neurosciencestuff
neurosciencestuff:

Size of personal space is affected by anxiety
The space surrounding the body (known by scientists as ‘peripersonal space’), which has previously been thought of as having a gradual boundary, has been given physical limits by new research into the relationship between anxiety and personal space.
New findings have allowed scientists to define the limit of the ‘peripersonal space’ surrounding the face as 20-40cm away. The study is published today in The Journal of Neuroscience.
As well as having numerical limits the specific distance was found to vary between individuals. Those with anxiety traits were found to have larger peripersonal space.
In an experiment, Dr Chiara Sambo and Dr Giandomenico Iannetti from UCL recorded the blink reflex - a defensive response to potentially dangerous stimuli at varying distances from subject’s face. They then compared the reflex data to the results of an anxiety test where subjects rated their levels of anxiety in various situations.
Those who scored highly on the anxiety test tended to react more strongly to stimuli 20cm from their face than subjects who got low scores on the anxiety test. Researchers classified those who reacted more strongly to further away stimuli as having a large ‘defensive peripersonal space’ (DPPS).
A larger DPPS means that those with high anxiety scores perceive threats as closer than non-anxious individuals when the stimulus is the same distance away. The research has led scientists to think that the brain controls the strength of defensive reflexes even though it cannot initiate them.
Dr Giandomenico Iannetti (UCL Neuroscience, Physiology and Pharmacology), lead author of the study, said: “This finding is the first objective measure of the size of the area surrounding the face that each individual considers at high-risk, and thus wants to protect through the most effective defensive motor responses.”
In the experiment, a group of 15 people aged 20 to 37 were chosen for study. Researchers applied an intense electrical stimulus to a specific nerve in the hand which causes the subject to blink. This is called the hand-blink reflex (HBR) which is not under conscious control of the brain.
This reflex was monitored with the subject holding their own hand at 4, 20, 40 and 60 cm away from the face. The magnitude of the reflex was used to determine how dangerous each stimulus was considered, and a larger response for stimuli further from the body indicated a larger DPPS.
Subjects also completed an anxiety test in which they self-scored their predicted level of anxiety in different situations. The results of this test were used to classify individuals as more or less anxious, and were compared to the data from the reflex experiment to determine if there was a link between the two tests.
Scientists hope that the findings can be used as a test to link defensive behaviours to levels of anxiety. This could be particularly useful determining risk assessment ability in those with jobs that encounter dangerous situations such as fire, police and military officers.

neurosciencestuff:

Size of personal space is affected by anxiety

The space surrounding the body (known by scientists as ‘peripersonal space’), which has previously been thought of as having a gradual boundary, has been given physical limits by new research into the relationship between anxiety and personal space.

New findings have allowed scientists to define the limit of the ‘peripersonal space’ surrounding the face as 20-40cm away. The study is published today in The Journal of Neuroscience.

As well as having numerical limits the specific distance was found to vary between individuals. Those with anxiety traits were found to have larger peripersonal space.

In an experiment, Dr Chiara Sambo and Dr Giandomenico Iannetti from UCL recorded the blink reflex - a defensive response to potentially dangerous stimuli at varying distances from subject’s face. They then compared the reflex data to the results of an anxiety test where subjects rated their levels of anxiety in various situations.

Those who scored highly on the anxiety test tended to react more strongly to stimuli 20cm from their face than subjects who got low scores on the anxiety test. Researchers classified those who reacted more strongly to further away stimuli as having a large ‘defensive peripersonal space’ (DPPS).

A larger DPPS means that those with high anxiety scores perceive threats as closer than non-anxious individuals when the stimulus is the same distance away. The research has led scientists to think that the brain controls the strength of defensive reflexes even though it cannot initiate them.

Dr Giandomenico Iannetti (UCL Neuroscience, Physiology and Pharmacology), lead author of the study, said: “This finding is the first objective measure of the size of the area surrounding the face that each individual considers at high-risk, and thus wants to protect through the most effective defensive motor responses.”

In the experiment, a group of 15 people aged 20 to 37 were chosen for study. Researchers applied an intense electrical stimulus to a specific nerve in the hand which causes the subject to blink. This is called the hand-blink reflex (HBR) which is not under conscious control of the brain.

This reflex was monitored with the subject holding their own hand at 4, 20, 40 and 60 cm away from the face. The magnitude of the reflex was used to determine how dangerous each stimulus was considered, and a larger response for stimuli further from the body indicated a larger DPPS.

Subjects also completed an anxiety test in which they self-scored their predicted level of anxiety in different situations. The results of this test were used to classify individuals as more or less anxious, and were compared to the data from the reflex experiment to determine if there was a link between the two tests.

Scientists hope that the findings can be used as a test to link defensive behaviours to levels of anxiety. This could be particularly useful determining risk assessment ability in those with jobs that encounter dangerous situations such as fire, police and military officers.

neurosciencestuff
neurosciencestuff:

High-Flying Pilots at Increased Risk of Brain Lesions
A new study suggests that pilots who fly at high altitudes may be at an increased risk for brain lesions. The study is published in the August 20, 2013, print issue of Neurology®, the medical journal of the American Academy of Neurology.
For the study, 102 U-2 United States Air Force pilots and 91 non-pilots between the ages of 26 and 50 underwent MRI brain scans. The scans measured the amount of white matter hyperintensities, or tiny brain lesions associated with memory decline in other neurological diseases. The groups were matched for age, education and health factors.
“Pilots who fly at altitudes above 18,000 feet are at risk for decompression sickness, a condition where gas or atmospheric pressure reaches lower levels than those within body tissues and forms bubbles,” said study author Stephen McGuire, MD, with the University of Texas in San Antonio, the US Air Force School of Aerospace Medicine and a Fellow of the American Academy of Neurology. “The risk for decompression sickness among Air Force pilots has tripled from 2006, probably due to more frequent and longer periods of exposure for pilots. To date however, we have been unable to demonstrate any permanent clinical neurocognitive or memory decline.”
Symptoms affecting the brain that sometimes accompany decompression sickness include slowed thought processes, confusion, unresponsiveness and permanent memory loss.
The study found that pilots had nearly four times the volume and three times the number of brain lesions as non-pilots. The results were the same whether or not the pilots had a history of symptoms of decompression sickness.
The research also found that while the lesions in non-pilots were mainly found in the frontal white matter, as occurs in normal aging, lesions in the pilots were evenly distributed throughout the brain.
“These results may be valuable in assessing risk for occupations that include high-altitude mountain climbing, deep sea diving and high-altitude flying,” McGuire said.

neurosciencestuff:

High-Flying Pilots at Increased Risk of Brain Lesions

A new study suggests that pilots who fly at high altitudes may be at an increased risk for brain lesions. The study is published in the August 20, 2013, print issue of Neurology®, the medical journal of the American Academy of Neurology.

For the study, 102 U-2 United States Air Force pilots and 91 non-pilots between the ages of 26 and 50 underwent MRI brain scans. The scans measured the amount of white matter hyperintensities, or tiny brain lesions associated with memory decline in other neurological diseases. The groups were matched for age, education and health factors.

“Pilots who fly at altitudes above 18,000 feet are at risk for decompression sickness, a condition where gas or atmospheric pressure reaches lower levels than those within body tissues and forms bubbles,” said study author Stephen McGuire, MD, with the University of Texas in San Antonio, the US Air Force School of Aerospace Medicine and a Fellow of the American Academy of Neurology. “The risk for decompression sickness among Air Force pilots has tripled from 2006, probably due to more frequent and longer periods of exposure for pilots. To date however, we have been unable to demonstrate any permanent clinical neurocognitive or memory decline.”

Symptoms affecting the brain that sometimes accompany decompression sickness include slowed thought processes, confusion, unresponsiveness and permanent memory loss.

The study found that pilots had nearly four times the volume and three times the number of brain lesions as non-pilots. The results were the same whether or not the pilots had a history of symptoms of decompression sickness.

The research also found that while the lesions in non-pilots were mainly found in the frontal white matter, as occurs in normal aging, lesions in the pilots were evenly distributed throughout the brain.

“These results may be valuable in assessing risk for occupations that include high-altitude mountain climbing, deep sea diving and high-altitude flying,” McGuire said.

neurosciencestuff
neurosciencestuff:

New models advance the study of deadly human prion diseases
By directly manipulating a portion of the prion protein-coding gene, Whitehead Institute researchers have created mouse models of two neurodegenerative diseases that are fatal in humans. The highly accurate reproduction of disease pathology seen with these models should advance the study of these unusual but deadly diseases. 
“By altering single amino acid codons in the gene coding for the prion protein, in the natural context of the genome—no over expression or other artificial manipulations—we can produce completely different neurodegenerative diseases, each of which spontaneously generates an infectious prion agent,” says Whitehead Member Susan Lindquist. “The work irrefutably establishes the prion hypothesis.”
According to the prion hypothesis, prion proteins infect by passing along their misfolded shape in templated fashion, unlike viruses or bacteria, which depend on DNA or RNA to transmit their information. Certain changes to the prion protein (PrP) create a misshapen structure, which is replicated by contact. The misfolded proteins accumulate, creating clumps that are toxic to surrounding tissue. 
PrP is expressed at high levels in the brain, and prion diseases, including Creutzfeldt-Jakob disease (CJD) in humans, bovine spongiform encephalopathy (BSE, or “mad cow disease”) in cows, and scrapie in sheep, wreak havoc on the brain and other neural tissues. Some prion diseases, like BSE, can be transmitted from feed animals to humans.
The study of these highly unusual but devastating prion diseases has to date been thwarted by a lack of animal models that faithfully mimic the disease processes in humans. However, Walker Jackson, a former postdoctoral researcher in Lindquist’s lab is changing that, creating novel mouse models of human fatal familial insomnia (FFI) and CJD. His research is reported online this week in the Proceedings of the National Academy of Sciences (PNAS).
To generate the models, Jackson created two mutated versions of the PrP-coding gene by changing a single codon—one of the three-nucleotide “words” in genes that code for the various amino acids in proteins. One mutation is known to cause FFI, while the other induces CJD. Unlike previous models that randomly inserted the mutations into the genome, occasionally increasing PrP expression, Jackson’s models faithfully mimic the human disease—from as to disease onset, to PrP production, to infectiousness. In the brain, his FFI mice develop neuronal loss in the thalamus and his CJD mice experience spongiosis in the hippocampus and the cerebellum, reflecting the damage seen in the brains of human patients.
“Walker (Jackson)’s work provides two extraordinary models of neurodegeneration,” says Lindquist, who is also a professor of biology at MIT. “Most mouse models produce pathology that only distantly resembles human diseases. These nail it, for two of the most enigmatic human diseases in the world.”
With the FFI and CJD models in hand, Jackson says he’s excited to investigate how the pathology of these diseases develops.
“Now we have two interesting models that are selectively targeting specific parts of the brain: the thalamus in FFI and the hippocampus in CJD,” says Jackson, who is now a Group Leader at the German Center for Neurodegenerative Disease. “But instead of focusing on areas that are heavily affected by the disease, we’ll be looking at the areas that seem to be resisting the disease to see what they’re doing. The protein is there, but for some reason, it’s not toxic.”
Initial characterization of one of the models (for FFI) was reporter earlier in Neuron.

neurosciencestuff:

New models advance the study of deadly human prion diseases

By directly manipulating a portion of the prion protein-coding gene, Whitehead Institute researchers have created mouse models of two neurodegenerative diseases that are fatal in humans. The highly accurate reproduction of disease pathology seen with these models should advance the study of these unusual but deadly diseases. 

“By altering single amino acid codons in the gene coding for the prion protein, in the natural context of the genome—no over expression or other artificial manipulations—we can produce completely different neurodegenerative diseases, each of which spontaneously generates an infectious prion agent,” says Whitehead Member Susan Lindquist. “The work irrefutably establishes the prion hypothesis.”

According to the prion hypothesis, prion proteins infect by passing along their misfolded shape in templated fashion, unlike viruses or bacteria, which depend on DNA or RNA to transmit their information. Certain changes to the prion protein (PrP) create a misshapen structure, which is replicated by contact. The misfolded proteins accumulate, creating clumps that are toxic to surrounding tissue. 

PrP is expressed at high levels in the brain, and prion diseases, including Creutzfeldt-Jakob disease (CJD) in humans, bovine spongiform encephalopathy (BSE, or “mad cow disease”) in cows, and scrapie in sheep, wreak havoc on the brain and other neural tissues. Some prion diseases, like BSE, can be transmitted from feed animals to humans.

The study of these highly unusual but devastating prion diseases has to date been thwarted by a lack of animal models that faithfully mimic the disease processes in humans. However, Walker Jackson, a former postdoctoral researcher in Lindquist’s lab is changing that, creating novel mouse models of human fatal familial insomnia (FFI) and CJD. His research is reported online this week in the Proceedings of the National Academy of Sciences (PNAS).

To generate the models, Jackson created two mutated versions of the PrP-coding gene by changing a single codon—one of the three-nucleotide “words” in genes that code for the various amino acids in proteins. One mutation is known to cause FFI, while the other induces CJD. Unlike previous models that randomly inserted the mutations into the genome, occasionally increasing PrP expression, Jackson’s models faithfully mimic the human disease—from as to disease onset, to PrP production, to infectiousness. In the brain, his FFI mice develop neuronal loss in the thalamus and his CJD mice experience spongiosis in the hippocampus and the cerebellum, reflecting the damage seen in the brains of human patients.

“Walker (Jackson)’s work provides two extraordinary models of neurodegeneration,” says Lindquist, who is also a professor of biology at MIT. “Most mouse models produce pathology that only distantly resembles human diseases. These nail it, for two of the most enigmatic human diseases in the world.”

With the FFI and CJD models in hand, Jackson says he’s excited to investigate how the pathology of these diseases develops.

“Now we have two interesting models that are selectively targeting specific parts of the brain: the thalamus in FFI and the hippocampus in CJD,” says Jackson, who is now a Group Leader at the German Center for Neurodegenerative Disease. “But instead of focusing on areas that are heavily affected by the disease, we’ll be looking at the areas that seem to be resisting the disease to see what they’re doing. The protein is there, but for some reason, it’s not toxic.”

Initial characterization of one of the models (for FFI) was reporter earlier in Neuron.

neurosciencestuff
neurosciencestuff:

Building Better Brain Implants: The Challenge of Longevity 
On August 20, JoVE, the Journal of Visualized Experiments will publish a technique from the Capadona Lab at Case Western Reserve University to accommodate two challenges inherent in brain-implantation technology, gauging the property changes that occur during implantation and measuring on a micro-scale. These new techniques open the doors for solving a great challenge for bioengineers — crafting a device that can withstand the physiological conditions in the brain for the long-term.
“We created an instrument to measure the mechanical properties of micro-scale biomedical implants, after being explanted from living animals,” explained the lab’s principal investigator, Dr. Jeffrey R. Capadona. By preserving the changing properties that occurred during implantation even after removal, the technique offers potential to create and test new materials for brain implant devices. It could result in producing longer lasting and better suited devices for the highly-tailored functions.
For implanted devices, withstanding the high-temperatures, moisture, and other in-vivo properties poses a challenge to longevity. Resulting changes in stiffness, etc, of an implanted material can trigger a greater inflammatory response. “Often, the body’s reaction to those implants causes the device to prematurely fail,” says Dr. Capadona, “In some cases, the patient requires regular brain surgery to replace or revise the implants.”
New implantation materials may help find solutions to restore motor function in individuals who have suffered from spinal cord injuries, stroke or multiple sclerosis. “Microelectrodes embedded chronically in the brain could hold promise for using neural activity to restore motor function in individuals who have, suffered from spinal cord injuries,” said Dr. Capadona.
Furthermore, Capadona and his colleagues’ method allows for measurement of mechanical properties using microsize scales. Previous methods typically require large or nano-sized samples of material, and data has to be scaled, which doesn’t always work.
When asked why Dr. Capadona and his colleagues published their methods with JoVE, he responded “We choose JoVE because of the novel format to show readers visually what we are doing. If a picture is worth [a] thousand words, a video is worth a million.”

neurosciencestuff:

Building Better Brain Implants: The Challenge of Longevity

On August 20, JoVE, the Journal of Visualized Experiments will publish a technique from the Capadona Lab at Case Western Reserve University to accommodate two challenges inherent in brain-implantation technology, gauging the property changes that occur during implantation and measuring on a micro-scale. These new techniques open the doors for solving a great challenge for bioengineers — crafting a device that can withstand the physiological conditions in the brain for the long-term.

“We created an instrument to measure the mechanical properties of micro-scale biomedical implants, after being explanted from living animals,” explained the lab’s principal investigator, Dr. Jeffrey R. Capadona. By preserving the changing properties that occurred during implantation even after removal, the technique offers potential to create and test new materials for brain implant devices. It could result in producing longer lasting and better suited devices for the highly-tailored functions.

For implanted devices, withstanding the high-temperatures, moisture, and other in-vivo properties poses a challenge to longevity. Resulting changes in stiffness, etc, of an implanted material can trigger a greater inflammatory response. “Often, the body’s reaction to those implants causes the device to prematurely fail,” says Dr. Capadona, “In some cases, the patient requires regular brain surgery to replace or revise the implants.”

New implantation materials may help find solutions to restore motor function in individuals who have suffered from spinal cord injuries, stroke or multiple sclerosis. “Microelectrodes embedded chronically in the brain could hold promise for using neural activity to restore motor function in individuals who have, suffered from spinal cord injuries,” said Dr. Capadona.

Furthermore, Capadona and his colleagues’ method allows for measurement of mechanical properties using microsize scales. Previous methods typically require large or nano-sized samples of material, and data has to be scaled, which doesn’t always work.

When asked why Dr. Capadona and his colleagues published their methods with JoVE, he responded “We choose JoVE because of the novel format to show readers visually what we are doing. If a picture is worth [a] thousand words, a video is worth a million.”

neurosciencestuff
neurosciencestuff:

Sleep deprivation linked to junk food cravings
A sleepless night makes us more likely to reach for doughnuts or pizza than for whole grains and leafy green vegetables, suggests a new study from UC Berkeley that examines the brain regions that control food choices. The findings shed new light on the link between poor sleep and obesity.
Using functional magnetic resonance imaging (fMRI), UC Berkeley researchers scanned the brains of 23 healthy young adults, first after a normal night’s sleep and next, after a sleepless night. They found impaired activity in the sleep-deprived brain’s frontal lobe, which governs complex decision-making, but increased activity in deeper brain centers that respond to rewards. Moreover, the participants favored unhealthy snack and junk foods when they were sleep deprived.
“What we have discovered is that high-level brain regions required for complex judgments and decisions become blunted by a lack of sleep, while more primal brain structures that control motivation and desire are amplified,” said Matthew Walker, a UC Berkeley professor of psychology and neuroscience and senior author of the study published today (Tuesday, Aug. 6) in the journal Nature Communications.
Moreover, he added, “high-calorie foods also became significantly more desirable when participants were sleep-deprived. This combination of altered brain activity and decision-making may help explain why people who sleep less also tend to be overweight or obese.”
Previous studies have linked poor sleep to greater appetites, particularly for sweet and salty foods, but the latest findings provide a specific brain mechanism explaining why food choices change for the worse following a sleepless night, Walker said.
“These results shed light on how the brain becomes impaired by sleep deprivation, leading to the selection of more unhealthy foods and, ultimately, higher rates of obesity,” said Stephanie Greer, a doctoral student in Walker’s Sleep and Neuroimaging Laboratory and lead author of the paper. Another co-author of the study is Andrea Goldstein, also a doctoral student in Walker’s lab.
In this newest study, researchers measured brain activity as participants viewed a series of 80 food images that ranged from high-to low-calorie and healthy and unhealthy, and rated their desire for each of the items. As an incentive, they were given the food they most craved after the MRI scan.
Food choices presented in the experiment ranged from fruits and vegetables, such as strawberries, apples and carrots, to high-calorie burgers, pizza and doughnuts. The latter are examples of the more popular choices following a sleepless night.
On a positive note, Walker said, the findings indicate that “getting enough sleep is one factor that can help promote weight control by priming the brain mechanisms governing appropriate food choices.”

Oh damn

neurosciencestuff:

Sleep deprivation linked to junk food cravings

A sleepless night makes us more likely to reach for doughnuts or pizza than for whole grains and leafy green vegetables, suggests a new study from UC Berkeley that examines the brain regions that control food choices. The findings shed new light on the link between poor sleep and obesity.

Using functional magnetic resonance imaging (fMRI), UC Berkeley researchers scanned the brains of 23 healthy young adults, first after a normal night’s sleep and next, after a sleepless night. They found impaired activity in the sleep-deprived brain’s frontal lobe, which governs complex decision-making, but increased activity in deeper brain centers that respond to rewards. Moreover, the participants favored unhealthy snack and junk foods when they were sleep deprived.

“What we have discovered is that high-level brain regions required for complex judgments and decisions become blunted by a lack of sleep, while more primal brain structures that control motivation and desire are amplified,” said Matthew Walker, a UC Berkeley professor of psychology and neuroscience and senior author of the study published today (Tuesday, Aug. 6) in the journal Nature Communications.

Moreover, he added, “high-calorie foods also became significantly more desirable when participants were sleep-deprived. This combination of altered brain activity and decision-making may help explain why people who sleep less also tend to be overweight or obese.”

Previous studies have linked poor sleep to greater appetites, particularly for sweet and salty foods, but the latest findings provide a specific brain mechanism explaining why food choices change for the worse following a sleepless night, Walker said.

“These results shed light on how the brain becomes impaired by sleep deprivation, leading to the selection of more unhealthy foods and, ultimately, higher rates of obesity,” said Stephanie Greer, a doctoral student in Walker’s Sleep and Neuroimaging Laboratory and lead author of the paper. Another co-author of the study is Andrea Goldstein, also a doctoral student in Walker’s lab.

In this newest study, researchers measured brain activity as participants viewed a series of 80 food images that ranged from high-to low-calorie and healthy and unhealthy, and rated their desire for each of the items. As an incentive, they were given the food they most craved after the MRI scan.

Food choices presented in the experiment ranged from fruits and vegetables, such as strawberries, apples and carrots, to high-calorie burgers, pizza and doughnuts. The latter are examples of the more popular choices following a sleepless night.

On a positive note, Walker said, the findings indicate that “getting enough sleep is one factor that can help promote weight control by priming the brain mechanisms governing appropriate food choices.”

Oh damn