the 2010 study and another that involved 68 undergraduate students at China’s Dalian University of Technology. The researchers revisited data obtained from using an MRI technique known as diffusion tensor imaging. The research team found improved density of the axons involved in brain connections but no change in myelin formation after two weeks. After a month, or about 11 hours of IBMT, both increases in axon density and myelin formation were found as measured by fractional anisotropy, axial diffusivity and radial diffusivity — the important indexes for measuring the integrity of white matter fibers.

"This dynamic pattern of white matter change involving the anterior cingulate cortex, a part of the brain network related to self-regulation, could provide a means for intervention to improve or prevent mental disorders," the authors concluded.

"When we got the results, we all got very excited because all of the other training exercises, like working-memory training or computer-based training, only have been shown to change myelination," Tang said. "We believe these changes may be reflective of the time of training involved in IBMT. We found a different pattern of neural plasticity induced by the training."

"This study gives us a much more detailed picture of what it is that is actually changing," Posner said. "We did confirm the exact locations of the white-matter changes that we had found previously. And now we show that both myelination and axon density are improving. The order of changes we found may be similar to changes found during brain development in early childhood, allowing a new way to reveal how such changes might influence emotional and cognitive development.”

The improved mood changes noted in this and earlier studies are based on self-ratings of subjects based on a standard six-dimensional mood-state measure, said Tang, who is now the director of Texas Tech University’s Neuroimaging Institute and holder of the Presidential Endowed Chair in Neuroscience in TTU’s psychology department.

Tang and Posner first reported findings related to IBMT in 2007, also in PNAS. They found that doing IBMT for five days prior to a mental math test led to low levels of the stress hormone cortisol among Chinese students. The experimental group also showed lower levels of anxiety, depression, anger and fatigue than students in a relaxation control group.

In 2009 in PNAS, Tang and his Chinese colleagues, with assistance from Posner and UO psychology professor Mary K. Rothbart, found that IBMT subjects in China had increased blood flow in the right anterior cingulate cortex after receiving training for 20 minutes a day over five days. Compared with the relaxation group, IBMT subjects also had lower heart rates and skin conductance responses, increased belly breathing amplitude and decreased chest respiration rates.

"These new findings provide fundamental new insights on how the brain responds in positive ways to new inputs and reflect the excellence in cognitive neuroscience research that has defined Michael Posner’s work at the University of Oregon," said Kimberly Andrews Espy, vice president for research and innovation. "The research by professors Posner and Tang also reflects the university’s long-running commitment to collaborate with institutions in Pacific Rim countries."

Provided by University of Oregon

Source: medicalxpress.com

June 11, 2012

A new study shows that changes in walking speed in late life may signal the early stages of dementia known as mild cognitive impairment (MCI). The research is published in the June 12, 2012, print issue of Neurology, the medical journal of the American Academy of Neurology.

"In our study, we used a new technique that included installing infrared sensors in the ceilings of homes, a system designed to detect walking movement in hallways,” said study author Hiroko Dodge, PhD, with Oregon Health and Science University in Portland and a member of the American Academy of Neurology. “By using this new monitoring method, we were able to get a better idea of how even subtle changes in walking speed may correlate with the development of MCI.”

The study involved 93 people age 70 or older who lived alone. Of those, 54 participants had no cognitive impairment, 31 had non-memory related MCI and eight had memory-related MCI. Participants were given memory and thinking tests and had their walking speed monitored at their homes unobtrusively over a three-year period. Participants were placed in groups of slow, moderate or fast based on their average weekly walking speed and how much their walking speed fluctuated at home.

The study found that people with non-memory related MCI were nine times more likely to be slow walkers than moderate or fast walkers and the amount of the fluctuation in walking speed was also associated with MCI.

"Further studies need to be done using larger groups of participants to determine whether walking speed and its fluctuations could be a predictor of future memory and thinking problems in the elderly,” said Dodge. “If we can detect dementia at its earliest phases, then we can work to maintain people’s independence, provide treatments and ultimately develop ways to prevent the disease from developing. Our in-home monitoring approach has a lot of potential to be used for sustaining independence of the elderly.”

Provided by American Academy of Neurology

Source: medicalxpress.com

ScienceDaily (June 11, 2012) — According to the Anxiety and Depression Association of America, one in eight children suffers from an anxiety disorder. And because many anxious children turn into severely anxious adults, early intervention can have a major impact on a patient’s life trajectory. The understandable reluctance to use psychiatric medications when it comes to children means child psychologists are always searching for viable therapeutic alternatives.

Now Prof. Yair Bar-Haim of Tel Aviv University’s School of Psychological Sciences and his fellow researchers are pursuing a new method to address childhood anxiety. Based on a computer program, the treatment uses a technique called Attention Bias Modification (ABM) to reduce anxiety by drawing children away from their tendency to dwell on potential threats, ultimately changing their thought patterns. In its initial clinical trial, the program was as effective as medication and cognitive therapy for children — with several distinct advantages.

The results of the trial were reported in the American Journal of Psychiatry.

Computers instead of capsules

Children are comfortable with computers, explains Prof. Bar-Haim. And because of the potential side effects of medications or the difficulty in obtaining cognitive behavioral therapy, such as the need for highly trained professionals, it is good to have an alternative treatment method. ABM treatments can be disseminated over the Internet or administered by personnel who don’t have to be Ph.D.s. “This could be a game-changer for providing treatment,” he says.

Anxious individuals have a heightened sensitivity towards threats that the average person would ignore, a sensitivity which creates and maintains anxiety, says Prof. Bar-Haim. One of the ways to measure a patient’s threat-related attention patterns is called the dot-probe test. The patient is presented with two pictures or words, one threatening and one neutral. These words then disappear and a dot appears where one of the pictures or words had been, and the patient is asked to press a button to indicate the dot’s location. A fast response time to a dot that appears in the place of the threatening picture or word indicates a bias towards threat.

To turn this test into a therapy, the location of the dot target is manipulated to appear more frequently beneath the neutral word or picture. Gradually, the patient begins to focus on that stimulus instead, predicting that this is where the dot will appear — helping to normalize the attention bias pattern and reduce anxiety.

Prof. Bar-Haim and his colleagues enlisted the participation of 40 pediatric patients with ongoing anxiety disorders and divided them into three groups. The first received the new ABM treatment; the second served as a placebo group where the dot appeared equally behind threatening and neutral images; and the third group was shown only neutral stimuli. Patients participated in one session a week for four weeks, completing 480 dot probe trials each session.

The children’s anxiety levels were measured before and after the training sessions using interviews and questionnaires. In both the placebo group and neutral images group, researchers found no significant change in the patients’ bias towards threatening stimuli. However, in the ABM group, there were marked differences in the participants’ threat bias. By the end of the trial, approximately 33 percent of the patients in this group no longer met the diagnostic criteria for anxiety disorder.

New methods for personalized treatment

These indications of the method’s success in treating children warrant further investigation, says Prof. Bar-Haim. In collaboration with the National Institute of Mental Health in the US, a large international trial involving his computer program is now being carried out at more than 20 sites across five continents.

The more options that exist for patients, the better that clinicians can tailor treatment for their patient’s individual needs, Prof. Bar-Haim observes. There are always patients for whom medication or cognitive therapy is not a viable option, he explains. “Psychological disorders are complex, and not every patient will respond well to every treatment. It’s great to have new methods that have a basis in neuroscience and clinical evidence.”

Source: Science Daily