Neuroscience

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Obama Seeking to Boost Study of Human Brain
The Obama administration is planning a decade-long scientific effort to examine the workings of the human brain and build a comprehensive map of its activity, seeking to do for the brain what the Human Genome Project did for genetics.
The project, which the administration has been looking to unveil as early as March, will include federal agencies, private foundations and teams of neuroscientists and nanoscientists in a concerted effort to advance the knowledge of the brain’s billions of neurons and gain greater insights into perception, actions and, ultimately, consciousness.
Scientists with the highest hopes for the project also see it as a way to develop the technology essential to understanding diseases like Alzheimer’s and Parkinson’s, as well as to find new therapies for a variety of mental illnesses.
Moreover, the project holds the potential of paving the way for advances in artificial intelligence.
The project, which could ultimately cost billions of dollars, is expected to be part of the president’s budget proposal next month. And, four scientists and representatives of research institutions said they had participated in planning for what is being called the Brain Activity Map project.
The details are not final, and it is not clear how much federal money would be proposed or approved for the project in a time of fiscal constraint or how far the research would be able to get without significant federal financing.
In his State of the Union address, President Obama cited brain research as an example of how the government should “invest in the best ideas.”
“Every dollar we invested to map the human genome returned $140 to our economy — every dollar,” he said. “Today our scientists are mapping the human brain to unlock the answers to Alzheimer’s. They’re developing drugs to regenerate damaged organs, devising new materials to make batteries 10 times more powerful. Now is not the time to gut these job-creating investments in science and innovation.”
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Obama Seeking to Boost Study of Human Brain

The Obama administration is planning a decade-long scientific effort to examine the workings of the human brain and build a comprehensive map of its activity, seeking to do for the brain what the Human Genome Project did for genetics.

The project, which the administration has been looking to unveil as early as March, will include federal agencies, private foundations and teams of neuroscientists and nanoscientists in a concerted effort to advance the knowledge of the brain’s billions of neurons and gain greater insights into perception, actions and, ultimately, consciousness.

Scientists with the highest hopes for the project also see it as a way to develop the technology essential to understanding diseases like Alzheimer’s and Parkinson’s, as well as to find new therapies for a variety of mental illnesses.

Moreover, the project holds the potential of paving the way for advances in artificial intelligence.

The project, which could ultimately cost billions of dollars, is expected to be part of the president’s budget proposal next month. And, four scientists and representatives of research institutions said they had participated in planning for what is being called the Brain Activity Map project.

The details are not final, and it is not clear how much federal money would be proposed or approved for the project in a time of fiscal constraint or how far the research would be able to get without significant federal financing.

In his State of the Union address, President Obama cited brain research as an example of how the government should “invest in the best ideas.”

“Every dollar we invested to map the human genome returned $140 to our economy — every dollar,” he said. “Today our scientists are mapping the human brain to unlock the answers to Alzheimer’s. They’re developing drugs to regenerate damaged organs, devising new materials to make batteries 10 times more powerful. Now is not the time to gut these job-creating investments in science and innovation.”

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Filed under brain neurodegenerative diseases mental illnesses Brain Activity Map project neuroscience science

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A sensational breakthrough: the first bionic hand that can feel
The first bionic hand that allows an amputee to feel what they are touching will be transplanted later this year in a pioneering operation that could introduce a new generation of artificial limbs with sensory perception.
The patient is an unnamed man in his 20s living in Rome who lost the lower part of his arm following an accident, said Silvestro Micera of the Ecole Polytechnique Federale de Lausanne in Switzerland.
The wiring of his new bionic hand will be connected to the patient’s nervous system with the hope that the man will be able to control the movements of the hand as well as receiving touch signals from the hand’s skin sensors.
Dr Micera said that the hand will be attached directly to the patient’s nervous system via electrodes clipped onto two of the arm’s main nerves, the median and the ulnar nerves.
This should allow the man to control the hand by his thoughts, as well as receiving sensory signals to his brain from the hand’s sensors. It will effectively provide a fast, bidirectional flow of information between the man’s nervous system and the prosthetic hand.
“This is real progress, real hope for amputees. It will be the first prosthetic that will provide real-time sensory feedback for grasping,” Dr Micera said.
“It is clear that the more sensory feeling an amputee has, the more likely you will get full acceptance of that limb,” he told the American Association for the Advancement of Science meeting in Boston.
“We could be on the cusp of providing new and more effective clinical solutions to amputees in the next year,” he said.

A sensational breakthrough: the first bionic hand that can feel

The first bionic hand that allows an amputee to feel what they are touching will be transplanted later this year in a pioneering operation that could introduce a new generation of artificial limbs with sensory perception.

The patient is an unnamed man in his 20s living in Rome who lost the lower part of his arm following an accident, said Silvestro Micera of the Ecole Polytechnique Federale de Lausanne in Switzerland.

The wiring of his new bionic hand will be connected to the patient’s nervous system with the hope that the man will be able to control the movements of the hand as well as receiving touch signals from the hand’s skin sensors.

Dr Micera said that the hand will be attached directly to the patient’s nervous system via electrodes clipped onto two of the arm’s main nerves, the median and the ulnar nerves.

This should allow the man to control the hand by his thoughts, as well as receiving sensory signals to his brain from the hand’s sensors. It will effectively provide a fast, bidirectional flow of information between the man’s nervous system and the prosthetic hand.

“This is real progress, real hope for amputees. It will be the first prosthetic that will provide real-time sensory feedback for grasping,” Dr Micera said.

“It is clear that the more sensory feeling an amputee has, the more likely you will get full acceptance of that limb,” he told the American Association for the Advancement of Science meeting in Boston.

“We could be on the cusp of providing new and more effective clinical solutions to amputees in the next year,” he said.

Filed under bionic hand prosthetics robotics artificial limbs neuroscience science

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Nano-machines for “Bionic Proteins”
Physicists of the University of Vienna together with researchers from the University of Natural Resources and Life Sciences Vienna developed nano-machines which recreate principal activities of proteins. They present the first versatile and modular example of a fully artificial protein-mimetic model system, thanks to the Vienna Scientific Cluster (VSC), a high performance computing infrastructure. These “bionic proteins” could play an important role in innovating pharmaceutical research. The results have now been published in the renowned journal “Physical Review Letters”.
Proteins are the fundamental building blocks of all living organism we currently know. Because of the large number and complexity of bio-molecular processes they are capable of, proteins are often referred to as “molecular machines”. Take for instance the proteins in your muscles: At each contraction stimulated by the brain, an uncountable number of proteins change their structures to create the collective motion of the contraction. This extraordinary process is performed by molecules which have a size of only about a nanometer, a billionth of a meter. Muscle contraction is just one of the numerous activities of proteins: There are proteins that transport cargo in the cells, proteins that construct other proteins, there are even cages in which proteins that “mis-behave” can be trapped for correction, and the list goes on and on. “Imitating these astonishing bio-mechanical properties of proteins and transferring them to a fully artificial system is our long term objective”, says Ivan Coluzza from the Faculty of Physics of the University of Vienna, who works on this project together with colleagues of the University of Natural Resources and Life Sciences Vienna.
Simulations thanks to Vienna Scientific Cluster (VSC)In a recent paper in Physical Review Letters, the team presented the first example of a fully artificial bio-mimetic model system capable of spontaneously self-knotting into a target structure. Using computer simulations, they reverse engineered proteins by focusing on the key elements that give them the ability to execute the program written in the genetic code. The computationally very intensive simulations have been made possible by access to the powerful Vienna Scientific Cluster (VSC), a high performance computing infrastructure operated jointly by the University of Vienna, the Vienna University of Technology and the University of Natural Resources and Life Sciences Vienna.Artificial proteins in the laboratoryThe team now works on realizing such artificial proteins in the laboratory using specially functionalized nanoparticles. The particles will then be connected into chains following the sequence determined by the computer simulations, such that the artificial proteins fold into the desired shapes. Such knotted nanostructures could be used as new stable drug delivery vehicles and as enzyme-like, but more stable, catalysts.

Nano-machines for “Bionic Proteins”

Physicists of the University of Vienna together with researchers from the University of Natural Resources and Life Sciences Vienna developed nano-machines which recreate principal activities of proteins. They present the first versatile and modular example of a fully artificial protein-mimetic model system, thanks to the Vienna Scientific Cluster (VSC), a high performance computing infrastructure. These “bionic proteins” could play an important role in innovating pharmaceutical research. The results have now been published in the renowned journal “Physical Review Letters”.

Proteins are the fundamental building blocks of all living organism we currently know. Because of the large number and complexity of bio-molecular processes they are capable of, proteins are often referred to as “molecular machines”. Take for instance the proteins in your muscles: At each contraction stimulated by the brain, an uncountable number of proteins change their structures to create the collective motion of the contraction. This extraordinary process is performed by molecules which have a size of only about a nanometer, a billionth of a meter. Muscle contraction is just one of the numerous activities of proteins: There are proteins that transport cargo in the cells, proteins that construct other proteins, there are even cages in which proteins that “mis-behave” can be trapped for correction, and the list goes on and on. “Imitating these astonishing bio-mechanical properties of proteins and transferring them to a fully artificial system is our long term objective”, says Ivan Coluzza from the Faculty of Physics of the University of Vienna, who works on this project together with colleagues of the University of Natural Resources and Life Sciences Vienna.

Simulations thanks to Vienna Scientific Cluster (VSC)
In a recent paper in Physical Review Letters, the team presented the first example of a fully artificial bio-mimetic model system capable of spontaneously self-knotting into a target structure. Using computer simulations, they reverse engineered proteins by focusing on the key elements that give them the ability to execute the program written in the genetic code. The computationally very intensive simulations have been made possible by access to the powerful Vienna Scientific Cluster (VSC), a high performance computing infrastructure operated jointly by the University of Vienna, the Vienna University of Technology and the University of Natural Resources and Life Sciences Vienna.

Artificial proteins in the laboratory
The team now works on realizing such artificial proteins in the laboratory using specially functionalized nanoparticles. The particles will then be connected into chains following the sequence determined by the computer simulations, such that the artificial proteins fold into the desired shapes. Such knotted nanostructures could be used as new stable drug delivery vehicles and as enzyme-like, but more stable, catalysts.

Filed under artificial proteins AI bionics robotics technology neuroscience science

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Blind brain receives “visual” cues for identifying object shape

A significant number of blind humans, not unlike bats and dolphins, can localize silent objects in their environment simply by making clicking sounds with their mouth and listening to the returning echoes. Some of these individuals have honed this skill to such a degree that they are not only able to localize an object, they are able to recognize the object’s size and shape – and even identify the material it is made from.

Researchers at Western University’s Brain and Mind Institute (BMI) used functional magnetic resonance imaging (fMRI) to study the brain of renowned blind echolocator Daniel Kish as he listened to recordings of his own mouth clicks and the echoes reflected back from different objects.

The results of this study, which was carried out in collaboration with colleagues based in Durham University in the U.K., the Rotman Research Institute at the Baycrest Hospital in Toronto, and World Access for the Blind, a not-for-profit organization based in California, appeared this week in the journal Neuropsychologia. In keeping with the previous research from this group, the researchers found that areas in Kish’s brain that were activated by the echoes corresponded to visual areas in the sighted brain.

But what has senior author and BMI Director Mel Goodale most excited about the new findings is that the particular areas in Kish’s brain that extract echo-based information about object shape are located in exactly the same brain regions that are activated by visual shape cues in the sighted brain.

"This work is shedding new light on just how plastic the human brain really is," says Goodale.

Lead author Stephen Arnott of Baycrest’s Rotman Research Institute explains, “This study implies that the processing of echoes for object shape in the blind brain can take advantage of the brain’s predisposition to process particular object features, such as shape, in particular brain regions – even though the sensory system conveying that information is very different.”

Kish lost both his eyes to cancer when he was only one-year old and taught himself to echolocate when he was a toddler. Interestingly, two other blind individuals who learned to echolocate much later in life do not show nearly the same level of brain activation in these ‘visual’ object areas as Kish.

(Source: communications.uwo.ca)

Filed under brain object localization object features blind humans neuroscience science

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Can Boosting Immunity Make You Smarter?
After spending a few days in bed with the flu, you may have felt a bit stupid. It is a common sensation, that your sickness is slowing down your brain. At first blush, though, it doesn’t make much sense. For one thing, flu viruses infect the lining of the airways, not the neurons in our brains. For another, the brain is walled off from the rest of the body by a series of microscopic defenses collectively known as the blood-brain barrier. It blocks most viruses and bacteria while allowing essential molecules like glucose to slip through. What ails the body, in other words, shouldn’t interfere with our thinking.
But over the past decade, Jonathan Kipnis, a neuroimmunologist in the University of Virginia School of Medicine’s department of neuroscience, has discovered a possible link, a modern twist on the age-old notion of the body-mind connection. His research suggests that the immune system engages the brain in an intricate dialogue that can influence our thought processes, coaxing our brains to work at their best.
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Can Boosting Immunity Make You Smarter?

After spending a few days in bed with the flu, you may have felt a bit stupid. It is a common sensation, that your sickness is slowing down your brain. At first blush, though, it doesn’t make much sense. For one thing, flu viruses infect the lining of the airways, not the neurons in our brains. For another, the brain is walled off from the rest of the body by a series of microscopic defenses collectively known as the blood-brain barrier. It blocks most viruses and bacteria while allowing essential molecules like glucose to slip through. What ails the body, in other words, shouldn’t interfere with our thinking.

But over the past decade, Jonathan Kipnis, a neuroimmunologist in the University of Virginia School of Medicine’s department of neuroscience, has discovered a possible link, a modern twist on the age-old notion of the body-mind connection. His research suggests that the immune system engages the brain in an intricate dialogue that can influence our thought processes, coaxing our brains to work at their best.

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Filed under immune system intelligence T cells white blood cells cognitive function neuroscience science

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When good habits go bad: Neuroscientist seeks roots of obsessive behavior, motion disorders

Learning, memory and habits are encoded in the strength of connections between neurons in the brain, the synapses. These connections aren’t meant to be fixed, they’re changeable, or plastic.

Duke University neurologist and neuroscientist Nicole Calakos studies what happens when those connections aren’t as adaptable as they should be in the basal ganglia, the brain’s “command center” for turning information into actions.

"The basal ganglia is the part of the brain that drives the car when you’re not thinking too hard about it," Calakos said. It’s also the part of the brain where neuroscientists are looking for the roots of obsessive-compulsive disorder, Huntington’s, Parkinson’s, and aspects of autism spectrum disorders.

In her most recent work, which she’ll discuss Saturday morning, Feb. 16 at the American Association for the Advancement of Science annual meeting in Boston, Calakos is mapping the defects in circuitry of the basal ganglia that underlie compulsive behavior. She is studying mice that have a synaptic defect that manifests itself as something like obsessive-compulsive behavior.

Calakos’ former colleague Guoping Feng developed the mice at Duke before moving to the McGovern Institute for Brain Research at MIT, where he now works. Feng was exploring the construction of synapses by knocking out genes one at a time. One set of mice ended up with facial lesions from endlessly grooming themselves until their faces were rubbed raw. When examining synaptic activity in the basal ganglia of these mice, Calakos’ group discovered that metabotropic glutamate receptors, or mGluRs, were overactive and this in turn, left their synapses less able to change. Scientists think overactivity of these receptors can cause many aspects of the autistic spectrum disorder Fragile X mental retardation.

"It’s an example of synaptic plasticity going awry," Calakos said. "They’re stuck with less adaptable synapses." Calakos is now using the mice to determine whether drugs that inhibit mGluRs can be used to improve their behavior and testing whether the circuit defects are a generalizable explanation for similar behaviors in other mouse models. This work may then lead to new understandings for compulsive behaviors and new treatment opportunities.

(Source: medicalxpress.com)

Filed under habits basal ganglia OCD compulsive behavior neuroscience science

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Queen’s University study aims to use stem cells to help save sight of diabetes sufferers
Scientists at Queen’s University Belfast are hoping to develop a novel approach that could save the sight of millions of diabetes sufferers using adult stem cells.
Currently millions of diabetics worldwide are at risk of sight loss due to a condition called Diabetic Retinopathy. This is when high blood sugar causes the blood vessels in the eye to become blocked or to leak. Failed blood flow harms the retina and leads to vision impairment and if left untreated can lead to blindness.
The novel REDDSTAR study (Repair of Diabetic Damage by Stromal Cell Administration) involving researchers from Queen’s Centre for Vision and Vascular Science in the School of Medicine, Dentistry and Biomedical Sciences, will see them isolating stem cells from donors, expanding them in a laboratory setting and re-delivering them to a patient where they help to repair the blood vessels in the eye. This is especially relevant to patients with diabetes were the vessels of the retina become damaged.
At present there are very few treatments available to control the progression of diabetic complications. There are no treatments which will improve glucose levels and simultaneously treat the diabetic complication.
The €6 million EU funded research is being carried out with NUI Galway and brings together experts from Northern Ireland, Ireland, Germany, the Netherlands, Denmark, Portugal and the US.
Professor Alan Stitt, Director of the Centre for Vision and Vascular Science in Queen’s and lead scientist for the project said: “The Queen’s component of the REDDSTAR study involves investigating the potential of a unique stem cell population to promote repair of damaged blood vessels in the retina during diabetes. The impact could be profound for patients, because regeneration of damaged retina could prevent progression of diabetic retinopathy and reduce the risk of vision loss.
“Currently available treatments for diabetic retinopathy are not always satisfactory. They focus on end-stages of the disease, carry many side effects and fail to address the root causes of the condition. A novel, alternative therapeutic approach is to harness adult stem cells to promote regeneration of the damaged retinal blood vessels and thereby prevent and/or reverse retinopathy.”
“This new research project is one of several regenerative medicine approaches ongoing in the centre. The approach is quite simple: we plan to isolate a very defined population of stem cells and then deliver them to sites in the body that have been damaged by diabetes. In the case of some patients with diabetes, they may gain enormous benefit from stem cell-mediated repair of damaged blood vessels in their retina. This is the first step towards an exciting new therapy in an area where it is desperately needed.”
The research focuses on specific adult stem-cells derived from bone-marrow. Which are being provided by Orbsen Therapeutics, a spin-out from the Science Foundation Ireland-funded Regenerative Medicine Institute (REMEDI) at NUI Galway.
The project will develop ways to grow the bone-marrow-derived stem cells. They will be tested in several preclinical models of diabetic complications at centres in Belfast, Galway, Munich, Berlin and Porto before human trials take place in Denmark.
Further information on the Centre for Vision and Vascular Science at Queen’s is available online at http://www.qub.ac.uk/research-centres/CentreforVisionandVascularScience/

Queen’s University study aims to use stem cells to help save sight of diabetes sufferers

Scientists at Queen’s University Belfast are hoping to develop a novel approach that could save the sight of millions of diabetes sufferers using adult stem cells.

Currently millions of diabetics worldwide are at risk of sight loss due to a condition called Diabetic Retinopathy. This is when high blood sugar causes the blood vessels in the eye to become blocked or to leak. Failed blood flow harms the retina and leads to vision impairment and if left untreated can lead to blindness.

The novel REDDSTAR study (Repair of Diabetic Damage by Stromal Cell Administration) involving researchers from Queen’s Centre for Vision and Vascular Science in the School of Medicine, Dentistry and Biomedical Sciences, will see them isolating stem cells from donors, expanding them in a laboratory setting and re-delivering them to a patient where they help to repair the blood vessels in the eye. This is especially relevant to patients with diabetes were the vessels of the retina become damaged.

At present there are very few treatments available to control the progression of diabetic complications. There are no treatments which will improve glucose levels and simultaneously treat the diabetic complication.

The €6 million EU funded research is being carried out with NUI Galway and brings together experts from Northern Ireland, Ireland, Germany, the Netherlands, Denmark, Portugal and the US.

Professor Alan Stitt, Director of the Centre for Vision and Vascular Science in Queen’s and lead scientist for the project said: “The Queen’s component of the REDDSTAR study involves investigating the potential of a unique stem cell population to promote repair of damaged blood vessels in the retina during diabetes. The impact could be profound for patients, because regeneration of damaged retina could prevent progression of diabetic retinopathy and reduce the risk of vision loss.

“Currently available treatments for diabetic retinopathy are not always satisfactory. They focus on end-stages of the disease, carry many side effects and fail to address the root causes of the condition. A novel, alternative therapeutic approach is to harness adult stem cells to promote regeneration of the damaged retinal blood vessels and thereby prevent and/or reverse retinopathy.”

“This new research project is one of several regenerative medicine approaches ongoing in the centre. The approach is quite simple: we plan to isolate a very defined population of stem cells and then deliver them to sites in the body that have been damaged by diabetes. In the case of some patients with diabetes, they may gain enormous benefit from stem cell-mediated repair of damaged blood vessels in their retina. This is the first step towards an exciting new therapy in an area where it is desperately needed.”

The research focuses on specific adult stem-cells derived from bone-marrow. Which are being provided by Orbsen Therapeutics, a spin-out from the Science Foundation Ireland-funded Regenerative Medicine Institute (REMEDI) at NUI Galway.

The project will develop ways to grow the bone-marrow-derived stem cells. They will be tested in several preclinical models of diabetic complications at centres in Belfast, Galway, Munich, Berlin and Porto before human trials take place in Denmark.

Further information on the Centre for Vision and Vascular Science at Queen’s is available online at http://www.qub.ac.uk/research-centres/CentreforVisionandVascularScience/

Filed under stem cells diabetes vision sight loss diabetic retinopathy REDDSTAR study medicine science

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Technique moves practical Alzheimer diagnosis one step closer to reality
Researchers at the University of Wisconsin-Madison School of Medicine and Public Health are moving closer to a significant milepost in the battle against Alzheimer’s disease: identifying the first signs of decline in the brain.
After years of frustrating failure to stop late-stage Alzheimer’s, it’s essential to find and treat the mild stages, says Sterling Johnson, professor of geriatrics. “We need to identify Alzheimer’s as early as possible, before the really destructive changes take place. Typically, by the time we diagnose Alzheimer’s disease, patients have already lost much of their brain capacity, and it’s difficult or impossible for them to recover.”
The earlier phases, before large numbers of brain cells have been killed, should be more amenable to treatment, Johnson says. Alzheimer’s disease is the largest single cause of dementia. Early symptoms include memory decline, eventually progressing to widespread cognitive and behavioral changes.
In a study published in the journal Cerebral Cortex in December, Johnson, Ozioma Okonkwo in the Department of Geriatrics, and colleagues reported on measurements of brain blood flow in 327 adults. The researchers used an advanced form of MRI to compare blood flow in people with Alzheimer’s, a preliminary stage called mild cognitive impairment, or those who had no symptoms but had a family history of Alzheimer’s.
Reduced blood flow signifies reduced activity in particular parts of the brain, often due to the atrophy of nerve cells. One affected structure, called the hippocampus, is necessary for making new memories. In mild to moderate cases of Alzheimer’s, 40 percent or more of the hippocampus has disappeared.
As expected, the Alzheimer’s patients had lower blood flow in several brain regions linked to memory. People with mild cognitive impairment had a milder version of the same deficits. And people whose mother (but not father) had Alzheimer’s had clear signs of reduced blood flow, even though they lacked symptoms.
Other techniques that can measure blood flow are more costly and require the use of radiation and injecting a drug tracer during the scan, Johnson says. If this non-invasive MRI technique continues to prove itself, it could be a key to detecting Alzheimer’s disease in its early, and hopefully more treatable, phases.
"In the new paper, we showed that the same areas that show up with more established scanning techniques also are identified with this MRI blood flow technique, in people with Alzheimer’s and mild cognitive impairment," says Johnson. "So this method is valid and reliable, and is now ready to begin deployment in treatment research with people at risk."

Technique moves practical Alzheimer diagnosis one step closer to reality

Researchers at the University of Wisconsin-Madison School of Medicine and Public Health are moving closer to a significant milepost in the battle against Alzheimer’s disease: identifying the first signs of decline in the brain.

After years of frustrating failure to stop late-stage Alzheimer’s, it’s essential to find and treat the mild stages, says Sterling Johnson, professor of geriatrics. “We need to identify Alzheimer’s as early as possible, before the really destructive changes take place. Typically, by the time we diagnose Alzheimer’s disease, patients have already lost much of their brain capacity, and it’s difficult or impossible for them to recover.”

The earlier phases, before large numbers of brain cells have been killed, should be more amenable to treatment, Johnson says. Alzheimer’s disease is the largest single cause of dementia. Early symptoms include memory decline, eventually progressing to widespread cognitive and behavioral changes.

In a study published in the journal Cerebral Cortex in December, Johnson, Ozioma Okonkwo in the Department of Geriatrics, and colleagues reported on measurements of brain blood flow in 327 adults. The researchers used an advanced form of MRI to compare blood flow in people with Alzheimer’s, a preliminary stage called mild cognitive impairment, or those who had no symptoms but had a family history of Alzheimer’s.

Reduced blood flow signifies reduced activity in particular parts of the brain, often due to the atrophy of nerve cells. One affected structure, called the hippocampus, is necessary for making new memories. In mild to moderate cases of Alzheimer’s, 40 percent or more of the hippocampus has disappeared.

As expected, the Alzheimer’s patients had lower blood flow in several brain regions linked to memory. People with mild cognitive impairment had a milder version of the same deficits. And people whose mother (but not father) had Alzheimer’s had clear signs of reduced blood flow, even though they lacked symptoms.

Other techniques that can measure blood flow are more costly and require the use of radiation and injecting a drug tracer during the scan, Johnson says. If this non-invasive MRI technique continues to prove itself, it could be a key to detecting Alzheimer’s disease in its early, and hopefully more treatable, phases.

"In the new paper, we showed that the same areas that show up with more established scanning techniques also are identified with this MRI blood flow technique, in people with Alzheimer’s and mild cognitive impairment," says Johnson. "So this method is valid and reliable, and is now ready to begin deployment in treatment research with people at risk."

Filed under dementia alzheimer's disease blood flow MRI blood flow technique neuroscience science

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Teaching the brain to speak again

Cynthia Thompson, a world-renowned researcher on stroke and brain damage, will discuss her groundbreaking research on aphasia and the neurolinguistic systems it affects Feb. 16 at the annual meeting of the American Association for the Advancement of Science (AAAS). An estimated one million Americans suffer from aphasia, affecting their ability to understand and/or produce spoken and/or written language.

For three decades, Thompson has played a crucial role in demonstrating the brain’s plasticity, or ability to change. “Not long ago, the conventional wisdom was that people only could recover language within three months to a year after the onset of stroke,” she says. “Today we know that, with appropriate training, patients can make gains as much as 10 years or more after a stroke.”

Thompson has probably contributed more findings on the effects of brain damage on language processing and the ways the brain and language recover from stroke than any other single researcher. Her particular interest is agrammatic aphasia, which impairs abstract knowledge of grammatical sentence structure and makes sentence production and understanding difficult.

Among the first researchers to use functional magnetic resonance imaging to study recovery from stroke, Thompson found that behavior treatment that focused on improving impaired language processing affects not only the ability to understand and produce language but also brain activity.

She found shifts in neural activity in both cerebral hemispheres associated with recovery, with the greatest recovery seen in undamaged brain regions within the language network engaged by healthy people, albeit regions recruited for various language activities.

"It’s a matter of ‘use it or lose it,’" Thompson says. "The brain has the capacity to learn and relearn throughout life, and it is directly affected by the activities we engage in. Language training that focuses on principles of normal language processing stimulates the recovery of neural networks that support language."

Thompson will discuss research she will conduct as principal investigator of a $12 million National Institutes of Health Clinical Research Center award to study biomarkers of recovery in aphasia.

Working with investigators from a number of universities, Thompson will explore the role blood flow plays in language recovery in chronic stroke patients. In addition, she will conduct cutting-edge, exploratory research using eye tracking to understand how people compute language as they hear it in real time. Eye-tracking techniques have been found to discern subtle problems underlying language deficits in acquired aphasia.

In a landmark 2010 study, she and colleagues discovered two critical variables related to understanding brain damage recovery. They found that stroke not only results in cell death in certain regions of the brain but that it also decreases blood flow (perfusion) to living cells that are adjacent (and sometimes even distant) to the lesion.

Until that study, hypoperfusion (diminished blood flow) was thought only to be associated with acute stroke. Her team also found that greater hypoperfusion led to poorer recovery.

(Source: eurekalert.org)

Filed under language aphasia brain damage stroke neural activity language processing neuroscience science

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Training speech networks to treat aphasia
About 80,000 people develop aphasia each year in the United States alone. Nearly all of these individuals have difficulty speaking. For example, some patients (nonfluent aphasics) have trouble producing sounds clearly, making it frustrating for them to speak and difficult for them to be understood. Other patients (fluent aphasics) may select the wrong sound in a word or mix up the order of the sounds. In the latter case, “kitchen” can become “chicken.” Blumstein’s idea is to use guided speech to help people who have suffered stroke-related brain damage to rebuild their neural speech infrastructure.
Blumstein has been studying aphasia and the neural basis of language her whole career. She uses brain imaging, acoustic analysis, and other lab-based techniques to study how the brain maps sound to meaning and meaning to sound.
What Blumstein and other scientists believe is that the brain organizes words into networks, linked both by similarity of meaning and similarity of sound. To say “pear,” a speaker will also activate other competing words like “apple” (which competes in meaning) and “bear”(which competes in sound). Despite this competition, normal speakers are able to select the correct word.
In a study published in the Journal of Cognitive Neuroscience in 2010, for example, she and her co-authors used functional magnetic resonance imaging to track neural activation patterns in the brains of 18 healthy volunteers as they spoke English words that had similar sounding “competitors” (“cape” and “gape” differ subtly in the first consonant by voicing, i.e. the timing of the onset of vocal cord vibration). Volunteers also spoke words without similar sounding competitors (“cake” has no voiced competitor in English; gake is not a word). What the researchers found is that neural activation within a network of brain regions was modulated differently when subjects said words that had competitors versus words that did not.
One way this competition-mediated difference is apparent in speech production is that words with competitors are produced differently from words that do not have competitors. For example, the voicing of the “t” in “tot” (with a voiced competitor ‘dot’) is produced with more voicing than the “t” in “top” (there is no ‘dop’ in English). Through acoustic analysis of the speech of people with aphasia, Blumstein has shown that this difference persists, suggesting that their word networks are still largely intact.

Training speech networks to treat aphasia

About 80,000 people develop aphasia each year in the United States alone. Nearly all of these individuals have difficulty speaking. For example, some patients (nonfluent aphasics) have trouble producing sounds clearly, making it frustrating for them to speak and difficult for them to be understood. Other patients (fluent aphasics) may select the wrong sound in a word or mix up the order of the sounds. In the latter case, “kitchen” can become “chicken.” Blumstein’s idea is to use guided speech to help people who have suffered stroke-related brain damage to rebuild their neural speech infrastructure.

Blumstein has been studying aphasia and the neural basis of language her whole career. She uses brain imaging, acoustic analysis, and other lab-based techniques to study how the brain maps sound to meaning and meaning to sound.

What Blumstein and other scientists believe is that the brain organizes words into networks, linked both by similarity of meaning and similarity of sound. To say “pear,” a speaker will also activate other competing words like “apple” (which competes in meaning) and “bear”(which competes in sound). Despite this competition, normal speakers are able to select the correct word.

In a study published in the Journal of Cognitive Neuroscience in 2010, for example, she and her co-authors used functional magnetic resonance imaging to track neural activation patterns in the brains of 18 healthy volunteers as they spoke English words that had similar sounding “competitors” (“cape” and “gape” differ subtly in the first consonant by voicing, i.e. the timing of the onset of vocal cord vibration). Volunteers also spoke words without similar sounding competitors (“cake” has no voiced competitor in English; gake is not a word). What the researchers found is that neural activation within a network of brain regions was modulated differently when subjects said words that had competitors versus words that did not.

One way this competition-mediated difference is apparent in speech production is that words with competitors are produced differently from words that do not have competitors. For example, the voicing of the “t” in “tot” (with a voiced competitor ‘dot’) is produced with more voicing than the “t” in “top” (there is no ‘dop’ in English). Through acoustic analysis of the speech of people with aphasia, Blumstein has shown that this difference persists, suggesting that their word networks are still largely intact.

Filed under aphasia brain damage language speech production neuroimaging neuroscience science

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