Neuroscience

Articles and news from the latest research reports.

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Eye movements reveal impaired reading in schizophrenia

A study of eye movements in schizophrenia patients provides new evidence of impaired reading fluency in individuals with the mental illness.

The findings, by researchers at McGill University in Montreal, could open avenues to earlier detection and intervention for people with the illness.
While schizophrenia patients are known to have abnormalities in language and in eye movements, until recently reading ability was believed to be unaffected. That is because most previous studies examined reading in schizophrenia using single-word reading tests, the McGill researchers conclude. Such tests aren’t sensitive to problems in reading fluency, which is affected by the context in which words appear and by eye movements that shift attention from one word to the next.
The McGill study, led by Ph.D. candidate Veronica Whitford and psychology professors Debra Titone and Gillian A. O’Driscoll, monitored how people move their eyes as they read simple sentences. The results, which were first published online last year, appear in the February issue of the Journal of Experimental Psychology: General.
Eye movement measures provide clear and objective indicators of how hard people are working as they read. For example, when struggling with a difficult sentence, people generally make smaller eye movements, spend more time looking at each word, and spend more time re-reading words. They also have more difficulty attending to upcoming words, so they plan their eye movements less efficiently.
The McGill study, which involved 20 schizophrenia outpatients and 16 non-psychiatric participants, showed that reading patterns in people with schizophrenia differed in several important ways from healthy participants matched for gender, age, and family social status. People with schizophrenia read more slowly, generated smaller eye movements, spent more time processing individual words, and spent more time re-reading. In addition, people with schizophrenia were less efficient at processing upcoming words to facilitate reading.
The researchers evaluated factors that could contribute to the problems in reading fluency among the schizophrenia outpatients – specifically, their ability to parse words into sound components and their ability to skillfully control eye movements in non-reading contexts. Both factors were found to contribute to the reading deficits.

Eye movements reveal impaired reading in schizophrenia

A study of eye movements in schizophrenia patients provides new evidence of impaired reading fluency in individuals with the mental illness.

The findings, by researchers at McGill University in Montreal, could open avenues to earlier detection and intervention for people with the illness.

While schizophrenia patients are known to have abnormalities in language and in eye movements, until recently reading ability was believed to be unaffected. That is because most previous studies examined reading in schizophrenia using single-word reading tests, the McGill researchers conclude. Such tests aren’t sensitive to problems in reading fluency, which is affected by the context in which words appear and by eye movements that shift attention from one word to the next.

The McGill study, led by Ph.D. candidate Veronica Whitford and psychology professors Debra Titone and Gillian A. O’Driscoll, monitored how people move their eyes as they read simple sentences. The results, which were first published online last year, appear in the February issue of the Journal of Experimental Psychology: General.

Eye movement measures provide clear and objective indicators of how hard people are working as they read. For example, when struggling with a difficult sentence, people generally make smaller eye movements, spend more time looking at each word, and spend more time re-reading words. They also have more difficulty attending to upcoming words, so they plan their eye movements less efficiently.

The McGill study, which involved 20 schizophrenia outpatients and 16 non-psychiatric participants, showed that reading patterns in people with schizophrenia differed in several important ways from healthy participants matched for gender, age, and family social status. People with schizophrenia read more slowly, generated smaller eye movements, spent more time processing individual words, and spent more time re-reading. In addition, people with schizophrenia were less efficient at processing upcoming words to facilitate reading.

The researchers evaluated factors that could contribute to the problems in reading fluency among the schizophrenia outpatients – specifically, their ability to parse words into sound components and their ability to skillfully control eye movements in non-reading contexts. Both factors were found to contribute to the reading deficits.

Filed under eye movements visual attention schizophrenia neuroscience medicine science

86 notes

Our primitive reflexes may be more sophisticated than they appear

Supposedly ‘primitive’ reflexes may involve more sophisticated brain function than previously thought, according to researchers at Imperial College London.

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The vestibular-ocular reflex (or VOR), common to most vertebrates, is what allows us to keep our eyes focused on a fixed point even while our heads are moving. Up until now, scientists had assumed this reflex was controlled by the lower brainstem, which regulates eating, sleeping and other low-level tasks.

Researchers at Imperial’s Division of Brain Sciences conducted tests to examine this reflex in left- and right-handed subjects, revealing that handedness plays a key role in the way it operates. This suggests that higher-level functions in the cortex, which govern handedness, are involved in the control of primitive reflexes such as the VOR.

The research, published in the Journal of Neuroscience, involved seating volunteers in a motorised chair which was then spun around at a speed of one revolution every four seconds. This allowed the experimenters to study the VOR by measuring the time it took for the eyes to adjust to the spinning motion. The subjects were then presented with what are known as bistable visual phenomena, optical illusions which appear to flip between two images. Famous examples include the duck which resembles a rabbit, and the cube outline which appears to come out of and go into the page simultaneously.

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Scientists already know that this bistable perception is controlled by a part of the cortex which governs more complex, decision-based tasks. Because of this, researcher Qadeer Arshad and his colleagues did not expect to find any link between the two processes.

They were surprised to find that processing bistable phenomena disrupted people’s ability to stabilise their gaze, following rightward rotation in right handers and leftward rotation in left handers. Arshad said “This is the first time that anything of this kind has been shown. Up until now, the vestibular-ocular reflex was considered a low-level reflex, not even approaching higher-order brain function. Now it seems that this primitive reflex was specialised into the cortex, the part of the brain which governs our sense of direction.”

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This study could help scientists understand why some people become dizzy through experiencing purely visual stimuli, such as flickering lights or busy supermarket aisles. Professor Adolfo Bronstein, a co-author on the paper, said “Most causes of dizziness start with an inner ear - or vestibular - disorder but this initial phase tends to settle quite rapidly.  In some patients, however, dizziness becomes a problematic long term problem and their dizziness becomes visually induced. The experimental set-up we used would be ideally suited to help us understand how visual stimuli could lead to long-term dizziness. In fact, we have already carried out research at Imperial around using complex visual stimuli to treat patients with long-term dizziness”

(Source: www3.imperial.ac.uk)

Filed under motor reflexes primitive reflexes vestibular-ocular reflex vision brain neuroscience science

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Memory appears susceptible to eradication of fear responses
Fear responses can only be erased when people learn something new while retrieving the fear memory. This is the conclusion of a study conducted by scientists from the University of Amsterdam (UvA) and published in the leading journal Science.
Researchers Dieuwke Sevenster MSc, Dr Tom Beckers and Prof. Merel Kindt have developed a method to determine whether an acquired fear response is susceptible to modification. By doing so, they have revealed the circumstances under which an acquired fear response can be eradicated. In order to measure whether a person actually learnt something new, the researchers used a measure for Prediction Error – in other words, the discrepancy between a person’s anticipation of what is going to happen and what actually happens.
No fear response
Cognitive Behavioural Therapy is currently the most common and effective type of treatment for people suffering from anxiety disorders. However, the effects are often short-lived and the fear returns in many patients. One major finding of Van Kindt’s research lab is that when participants were given propranolol, a beta blocker, while retrieving a specific fear memory, the acquired fear response was shown to be totally erased a day or month later. The researchers repeatedly found that the fear did not come back, despite the use of techniques specifically aimed to make it return. This indicates that the fear memory was either fully eradicated, or could no longer be accessed. One crucial finding was that while participants could still remember the association with the fear, that particular memory no longer triggered the former fear response.
Fear conditioning
For their study the researchers used a fear conditioning procedure in which a specific picture was followed by a nasty painful stimulus. While the participants viewed the pictures, the researchers measured the anticipation of the painful stimulus as well as the more autonomous fear response on the basis of the startle reflex.
The current findings will contribute to the further development of more effective and efficient therapies for patients suffering from excessive anxiety disorders, such as trauma victims. There was no independent measure to indicate whether the memory is susceptible to modification up until now. The researchers have shown that the fear response can be eradicated completely, provided that the person concerned actually learns something new while retrieving the fear memory.
(Image: iStock)

Memory appears susceptible to eradication of fear responses

Fear responses can only be erased when people learn something new while retrieving the fear memory. This is the conclusion of a study conducted by scientists from the University of Amsterdam (UvA) and published in the leading journal Science.

Researchers Dieuwke Sevenster MSc, Dr Tom Beckers and Prof. Merel Kindt have developed a method to determine whether an acquired fear response is susceptible to modification. By doing so, they have revealed the circumstances under which an acquired fear response can be eradicated. In order to measure whether a person actually learnt something new, the researchers used a measure for Prediction Error – in other words, the discrepancy between a person’s anticipation of what is going to happen and what actually happens.

No fear response

Cognitive Behavioural Therapy is currently the most common and effective type of treatment for people suffering from anxiety disorders. However, the effects are often short-lived and the fear returns in many patients. One major finding of Van Kindt’s research lab is that when participants were given propranolol, a beta blocker, while retrieving a specific fear memory, the acquired fear response was shown to be totally erased a day or month later. The researchers repeatedly found that the fear did not come back, despite the use of techniques specifically aimed to make it return. This indicates that the fear memory was either fully eradicated, or could no longer be accessed. One crucial finding was that while participants could still remember the association with the fear, that particular memory no longer triggered the former fear response.

Fear conditioning

For their study the researchers used a fear conditioning procedure in which a specific picture was followed by a nasty painful stimulus. While the participants viewed the pictures, the researchers measured the anticipation of the painful stimulus as well as the more autonomous fear response on the basis of the startle reflex.

The current findings will contribute to the further development of more effective and efficient therapies for patients suffering from excessive anxiety disorders, such as trauma victims. There was no independent measure to indicate whether the memory is susceptible to modification up until now. The researchers have shown that the fear response can be eradicated completely, provided that the person concerned actually learns something new while retrieving the fear memory.

(Image: iStock)

Filed under memory amnesia anxiety learning fear conditioning fear psychology neuroscience science

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Neuronal activity induces tau release from healthy neurons
Researchers from King’s College London have discovered that neuronal activity can stimulate tau release from healthy neurons in the absence of cell death. The results published by Diane Hanger and her colleagues in EMBO reports show that treatment of neurons with known biological signaling molecules increases the release of tau into the culture medium. The release of tau from cortical neurons is therefore a physiological process that can be regulated by neuronal activity.
Tau proteins stabilize microtubules, the long threads of polymers that help to maintain the structure of the cell. However, in Alzheimer’s disease or certain types of dementia, tau accumulates in neurons or glial cells, where it contributes to neurodegeneration.
In addition to intracellular aggregation, recent experiments have shown that tau is released from neuronal cells and taken up by neighboring cells, which allows the spread of aggregated tau across the brain. This release could occur passively from dying neuronal cells, though some evidence suggests it might take place before neuronal cell death and neurodegeneration. The new findings indicate that tau release is an active process in healthy neurons and this could be altered in diseased brains.
“Our findings suggest that altered tau release is likely to occur in response to changes in neuronal excitability in the Alzheimer’s brain. Secreted tau could therefore be involved in the propagation of tau pathology in tauopathies, a group of neurodegenerative diseases associated with the accumulation of tau proteins in the brain,” commented Diane Hanger, Reader in the Department of Neuroscience at King’s College London. In these experiments, Amy Pooler, the lead author, revealed that molecules such as potassium chloride, glutamate or an AMPA receptor agonist could release tau from cortical neurons in an active physiological process that is, at least partially, dependent on pre-synaptic vesicle secretion.
The new findings by the scientists indicate that tau has previously unknown roles in biological signaling between cells, in addition to its well-established role in stabilizing microtubules.
“We believe that targeting the release of tau could be explored as a new therapeutic approach for the treatment of Alzheimer’s disease and related tauopathies,” said Hanger. Additional studies are needed in model organisms to test this hypothesis further.
(Image: Patrick Hoesly)

Neuronal activity induces tau release from healthy neurons

Researchers from King’s College London have discovered that neuronal activity can stimulate tau release from healthy neurons in the absence of cell death. The results published by Diane Hanger and her colleagues in EMBO reports show that treatment of neurons with known biological signaling molecules increases the release of tau into the culture medium. The release of tau from cortical neurons is therefore a physiological process that can be regulated by neuronal activity.

Tau proteins stabilize microtubules, the long threads of polymers that help to maintain the structure of the cell. However, in Alzheimer’s disease or certain types of dementia, tau accumulates in neurons or glial cells, where it contributes to neurodegeneration.

In addition to intracellular aggregation, recent experiments have shown that tau is released from neuronal cells and taken up by neighboring cells, which allows the spread of aggregated tau across the brain. This release could occur passively from dying neuronal cells, though some evidence suggests it might take place before neuronal cell death and neurodegeneration. The new findings indicate that tau release is an active process in healthy neurons and this could be altered in diseased brains.

“Our findings suggest that altered tau release is likely to occur in response to changes in neuronal excitability in the Alzheimer’s brain. Secreted tau could therefore be involved in the propagation of tau pathology in tauopathies, a group of neurodegenerative diseases associated with the accumulation of tau proteins in the brain,” commented Diane Hanger, Reader in the Department of Neuroscience at King’s College London. In these experiments, Amy Pooler, the lead author, revealed that molecules such as potassium chloride, glutamate or an AMPA receptor agonist could release tau from cortical neurons in an active physiological process that is, at least partially, dependent on pre-synaptic vesicle secretion.

The new findings by the scientists indicate that tau has previously unknown roles in biological signaling between cells, in addition to its well-established role in stabilizing microtubules.

“We believe that targeting the release of tau could be explored as a new therapeutic approach for the treatment of Alzheimer’s disease and related tauopathies,” said Hanger. Additional studies are needed in model organisms to test this hypothesis further.

(Image: Patrick Hoesly)

Filed under neurons neuronal activity tau proteins neurodegeneration alzheimer's disease neuroscience science

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Paving the way for better sleep in Alzheimer’s
A new sleep pattern monitoring system has been developed by UK researchers to help spot sleep disturbance in people diagnosed with early dementia. The system, known as PAViS, could be used remotely by healthcare workers to view sleep profiles and analyse sleep patterns based on sensory data gathered at the patient’s home.
Writing in the International Journal of Computers in Healthcare, Huiru Zheng and colleagues at the University of Ulster at Jordanstown, County Antrim, Northern Ireland explain how sleep disturbance is one of the most distressing of symptoms in Alzheimer’s disease and might also be an early indicator of the onset of the disease in some cases. They point out that so-called “telecare” systems allow healthcare workers to monitor patient activity whether in normal or supported housing.
There are almost half a million people in the UK with Alzheimer’s disease and for many of those sleep disorders and disruptive nocturnal behaviour present a significant clinical problem for healthcare workers and are a cause of distress for caregivers. Sleep-related problems generally worsen as the disease progresses and are an indicator of cognitive impairment and lead to the patient being less alert than would be expected during waking hours as well as reducing their overall wellbeing.
Various systems have been developed in recent years to monitor sleeping patients. However, these would often tend to involve other people in the patient’s home as well as simply monitoring sleep patterns rather than long-term monitoring and analysis of sleep profiles for assessing sleep quality. PAViS, pattern analysis and visualisation system, circumvents the problems and allows healthcare workers to quickly see shifts in sleep pattern and detect unusual patterns in order to assess the changes in health condition of people with early dementia over the course of weeks and months. Data are collected from infrared movement detectors and sensors on bedroom and other doors in the patient’s home. This provides a non-invasive, pervasive and objective monitoring and assessment solution, the team says.

Paving the way for better sleep in Alzheimer’s

A new sleep pattern monitoring system has been developed by UK researchers to help spot sleep disturbance in people diagnosed with early dementia. The system, known as PAViS, could be used remotely by healthcare workers to view sleep profiles and analyse sleep patterns based on sensory data gathered at the patient’s home.

Writing in the International Journal of Computers in Healthcare, Huiru Zheng and colleagues at the University of Ulster at Jordanstown, County Antrim, Northern Ireland explain how sleep disturbance is one of the most distressing of symptoms in Alzheimer’s disease and might also be an early indicator of the onset of the disease in some cases. They point out that so-called “telecare” systems allow healthcare workers to monitor patient activity whether in normal or supported housing.

There are almost half a million people in the UK with Alzheimer’s disease and for many of those sleep disorders and disruptive nocturnal behaviour present a significant clinical problem for healthcare workers and are a cause of distress for caregivers. Sleep-related problems generally worsen as the disease progresses and are an indicator of cognitive impairment and lead to the patient being less alert than would be expected during waking hours as well as reducing their overall wellbeing.

Various systems have been developed in recent years to monitor sleeping patients. However, these would often tend to involve other people in the patient’s home as well as simply monitoring sleep patterns rather than long-term monitoring and analysis of sleep profiles for assessing sleep quality. PAViS, pattern analysis and visualisation system, circumvents the problems and allows healthcare workers to quickly see shifts in sleep pattern and detect unusual patterns in order to assess the changes in health condition of people with early dementia over the course of weeks and months. Data are collected from infrared movement detectors and sensors on bedroom and other doors in the patient’s home. This provides a non-invasive, pervasive and objective monitoring and assessment solution, the team says.

Filed under dementia alzheimer's disease sleep sleep patterns PAViS neuroscience science

54 notes

Fighting disease deep inside the brain
Some 90,000 patients per year are treated for Parkinson’s disease, a number that is expected to rise by 25 percent annually. Deep Brain Stimulation (DBS), which consists of electrically stimulating the central or peripheral nervous system, is currently standard practice for treating Parkinson’s, but it can involve long, expensive surgeries with dramatic side effects. Miniature, ultra-flexible electrodes developed in Switzerland, however, could be the answer to more successful treatment for this and a host of other health issues.
Today, Professor Philippe Renaud of the École Polytechnique Fédérale de Lausanne (EPFL) in Switzerland reports on soft arrays of miniature electrodes developed in his Microsystems Laboratory that open new possibilities for more accurate and local DBS. At the 2013 Annual Meeting of the American Association for the Advancement of Science (AAAS) in Boston, in a symposium called “Engineering the Nervous System: Solutions to Restore Sight, Hearing, and Mobility,” he announces the start of clinical trials and early, yet promising results in patients, and describes new developments in ultra-flexible electronics that can conform to the contours of the brainstem—in the brain itself—for treating other disorders.
At AAAS, Renaud outlines the technology behind these novel electronic interfaces with the nervous system, the associated challenges, and their immense potential to enhance DBS and treat disease, even how ultra flexible electronics could lead to the auditory implants of the future and the restoration of hearing. “Although Deep Brain Stimulation has been used for the past two decades, we see little progress in its clinical outcomes,” Renaud says. “Microelectrodes have the potential to open new therapeutic routes, with more efficiency and fewer side effects through a much better and finer control of electrical activation zones.” The preliminary clinical trials related to this research are being done in conjunction with EPFL spin-off company Aleva Neurotherapeutics, the first company in the world to introduce microelectrodes in Deep Brain Stimulation leading to more precise directional stimulation.

Fighting disease deep inside the brain

Some 90,000 patients per year are treated for Parkinson’s disease, a number that is expected to rise by 25 percent annually. Deep Brain Stimulation (DBS), which consists of electrically stimulating the central or peripheral nervous system, is currently standard practice for treating Parkinson’s, but it can involve long, expensive surgeries with dramatic side effects. Miniature, ultra-flexible electrodes developed in Switzerland, however, could be the answer to more successful treatment for this and a host of other health issues.

Today, Professor Philippe Renaud of the École Polytechnique Fédérale de Lausanne (EPFL) in Switzerland reports on soft arrays of miniature electrodes developed in his Microsystems Laboratory that open new possibilities for more accurate and local DBS. At the 2013 Annual Meeting of the American Association for the Advancement of Science (AAAS) in Boston, in a symposium called “Engineering the Nervous System: Solutions to Restore Sight, Hearing, and Mobility,” he announces the start of clinical trials and early, yet promising results in patients, and describes new developments in ultra-flexible electronics that can conform to the contours of the brainstem—in the brain itself—for treating other disorders.

At AAAS, Renaud outlines the technology behind these novel electronic interfaces with the nervous system, the associated challenges, and their immense potential to enhance DBS and treat disease, even how ultra flexible electronics could lead to the auditory implants of the future and the restoration of hearing. “Although Deep Brain Stimulation has been used for the past two decades, we see little progress in its clinical outcomes,” Renaud says. “Microelectrodes have the potential to open new therapeutic routes, with more efficiency and fewer side effects through a much better and finer control of electrical activation zones.” The preliminary clinical trials related to this research are being done in conjunction with EPFL spin-off company Aleva Neurotherapeutics, the first company in the world to introduce microelectrodes in Deep Brain Stimulation leading to more precise directional stimulation.

Filed under deep brain stimulation electrodes microelectrodes electrical stimulation neuroscience science

63 notes

Shedding New Light on Infant Brain Development
A new study by Columbia Engineering researchers finds that the infant brain does not control its blood flow in the same way as the adult brain. The findings, which the scientists say could change the way researchers study brain development in infants and children, are published in the February 18 Early Online edition of Proceedings of the National Academy of Sciences (PNAS).
“The control of blood flow in the brain is very important,” says Elizabeth Hillman, associate professor of biomedical engineering and of radiology, who led the research study in her Laboratory for Functional Optical Imaging at Columbia. “Not only are regionally specific increases in blood flow necessary for normal brain function, but these blood-flow increases form the basis of signals measured in fMRI, a critical imaging tool used widely in adults and children to assess brain function. Many prior fMRI studies have overlooked the possibility that the infant brain controls blood flow differently.”
“Our results are fascinating,” says Mariel Kozberg, a neurobiology MD-PhD candidate who works under Hillman and is the lead author of the PNAS paper. “We found that the immature brain does not generate localized blood-flow increases in response to stimuli. By tracking changes in blood-flow control with increasing age, we observed the brain gradually developing its ability to increase local blood flow and, by adulthood, generate a large blood-flow response.”
The study results suggest that fMRI experiments in infants and children should be carefully designed to ensure that maturation of blood-flow control can be delineated from changes in neuronal development. “On the other hand,” says Hillman, “our findings also suggest that vascular development may be an important new factor to consider in normal and abnormal brain development, so our findings could represent new markers of normal and abnormal brain development that could potentially be related to a range of neurological or even psychological conditions.”

Shedding New Light on Infant Brain Development

A new study by Columbia Engineering researchers finds that the infant brain does not control its blood flow in the same way as the adult brain. The findings, which the scientists say could change the way researchers study brain development in infants and children, are published in the February 18 Early Online edition of Proceedings of the National Academy of Sciences (PNAS).

“The control of blood flow in the brain is very important,” says Elizabeth Hillman, associate professor of biomedical engineering and of radiology, who led the research study in her Laboratory for Functional Optical Imaging at Columbia. “Not only are regionally specific increases in blood flow necessary for normal brain function, but these blood-flow increases form the basis of signals measured in fMRI, a critical imaging tool used widely in adults and children to assess brain function. Many prior fMRI studies have overlooked the possibility that the infant brain controls blood flow differently.”

“Our results are fascinating,” says Mariel Kozberg, a neurobiology MD-PhD candidate who works under Hillman and is the lead author of the PNAS paper. “We found that the immature brain does not generate localized blood-flow increases in response to stimuli. By tracking changes in blood-flow control with increasing age, we observed the brain gradually developing its ability to increase local blood flow and, by adulthood, generate a large blood-flow response.”

The study results suggest that fMRI experiments in infants and children should be carefully designed to ensure that maturation of blood-flow control can be delineated from changes in neuronal development. “On the other hand,” says Hillman, “our findings also suggest that vascular development may be an important new factor to consider in normal and abnormal brain development, so our findings could represent new markers of normal and abnormal brain development that could potentially be related to a range of neurological or even psychological conditions.”

Filed under brain brain function neuronal development brain development infants blood flow neuroscience science

90 notes

Brain plasticity
Babies’ brains are highly plastic, meaning they’re constantly adapting as they learn and respond to the world and people around them.
Daphne Maurer, director of the Visual Development Laboratory at McMaster University in Hamilton, Ontario, has found clues as to when plasticity might be locked off in babies and how in some adults it actually may persist unbeknown to them.

Brain plasticity

Babies’ brains are highly plastic, meaning they’re constantly adapting as they learn and respond to the world and people around them.

Daphne Maurer, director of the Visual Development Laboratory at McMaster University in Hamilton, Ontario, has found clues as to when plasticity might be locked off in babies and how in some adults it actually may persist unbeknown to them.

Filed under infants brain development plasticity vision synesthesia neuroscience science

363 notes

Scans reveal intricate brain wiring

Scientists are set to release the first batch of data from a project designed to create the first map of the human brain.

The project could help shed light on why some people are naturally scientific, musical or artistic.

Some of the first images were shown at the American Association for the Advancement of Science meeting in Boston.

I found out how researchers are developing new brain imaging techniques for the project by having my own brain scanned.

Scientists at Massachusetts General Hospital are pushing brain imaging to its limit using a purpose built scanner. It is one of the most powerful scanners in the world.

The scanner’s magnets need 22MW of electricity - enough to power a nuclear submarine.

The researchers invited me to have my brain scanned. I was asked if I wanted “the 10-minute job or the 45-minute ‘full monty’” which would give one of the most detailed scans of the brain ever carried out. Only 50 such scans have ever been done.

I went for the full monty.

It was a pleasant experience enclosed in the scanner’s vast twin magnets. Powerful and rapidly changing magnetic fields were looking to see tiny particles of water travelling along the larger nerve fibres.

By following the droplets, the scientists in the adjoining cubicle are able to trace the major connections within my brain.

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Filed under brain brain imaging Human Connectome Project wiring diagram neuroscience science

230 notes

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.”
Read more

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.”

Read more

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

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