Neuroscience

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Posts tagged neuroscience

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Study shows cogntive benefit of lifelong bilingualism
Seniors who have spoken two languages since childhood are faster than single-language speakers at switching from one task to another, according to a study published in the January 9 issue of The Journal of Neuroscience. Compared to their monolingual peers, lifelong bilinguals also show different patterns of brain activity when making the switch, the study found.
The findings suggest the value of regular stimulating mental activity across the lifetime. As people age, cognitive flexibility — the ability to adapt to unfamiliar or unexpected circumstances — and related “executive” functions decline. Recent studies suggest lifelong bilingualism may reduce this decline — a boost that may stem from the experience of constantly switching between languages. However, how brain activity differs between older bilinguals and monolinguals was previously unclear.
In the current study, Brian T. Gold, PhD, and colleagues at the University of Kentucky College of Medicine, used functional magnetic resonance imaging (fMRI) to compare the brain activity of healthy bilingual seniors (ages 60-68) with that of healthy monolingual seniors as they completed a task that tested their cognitive flexibility. The researchers found that both groups performed the task accurately. However, bilingual seniors were faster at completing the task than their monolingual peers despite expending less energy in the frontal cortex — an area known to be involved in task switching.
“This study provides some of the first evidence of an association between a particular cognitively stimulating activity — in this case, speaking multiple languages on a daily basis — and brain function,” said John L. Woodard, PhD, an aging expert from Wayne State University, who was not involved with the study. “The authors provide clear evidence of a different pattern of neural functioning in bilingual versus monolingual individuals.”
The researchers also measured the brain activity of younger bilingual and monolingual adults while they performed the cognitive flexibility task.
Overall, the young adults were faster than the seniors at performing the task. Being bilingual did not affect task performance or brain activity in the young participants. In contrast, older bilinguals performed the task faster than their monolingual peers and expended less energy in the frontal parts of their brain.
“This suggests that bilingual seniors use their brains more efficiently than monolingual seniors,” Gold said. “Together, these results suggest that lifelong bilingualism may exert its strongest benefits on the functioning of frontal brain regions in aging.”
(Image: Harriet Russell)

Study shows cogntive benefit of lifelong bilingualism

Seniors who have spoken two languages since childhood are faster than single-language speakers at switching from one task to another, according to a study published in the January 9 issue of The Journal of Neuroscience. Compared to their monolingual peers, lifelong bilinguals also show different patterns of brain activity when making the switch, the study found.

The findings suggest the value of regular stimulating mental activity across the lifetime. As people age, cognitive flexibility — the ability to adapt to unfamiliar or unexpected circumstances — and related “executive” functions decline. Recent studies suggest lifelong bilingualism may reduce this decline — a boost that may stem from the experience of constantly switching between languages. However, how brain activity differs between older bilinguals and monolinguals was previously unclear.

In the current study, Brian T. Gold, PhD, and colleagues at the University of Kentucky College of Medicine, used functional magnetic resonance imaging (fMRI) to compare the brain activity of healthy bilingual seniors (ages 60-68) with that of healthy monolingual seniors as they completed a task that tested their cognitive flexibility. The researchers found that both groups performed the task accurately. However, bilingual seniors were faster at completing the task than their monolingual peers despite expending less energy in the frontal cortex — an area known to be involved in task switching.

“This study provides some of the first evidence of an association between a particular cognitively stimulating activity — in this case, speaking multiple languages on a daily basis — and brain function,” said John L. Woodard, PhD, an aging expert from Wayne State University, who was not involved with the study. “The authors provide clear evidence of a different pattern of neural functioning in bilingual versus monolingual individuals.”

The researchers also measured the brain activity of younger bilingual and monolingual adults while they performed the cognitive flexibility task.

Overall, the young adults were faster than the seniors at performing the task. Being bilingual did not affect task performance or brain activity in the young participants. In contrast, older bilinguals performed the task faster than their monolingual peers and expended less energy in the frontal parts of their brain.

“This suggests that bilingual seniors use their brains more efficiently than monolingual seniors,” Gold said. “Together, these results suggest that lifelong bilingualism may exert its strongest benefits on the functioning of frontal brain regions in aging.”

(Image: Harriet Russell)

Filed under bilingualism brain activity cognitive flexibility cognition aging psychology neuroscience science

146 notes

Simulated Mars Mission Reveals Body’s Sodium Rhythms
Clinical pharmacologist Jens Titze, M.D., knew he had a one-of-a-kind scientific opportunity: the Russians were going to simulate a flight to Mars, and he was invited to study the participating cosmonauts.
Titze, now an associate professor of Medicine at Vanderbilt University, wanted to explore long-term sodium balance in humans. He didn’t believe the textbook view – that the salt we eat is rapidly excreted in urine to maintain relatively constant body sodium levels. The “Mars500” simulation gave him the chance to keep salt intake constant and monitor urine sodium levels in humans over a long period of time.
Now, in the Jan. 8 issue of Cell Metabolism, Titze and his colleagues report that – in contrast to the prevailing dogma – sodium levels fluctuate rhythmically with 7-day and monthly cycles. The findings, which demonstrate that sodium is stored in the body, have implications for blood pressure control, hypertension and salt-associated cardiovascular risk.
Titze’s interest in sodium balance was sparked by human space flight simulation studies he conducted in the 1990s that showed rhythmic variations in sodium urine excretion.“It was so clear to me that sodium must be stored in the body, but no one wanted to hear about that because it was so different from the textbook view,” he said.
He and his team persisted with animal studies and demonstrated that the skin stores sodium and that the immune system regulates sodium release from the skin.
In 2005, planning began for Mars500 – a collaboration between Russia, the European Union and China to prepare for manned spaceflight to Mars. Mars500 was conducted at a research facility in Moscow between 2007 and 2011 in three phases: a 15-day phase to test the equipment, a 105-day phase, and a 520-day phase to simulate a full-length manned mission.
Crews of healthy male cosmonauts volunteered to live and work in an enclosed habitat of sealed interconnecting modules, as if they were on an international space station. Titze and his colleagues organized the food for the mission and secured commitments from the participants to consume all of the food and to collect all urine each day. They studied twelve men: six for the full 105-day phase of the program, and six for the first 205 days of the 520-day phase.
“It was the participants’ stamina to precisely adhere to the daily menu plans and to accurately collect their urine for months that allowed scientific discovery,” Titze said. The researchers found that nearly all (95 percent) of the ingested salt was excreted in the urine, but not on a daily basis. Instead, at constant salt intake, sodium excretion fluctuated with a weekly rhythm, resulting in sodium storage. The levels of the hormones aldosterone (a regulator of sodium excretion) and cortisol (no known major role in sodium balance) also fluctuated weekly.
Changes in total body sodium levels fluctuated on monthly and longer cycles, Titze said. Sodium storage on this longer cycle was independent of salt intake and did not include weight gain, supporting the idea that sodium is stored without accompanying increases in water.
The findings suggest that current medical practice and studies that rely on 24-hour urine samples to determine salt intake are not accurate, he said. “We understand now that there are 7-day and monthly sodium clocks that are ticking, so a one-day snapshot shouldn’t be used to determine salt intake.”
Using newly developed magnetic resonance imaging (MRI) technologies to view sodium, Titze and his colleagues have found that humans store sodium in skin (as they found in their animal studies) and in muscle.
The investigators suspect that genes related to the circadian “clock” genes, which regulate daily rhythms, may be involved in sodium storage and release. “We find these long rhythms of sodium storage in the body particularly intriguing,” Titze said. “The observations open up entirely new avenues for research.”

Simulated Mars Mission Reveals Body’s Sodium Rhythms

Clinical pharmacologist Jens Titze, M.D., knew he had a one-of-a-kind scientific opportunity: the Russians were going to simulate a flight to Mars, and he was invited to study the participating cosmonauts.

Titze, now an associate professor of Medicine at Vanderbilt University, wanted to explore long-term sodium balance in humans. He didn’t believe the textbook view – that the salt we eat is rapidly excreted in urine to maintain relatively constant body sodium levels. The “Mars500” simulation gave him the chance to keep salt intake constant and monitor urine sodium levels in humans over a long period of time.

Now, in the Jan. 8 issue of Cell Metabolism, Titze and his colleagues report that – in contrast to the prevailing dogma – sodium levels fluctuate rhythmically with 7-day and monthly cycles. The findings, which demonstrate that sodium is stored in the body, have implications for blood pressure control, hypertension and salt-associated cardiovascular risk.

Titze’s interest in sodium balance was sparked by human space flight simulation studies he conducted in the 1990s that showed rhythmic variations in sodium urine excretion.
“It was so clear to me that sodium must be stored in the body, but no one wanted to hear about that because it was so different from the textbook view,” he said.

He and his team persisted with animal studies and demonstrated that the skin stores sodium and that the immune system regulates sodium release from the skin.

In 2005, planning began for Mars500 – a collaboration between Russia, the European Union and China to prepare for manned spaceflight to Mars. Mars500 was conducted at a research facility in Moscow between 2007 and 2011 in three phases: a 15-day phase to test the equipment, a 105-day phase, and a 520-day phase to simulate a full-length manned mission.

Crews of healthy male cosmonauts volunteered to live and work in an enclosed habitat of sealed interconnecting modules, as if they were on an international space station. Titze and his colleagues organized the food for the mission and secured commitments from the participants to consume all of the food and to collect all urine each day. They studied twelve men: six for the full 105-day phase of the program, and six for the first 205 days of the 520-day phase.

“It was the participants’ stamina to precisely adhere to the daily menu plans and to accurately collect their urine for months that allowed scientific discovery,” Titze said. The researchers found that nearly all (95 percent) of the ingested salt was excreted in the urine, but not on a daily basis. Instead, at constant salt intake, sodium excretion fluctuated with a weekly rhythm, resulting in sodium storage. The levels of the hormones aldosterone (a regulator of sodium excretion) and cortisol (no known major role in sodium balance) also fluctuated weekly.

Changes in total body sodium levels fluctuated on monthly and longer cycles, Titze said. Sodium storage on this longer cycle was independent of salt intake and did not include weight gain, supporting the idea that sodium is stored without accompanying increases in water.

The findings suggest that current medical practice and studies that rely on 24-hour urine samples to determine salt intake are not accurate, he said. “We understand now that there are 7-day and monthly sodium clocks that are ticking, so a one-day snapshot shouldn’t be used to determine salt intake.”

Using newly developed magnetic resonance imaging (MRI) technologies to view sodium, Titze and his colleagues have found that humans store sodium in skin (as they found in their animal studies) and in muscle.

The investigators suspect that genes related to the circadian “clock” genes, which regulate daily rhythms, may be involved in sodium storage and release. “We find these long rhythms of sodium storage in the body particularly intriguing,” Titze said. “The observations open up entirely new avenues for research.”

Filed under Mars500 simulation immune system sodium sodium balance space mission 520-day simulation neuroscience science

217 notes

520-Day Simulated Mission to Mars Reveals Critical Data about Sleep and Activity Needs for Astronauts
In the first study of its kind, a team of researchers led by faculty at the Perelman School of Medicine at the University of Pennsylvania and the Baylor College of Medicine, has analyzed data on the impact of prolonged operational confinement on sleep, performance, and mood in astronauts from a groundbreaking international effort to simulate a 520-day space mission to Mars. The findings, published online-first in the Proceedings of the National Academy of Sciences, revealed alterations of life-sustaining sleep patterns and neurobehavioral consequences for crew members that must be addressed for successful adaption to prolonged space missions.
"The success of human interplanetary spaceflight, which is anticipated to be in this century, will depend on the ability of astronauts to remain confined and isolated from Earth much longer than previous missions or simulations," said David F. Dinges, PhD, professor and chief, Division of Sleep and Chronobiology in the Department of Psychiatry at the Perelman School of Medicine, and co-lead author of the new study. "This is the first investigation to pinpoint the crucial role that sleep-wake cycles will play in extended space missions."
The 520-day simulation, which was developed by the Institute for Biomedical Problems (IBMP) of the Russian Academy of Sciences, and sponsored in part by the European Space Agency (ESA), was initiated on June 3, 2010 when the hatches were closed on a 550-cubic-meter IBMP spacecraft-like confinement facility in Russia. The simulated mission, involving an international, six-man team of volunteers, involved more than 90 experiments and realistic scenarios to gather valuable psychological and medical data on the effects of a long-term deep space flight. The 520-day mission was broken into three phases: 250 days for the trip to Mars, 30 days on the surface, and 240 days for the return to Earth.
“As the only U.S. research team involved with the Mars 520-day simulation, the study required international coordination and strong collaborations to ensure that the experiments were conducted in a thorough and rigorous manner,” said Jeffrey P. Sutton, MD, PhD, professor and director, Center for Space Medicine at Baylor College of Medicine, and senior study author. The investigators monitored the crew’s rest-activity patterns, performance and psychological responses to determine the extent to which sleep loss, fatigue, stress, mood changes and conflicts occurred during the mission.
Measurements included continuous recordings of body movements using wrist actigraphy (a noninvasive means of estimating sleep and movement intensity), and light exposure and weekly computer-based neurobehavioral assessments to identify changes in the crew’s activity levels, sleep quantity and quality, sleep–wake intervals, alertness performance, and workload throughout the 17 months of mission confinement.
Data from the actigraph devices revealed that crew sedentariness increased across the mission, as illustrated by decreased waking movement and increased sleep and rest times. The majority of crewmembers also experienced one or more disturbances of sleep quality, alertness deficits, or altered sleep–wake intervals and timing, suggesting inadequate circadian synchronization.
"Taken together, these measurements point to the need to identify markers of differential vulnerability to abnormal decrease in muscular movement and sleep– wake changes in crew members during the prolonged isolation of exploration spaceflight and the need to ensure maintenance of the Earth’s natural circadian rhythm, sleep quantity and quality, and optimal activity levels during exploration missions," said Mathias Basner, MD, PhD, MSc, assistant professor of Sleep and Chronobiology in Psychiatry at Penn, and co-lead author.
The research team concludes that successful adaptation to such missions will require crews to transit in spacecraft and live in surface habitats that artificially mimic aspects of Earth’s sleep-wake activity cycles, such as appropriately timed light exposure, food intake, and exercise. This dynamic will be necessary to maintain neurocognition and human behavior throughout the flight.

520-Day Simulated Mission to Mars Reveals Critical Data about Sleep and Activity Needs for Astronauts

In the first study of its kind, a team of researchers led by faculty at the Perelman School of Medicine at the University of Pennsylvania and the Baylor College of Medicine, has analyzed data on the impact of prolonged operational confinement on sleep, performance, and mood in astronauts from a groundbreaking international effort to simulate a 520-day space mission to Mars. The findings, published online-first in the Proceedings of the National Academy of Sciences, revealed alterations of life-sustaining sleep patterns and neurobehavioral consequences for crew members that must be addressed for successful adaption to prolonged space missions.

"The success of human interplanetary spaceflight, which is anticipated to be in this century, will depend on the ability of astronauts to remain confined and isolated from Earth much longer than previous missions or simulations," said David F. Dinges, PhD, professor and chief, Division of Sleep and Chronobiology in the Department of Psychiatry at the Perelman School of Medicine, and co-lead author of the new study. "This is the first investigation to pinpoint the crucial role that sleep-wake cycles will play in extended space missions."

The 520-day simulation, which was developed by the Institute for Biomedical Problems (IBMP) of the Russian Academy of Sciences, and sponsored in part by the European Space Agency (ESA), was initiated on June 3, 2010 when the hatches were closed on a 550-cubic-meter IBMP spacecraft-like confinement facility in Russia. The simulated mission, involving an international, six-man team of volunteers, involved more than 90 experiments and realistic scenarios to gather valuable psychological and medical data on the effects of a long-term deep space flight. The 520-day mission was broken into three phases: 250 days for the trip to Mars, 30 days on the surface, and 240 days for the return to Earth.

“As the only U.S. research team involved with the Mars 520-day simulation, the study required international coordination and strong collaborations to ensure that the experiments were conducted in a thorough and rigorous manner,” said Jeffrey P. Sutton, MD, PhD, professor and director, Center for Space Medicine at Baylor College of Medicine, and senior study author. The investigators monitored the crew’s rest-activity patterns, performance and psychological responses to determine the extent to which sleep loss, fatigue, stress, mood changes and conflicts occurred during the mission.

Measurements included continuous recordings of body movements using wrist actigraphy (a noninvasive means of estimating sleep and movement intensity), and light exposure and weekly computer-based neurobehavioral assessments to identify changes in the crew’s activity levels, sleep quantity and quality, sleep–wake intervals, alertness performance, and workload throughout the 17 months of mission confinement.

Data from the actigraph devices revealed that crew sedentariness increased across the mission, as illustrated by decreased waking movement and increased sleep and rest times. The majority of crewmembers also experienced one or more disturbances of sleep quality, alertness deficits, or altered sleep–wake intervals and timing, suggesting inadequate circadian synchronization.

"Taken together, these measurements point to the need to identify markers of differential vulnerability to abnormal decrease in muscular movement and sleep– wake changes in crew members during the prolonged isolation of exploration spaceflight and the need to ensure maintenance of the Earth’s natural circadian rhythm, sleep quantity and quality, and optimal activity levels during exploration missions," said Mathias Basner, MD, PhD, MSc, assistant professor of Sleep and Chronobiology in Psychiatry at Penn, and co-lead author.

The research team concludes that successful adaptation to such missions will require crews to transit in spacecraft and live in surface habitats that artificially mimic aspects of Earth’s sleep-wake activity cycles, such as appropriately timed light exposure, food intake, and exercise. This dynamic will be necessary to maintain neurocognition and human behavior throughout the flight.

Filed under 520-day simulation astronauts muscular movement sleep sleep-wake cycles space missions circadian rhythms neuroscience science

225 notes

Out of Sight, Out of Mind? How the brain codes its surroundings beyond the field of view
Even when they are not directly in sight, we are aware of our surroundings: so it is that when our eyes are fixed on an interesting book, for example, we know that the door is to the right, the bookshelf is to the left and the window is behind us. However, research into the brain has so far concerned itself predominantly with how information from our field of vision is coded in the visual cortex. To date it has not been known how the brain codes our surroundings beyond the field of view from an egocentric perspective (that is, from the point of view of the observer).
In the latest issue of the renowned journal Current Biology, Andreas Schindler und Andreas Bartels, scientists at the Werner Reichardt Center for Integrative Neuroscience (CIN) of the University of Tübingen, present for the first time direct evidence of this kind of spatial information in the brain.
The participants in their study found themselves in the center of a virtual octagonal room, with a unique object in each corner. As the brain’s activity was monitored by means of functional magnetic resonance imaging, the participants stood in front of one corner and looked at its object. Now they were instructed to determine the position of a second randomly chosen object within the room relative to their current perspective (for example, the object behind them). After a few trials the participant turned around so that the next object was brought into the field of view and the task was set up again. The whole procedure was repeated until every object had been looked at once.
The scientists discovered that patterns of activity in the parietal cortex code the participant’s egocentric position, that is, the relative position to his or her surroundings. The spatial information discovered there proved to be independent of the particular object, its absolute position in the room or that of the observer – i.e. it encoded egocentric spatial information of the three-dimensional surroundings. This result turns out to be particularly interesting because damage to the brain in the parietal cortex can lead to serious disruption of egocentric spatial awareness. Hence it is difficult for patients suffering from optical ataxia to carry out coordinated grasping movements. Lesions in the parietal cortex can also lead to a symptom called spatial neglect where patients have difficulties in perceiving their surroundings on the side opposite to the lesion. The brain areas identified in the present study coincided precisely with the areas of brain damage in such patients and provide for the first time insights regarding their function in the healthy brain.

Out of Sight, Out of Mind? How the brain codes its surroundings beyond the field of view

Even when they are not directly in sight, we are aware of our surroundings: so it is that when our eyes are fixed on an interesting book, for example, we know that the door is to the right, the bookshelf is to the left and the window is behind us. However, research into the brain has so far concerned itself predominantly with how information from our field of vision is coded in the visual cortex. To date it has not been known how the brain codes our surroundings beyond the field of view from an egocentric perspective (that is, from the point of view of the observer).

In the latest issue of the renowned journal Current Biology, Andreas Schindler und Andreas Bartels, scientists at the Werner Reichardt Center for Integrative Neuroscience (CIN) of the University of Tübingen, present for the first time direct evidence of this kind of spatial information in the brain.

The participants in their study found themselves in the center of a virtual octagonal room, with a unique object in each corner. As the brain’s activity was monitored by means of functional magnetic resonance imaging, the participants stood in front of one corner and looked at its object. Now they were instructed to determine the position of a second randomly chosen object within the room relative to their current perspective (for example, the object behind them). After a few trials the participant turned around so that the next object was brought into the field of view and the task was set up again. The whole procedure was repeated until every object had been looked at once.

The scientists discovered that patterns of activity in the parietal cortex code the participant’s egocentric position, that is, the relative position to his or her surroundings. The spatial information discovered there proved to be independent of the particular object, its absolute position in the room or that of the observer – i.e. it encoded egocentric spatial information of the three-dimensional surroundings. This result turns out to be particularly interesting because damage to the brain in the parietal cortex can lead to serious disruption of egocentric spatial awareness. Hence it is difficult for patients suffering from optical ataxia to carry out coordinated grasping movements. Lesions in the parietal cortex can also lead to a symptom called spatial neglect where patients have difficulties in perceiving their surroundings on the side opposite to the lesion. The brain areas identified in the present study coincided precisely with the areas of brain damage in such patients and provide for the first time insights regarding their function in the healthy brain.

Filed under brain brain activity visual cortex spatial awareness parietal cortex neuroscience science

46 notes

Cell Loss in the Brain Relates to Variations in Individual Symptoms in Huntington’s Disease

Scientists have wrestled to understand why Huntington’s disease, which is caused by a single gene mutation, can produce such variable symptoms. An authoritative review by a group of leading experts summarizes the progress relating cell loss in the striatum and cerebral cortex to symptom profile in Huntington’s disease, suggesting a possible direction for developing targeted therapies. The article is published in the latest issue of the Journal of Huntington’s Disease.

Huntington’s disease (HD) is an inherited progressive neurological disorder for which there is presently no cure. It is caused by a dominant mutation in the HD gene leading to expression of mutant huntingtin (HTT) protein. Expression of mutant HTT causes subtle changes in cellular functions, which ultimately results in jerking, uncontrollable movements, progressive psychiatric difficulties, and loss of mental abilities.

Although it is caused by a single gene, there are major variations in the symptoms of HD. The pattern of symptoms shown by each individual during the course of the disease can differ considerably and present as varying degrees of movement disturbances, cognitive decline, and mood and behavioral changes. Disease duration is typically between ten and twenty years.

Recent investigations have focused on what the presence of the defective gene does to various structures in the brain and understanding the relationship between changes in the brain and the variability in symptom profiles in Huntington’s disease.

Analyses of post-mortem human HD tissue suggest that the variation in clinical symptoms in HD is strongly associated with the variable pattern of neurodegeneration in two major regions of the brain, the striatum and the cerebral cortex. The neurodegeneration of the striatum generally follows an ordered and topographical distribution, but comparison of post-mortem human HD tissue and in vivo neuroimaging techniques reveal that the disease produces a striking bilateral atrophy of the striatum, which in these recent studies has been found to be highly variable.

“What is especially interesting is that recent findings suggest that the pattern of striatal cell death shows regional differences between cases in the functionally and neurochemically distinct striosomal and matrix compartments of the striatum which correspond with symptom variation,” says author Richard L.M. Faull, MB, ChB, PhD, DSc, Director of the Centre for Brain Research, University of Auckland, New Zealand.

“Our own recent detailed quantitative study using stereological cell counting in the post-mortem human HD cortex has complemented and expanded the neuroimaging studies by providing a cortical cellular basis of symptom heterogeneity in HD,” continues Dr Faull. “In particular, HD cases which were dominated by motor dysfunction showed a major total cell loss (28% loss) in the primary motor cortex but no cell loss in the limbic cingulate cortex, whereas cases where mood symptoms predominated showed a total of 54% neuronal loss in the limbic cingulate cortex but no cell loss in the motor cortex. This suggests that the variable neuronal loss and alterations in the circuitry of the primary motor cortex and anterior cingulate cortex associated with the variable compartmental pattern of cell degeneration in the striatum contribute to the differential impairments of motor and mood functions in HD.”

The authors note that there are still questions to be answered in the field of HD pathology, such as, how and when pathological neuronal loss occurs; whether the progressive loss of neurons in the striatum is the primary process or is consequential to cortical cell dysfunction; and how these changes relate to symptom profiles.

“What is clear however is that the diverse symptoms of HD patients appear to relate to the heterogeneity of cell loss in both the striatum and cerebral cortex,” the authors conclude. “While there is currently no cure, this contemporary evidence suggests that possible genetic therapies aimed at HD gene silencing should be directed towards intervention at both the cerebral cortex and the striatum in the human brain. This poses challenging problems requiring the application of gene silencing therapies to quite widespread regions of the forebrain which may be assisted via CSF delivery systems using gene suppression agents that cross the CSF/brain barrier.”

(Source: iospress.nl)

Filed under huntington’s disease neurodegeneration cell loss neuroimaging cognitive decline neuroscience science

71 notes

Cognitive deficits from concussions still present after two months
The ability to focus and switch tasks readily amid distractions was compromised for up to two months following brain concussions suffered by high school athletes, according to a study at the University of Oregon.
Research team members, in an interview, said the discovery suggests that some athletes may need longer recovery periods than current practices dictate to lower the risk of subsequent concussions. Conventional wisdom, said lead author David Howell, a graduate student in the UO Department of Human Physiology, says that typical recovery from concussion takes seven to 10 days.
"The differences we detected may be a matter of milliseconds between a concussed person and a control subject, but as far as brain time goes that difference for a linebacker returning to competition too soon could mean the difference between another injury or successfully preparing to safely tackle an oncoming running back," Howell said.
The findings are based on cognitive exercises used five times over the two months with a pair of sensitive computer-based measuring tools — the attentional network test and the task-switching test. The study focused on the effects of concussions to the frontal region of the brain, which is responsible for working, or short-term, memory and executive function, said Li-Shan Chou, professor of human physiology and director of the UO Motion Analysis Laboratory.
The study was published online ahead of print by Medicine & Science in Sports & Exercise, the official journal of the American College of Sports Medicine.

Cognitive deficits from concussions still present after two months

The ability to focus and switch tasks readily amid distractions was compromised for up to two months following brain concussions suffered by high school athletes, according to a study at the University of Oregon.

Research team members, in an interview, said the discovery suggests that some athletes may need longer recovery periods than current practices dictate to lower the risk of subsequent concussions. Conventional wisdom, said lead author David Howell, a graduate student in the UO Department of Human Physiology, says that typical recovery from concussion takes seven to 10 days.

"The differences we detected may be a matter of milliseconds between a concussed person and a control subject, but as far as brain time goes that difference for a linebacker returning to competition too soon could mean the difference between another injury or successfully preparing to safely tackle an oncoming running back," Howell said.

The findings are based on cognitive exercises used five times over the two months with a pair of sensitive computer-based measuring tools — the attentional network test and the task-switching test. The study focused on the effects of concussions to the frontal region of the brain, which is responsible for working, or short-term, memory and executive function, said Li-Shan Chou, professor of human physiology and director of the UO Motion Analysis Laboratory.

The study was published online ahead of print by Medicine & Science in Sports & Exercise, the official journal of the American College of Sports Medicine.

Filed under brain concussion brain injury cognitive deficits psychology neuroscience science

152 notes

Detrimental effect of obesity on lesions associated with Alzheimer’s disease
Researchers from Inserm and the Université Lille/Université Lille Nord de France have recently used a neurodegeneration model of Alzheimer’s disease to provide experimental evidence of the relationship between obesity and disorders linked to the tau protein. This research was conducted on mice and is published in the Diabetes review: it corroborates the theory that metabolic anomalies contribute massively to the development of dementia.
In France, more than 860,000 people suffer from Alzheimer’s disease and related disorders, making them the largest cause of age-related loss of intellectual function. Cognitive impairments observed in Alzheimer’s disease result from the accumulation of abnormal tau proteins in nerve cells undergoing degeneration (see the picture below). We know that obesity, a major risk factor in the development of insulin resistance and type 2 diabetes, increases the risk of dementia during the aging process. However, the effects of obesity on ‘Taupathies’ (i.e. tau protein-related disorders), including Alzheimer’s disease, were not clearly understood. In particular, researchers assumed that insulin resistance played a major role in terms of the effects of obesity.
The “Alzheimer & Tauopathies” team from mixed research unit 837 (Inserm/Université Lille 2/Université Lille Nord de France) directed by Dr. Luc Buée, in collaboration with mixed research unit 1011 “Nuclear receptors, cardiovascular diseases and diabetes”, have just demonstrated, in mice, that obese subjects develop aggravated disorders. To achieve this result, young transgenic mice, who develop tau-related neurodegeneration progressively with age, were put on a high-fat diet for five months, leading to progressive obesity.
“At the end of this diet, the obese mice had developed an aggravated disorder both from the point of view of memory and modifications to the Tau protein”, explains David Blum, in charge of research at Inserm.
This study uses a neurodenegeneration model of Alzheimer’s disease to provide experimental evidence of the relationship between obesity and disorders linked to the tau protein. Furthermore, it indicates that insulin resistance is not the aggravating factor, as was suggested in previous studies.
“Our research supports the theory that environmental factors contribute massively to the development of this neurodegenerative disorder” underlines the researcher. “Our work is now focussing on identifying the factors responsible for this aggravation” he adds.

Detrimental effect of obesity on lesions associated with Alzheimer’s disease

Researchers from Inserm and the Université Lille/Université Lille Nord de France have recently used a neurodegeneration model of Alzheimer’s disease to provide experimental evidence of the relationship between obesity and disorders linked to the tau protein. This research was conducted on mice and is published in the Diabetes review: it corroborates the theory that metabolic anomalies contribute massively to the development of dementia.

In France, more than 860,000 people suffer from Alzheimer’s disease and related disorders, making them the largest cause of age-related loss of intellectual function. Cognitive impairments observed in Alzheimer’s disease result from the accumulation of abnormal tau proteins in nerve cells undergoing degeneration (see the picture below). We know that obesity, a major risk factor in the development of insulin resistance and type 2 diabetes, increases the risk of dementia during the aging process. However, the effects of obesity on ‘Taupathies’ (i.e. tau protein-related disorders), including Alzheimer’s disease, were not clearly understood. In particular, researchers assumed that insulin resistance played a major role in terms of the effects of obesity.

The “Alzheimer & Tauopathies” team from mixed research unit 837 (Inserm/Université Lille 2/Université Lille Nord de France) directed by Dr. Luc Buée, in collaboration with mixed research unit 1011 “Nuclear receptors, cardiovascular diseases and diabetes”, have just demonstrated, in mice, that obese subjects develop aggravated disorders. To achieve this result, young transgenic mice, who develop tau-related neurodegeneration progressively with age, were put on a high-fat diet for five months, leading to progressive obesity.

“At the end of this diet, the obese mice had developed an aggravated disorder both from the point of view of memory and modifications to the Tau protein”, explains David Blum, in charge of research at Inserm.

This study uses a neurodenegeneration model of Alzheimer’s disease to provide experimental evidence of the relationship between obesity and disorders linked to the tau protein. Furthermore, it indicates that insulin resistance is not the aggravating factor, as was suggested in previous studies.

“Our research supports the theory that environmental factors contribute massively to the development of this neurodegenerative disorder” underlines the researcher. “Our work is now focussing on identifying the factors responsible for this aggravation” he adds.

Filed under tau protein neurodegenerative disorders obesity alzheimer's disease cognitive decline neuroscience science

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Molecular ‘Two-Way Radio’ Directs Nerve Cell Branching And Connectivity
Working with fruit flies, Johns Hopkins scientists have decoded the activity of protein signals that let certain nerve cells know when and where to branch so that they reach and connect to their correct muscle targets. The proteins’ mammalian counterparts are known to have signaling roles in immunity, nervous system and heart development, and tumor progression, suggesting broad implications for human disease research. A report of the research was published online Nov. 21 in the journal Neuron.
To control muscle movements, fruit flies, like other animals, have a set of nerve cells called motor neurons that connect muscle fibers to the nerve cord, a structure similar to the spinal cord, which in turn connects to the brain. During embryonic development, the nerve cells send wire-like projections, or axons, from the nerve cord structure out to their targets. Initially, multiple axons travel together in a convoy, but as they move forward, some axons must exit the “highway” at specific points to reach particular targets.
In their experiments, the researchers learned that axons travelling together have proteins on their surfaces that act like two-way radios, allowing the axons to communicate with each other and coordinate their travel patterns, thus ensuring that every muscle fiber gets connected to a nerve cell. “When axons fail to branch, or when they branch too early and too often, fruits flies, and presumably other animals, can be left without crucial muscle-nerve connections,” says Alex Kolodkin, Ph.D., a Howard Hughes investigator and professor of neuroscience at the Institute for Basic Biomedical Sciences at the Johns Hopkins University School of Medicine.
At the center of the communications system, Kolodkin says, is a protein called Sema-1a, already known to reside on the surface of motor neuron axons. If a neighboring axon has a different protein, called PlexA, on its surface, it will be repulsed by Sema-1a and will turn away from the axon bundle. So Sema-1a acts as an instructional signal and PlexA as its receptor. In the fruit fly study, the scientists discovered that Sema-1a can also act as a receptor for PlexA. “We used to think that this pair of surface proteins acted as a one-way radio, with information flowing in a single direction,” says Kolodkin. “What we found is that instructional information flows both ways.”
The Johns Hopkins team identified the “two-way” system by knocking out and otherwise manipulating fruit fly genes and then watching what happened to motor neuron branching. In these experiments, the researchers uncovered still other proteins located within the motor axons that Sema-1a interacts with after receiving a PlexA signal. When the gene for a protein called Pebble was deleted, for example, motor axons bunched together and didn’t branch. When the gene for RhoGAPp190 was deleted, motor axons branched too soon and failed to recognize their target muscles.
Through a series of biochemical tests, Kolodkin’s team found that Pebble and RhoGAPp190 both act on a third protein, Rho1. When Rho1 is activated, it collapses the supporting structures within an axon, making it “limp” and unable to continue toward a target. Sema-1a can bind to Pebble or to RhoGAPp190, and subsequently, these proteins can bind to Rho1. Binding to Pebble activates Rho1, causing axons to branch away from each other. However, binding to RhoGAPp190 shuts down Rho1, causing axons to remain bunched together. Thus, says Kolodkin, balance in the amounts of available Pebble and RhoGAPp190 can determine axon behavior, although what determines this balance is still unknown.
“This signaling is complex and we still don’t understand how it’s all controlled, but we’re one step closer now,” says Kolodkin. He notes that “a relative” of the Sema-1a protein in humans has already been implicated in schizophrenia, although details of this protein’s role in disease remain unclear. “Our experiments affirm how important this protein is to study and understand,” adds Kolodkin.

Molecular ‘Two-Way Radio’ Directs Nerve Cell Branching And Connectivity

Working with fruit flies, Johns Hopkins scientists have decoded the activity of protein signals that let certain nerve cells know when and where to branch so that they reach and connect to their correct muscle targets. The proteins’ mammalian counterparts are known to have signaling roles in immunity, nervous system and heart development, and tumor progression, suggesting broad implications for human disease research. A report of the research was published online Nov. 21 in the journal Neuron.

To control muscle movements, fruit flies, like other animals, have a set of nerve cells called motor neurons that connect muscle fibers to the nerve cord, a structure similar to the spinal cord, which in turn connects to the brain. During embryonic development, the nerve cells send wire-like projections, or axons, from the nerve cord structure out to their targets. Initially, multiple axons travel together in a convoy, but as they move forward, some axons must exit the “highway” at specific points to reach particular targets.

In their experiments, the researchers learned that axons travelling together have proteins on their surfaces that act like two-way radios, allowing the axons to communicate with each other and coordinate their travel patterns, thus ensuring that every muscle fiber gets connected to a nerve cell. “When axons fail to branch, or when they branch too early and too often, fruits flies, and presumably other animals, can be left without crucial muscle-nerve connections,” says Alex Kolodkin, Ph.D., a Howard Hughes investigator and professor of neuroscience at the Institute for Basic Biomedical Sciences at the Johns Hopkins University School of Medicine.

At the center of the communications system, Kolodkin says, is a protein called Sema-1a, already known to reside on the surface of motor neuron axons. If a neighboring axon has a different protein, called PlexA, on its surface, it will be repulsed by Sema-1a and will turn away from the axon bundle. So Sema-1a acts as an instructional signal and PlexA as its receptor. In the fruit fly study, the scientists discovered that Sema-1a can also act as a receptor for PlexA. “We used to think that this pair of surface proteins acted as a one-way radio, with information flowing in a single direction,” says Kolodkin. “What we found is that instructional information flows both ways.”

The Johns Hopkins team identified the “two-way” system by knocking out and otherwise manipulating fruit fly genes and then watching what happened to motor neuron branching. In these experiments, the researchers uncovered still other proteins located within the motor axons that Sema-1a interacts with after receiving a PlexA signal. When the gene for a protein called Pebble was deleted, for example, motor axons bunched together and didn’t branch. When the gene for RhoGAPp190 was deleted, motor axons branched too soon and failed to recognize their target muscles.

Through a series of biochemical tests, Kolodkin’s team found that Pebble and RhoGAPp190 both act on a third protein, Rho1. When Rho1 is activated, it collapses the supporting structures within an axon, making it “limp” and unable to continue toward a target. Sema-1a can bind to Pebble or to RhoGAPp190, and subsequently, these proteins can bind to Rho1. Binding to Pebble activates Rho1, causing axons to branch away from each other. However, binding to RhoGAPp190 shuts down Rho1, causing axons to remain bunched together. Thus, says Kolodkin, balance in the amounts of available Pebble and RhoGAPp190 can determine axon behavior, although what determines this balance is still unknown.

“This signaling is complex and we still don’t understand how it’s all controlled, but we’re one step closer now,” says Kolodkin. He notes that “a relative” of the Sema-1a protein in humans has already been implicated in schizophrenia, although details of this protein’s role in disease remain unclear. “Our experiments affirm how important this protein is to study and understand,” adds Kolodkin.

Filed under fruit flies nerve cells proteins motor neurons muscle movements nerve disorders neuroscience science

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Mechanism of hearing is similar to car battery
University of Iowa biologist Daniel Eberl and his colleagues have shown that one of the mechanisms involved in hearing is similar to the battery in your car.
And if that isn’t interesting enough, the UI scientists advanced their knowledge of human hearing by studying a similar auditory system in fruit flies—and by making use of the fruit fly “love song.”
To see how the mechanism of hearing resembles a battery, you need to know that the auditory system of the fruit fly contains a protein that functions as a sodium/potassium pump, often called the sodium pump for short, and is highly expressed in a specialized support cell called the scolopale cell.
The scolopale cell is important because it wraps around the sensory endings in the fly’s ear and makes a tight extra-cellular cavity or compartment around them called the scolopale space.
“You could think of these compartments as similar to the compartments of a battery that need to be charged up so they can drive electrons through circuits,” says Eberl, whose paper made the cover of the journal Proceedings of the National Academy of Sciences. “In the auditory system, the charge in the scolopale space drives ions, or electrically charged atoms, through membrane channels in the sensory endings that open briefly in response to activation by sounds.
“Our work shows that the sodium pump plays a particularly important role in this cell to help replenish or recharge this compartment with the right ions. The human ear also relies on a compartment called the scala media, which similarly drives ions into the sensory cells of the ear,” he says.
How was the research done? This is where the fruit fly love song comes into play.
Testing whether or not a fruit fly can hear the love song—a sound generated by a vibrating wing—enables Eberl to learn whether electrical recharging is occurring in the fly ear. The fruit fly love song played a role in the research by stimulating the fly to move whenever a sound was emitted and received.
“In these experiments we tested the fly’s hearing by inserting tiny electrodes in the fly’s antenna, then measuring the electrical responses when we play back computer-generated love songs,” he says.
Eberl notes there are many similarities between fruit fly and human mechanisms of hearing. That means his work on the fly model to identify additional new components required for generating the correct ion balance in the ear will help scientists to understand the human process in more detail.

Mechanism of hearing is similar to car battery

University of Iowa biologist Daniel Eberl and his colleagues have shown that one of the mechanisms involved in hearing is similar to the battery in your car.

And if that isn’t interesting enough, the UI scientists advanced their knowledge of human hearing by studying a similar auditory system in fruit flies—and by making use of the fruit fly “love song.”

To see how the mechanism of hearing resembles a battery, you need to know that the auditory system of the fruit fly contains a protein that functions as a sodium/potassium pump, often called the sodium pump for short, and is highly expressed in a specialized support cell called the scolopale cell.

The scolopale cell is important because it wraps around the sensory endings in the fly’s ear and makes a tight extra-cellular cavity or compartment around them called the scolopale space.

“You could think of these compartments as similar to the compartments of a battery that need to be charged up so they can drive electrons through circuits,” says Eberl, whose paper made the cover of the journal Proceedings of the National Academy of Sciences. “In the auditory system, the charge in the scolopale space drives ions, or electrically charged atoms, through membrane channels in the sensory endings that open briefly in response to activation by sounds.

“Our work shows that the sodium pump plays a particularly important role in this cell to help replenish or recharge this compartment with the right ions. The human ear also relies on a compartment called the scala media, which similarly drives ions into the sensory cells of the ear,” he says.

How was the research done? This is where the fruit fly love song comes into play.

Testing whether or not a fruit fly can hear the love song—a sound generated by a vibrating wing—enables Eberl to learn whether electrical recharging is occurring in the fly ear. The fruit fly love song played a role in the research by stimulating the fly to move whenever a sound was emitted and received.

“In these experiments we tested the fly’s hearing by inserting tiny electrodes in the fly’s antenna, then measuring the electrical responses when we play back computer-generated love songs,” he says.

Eberl notes there are many similarities between fruit fly and human mechanisms of hearing. That means his work on the fly model to identify additional new components required for generating the correct ion balance in the ear will help scientists to understand the human process in more detail.

Filed under hearing auditory system fruit flies sodium pump scala media ions neuroscience science

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All in the family: A genetic link between epilepsy and migraine

New research reveals a shared genetic susceptibility to epilepsy and migraine. Findings published in Epilepsia (DOI: 10.1111/epi.12072), a journal of the International League Against Epilepsy (ILAE), indicate that having a strong family history of seizure disorders increases the chance of having migraine with aura (MA).

Medical evidence has established that migraine and epilepsy often co-occur in patients; this co-occurrence is called “comorbidity.” Previous studies have found that people with epilepsy are substantially more likely than the general population to have migraine headache. However, it is not clear whether that comorbidity results from a shared genetic cause.

"Epilepsy and migraine are each individually influenced by genetic factors," explains lead author Dr. Melodie Winawer from Columbia University Medical Center in New York. "Our study is the first to confirm a shared genetic susceptibility to epilepsy and migraine in a large population of patients with common forms of epilepsy."

For the present study, Dr. Winawer and colleagues analyzed data collected from participants in the Epilepsy Phenome/Genome Project (EPGP)—a genetic study of epilepsy patients and families from 27 clinical centers in the U.S., Canada, Argentina, Australia, and New Zealand. The study examined one aspect of EPGP: sibling and parent-child pairs with focal epilepsy or generalized epilepsy of unknown cause. Most people with epilepsy have no family members affected with epilepsy. EPGP was designed to look at those rare families with more than one individual with epilepsy, in order to increase the chance of finding genetic causes of epilepsy.

Analysis of 730 participants with epilepsy from 501 families demonstrated that the prevalence of MA—when additional symptoms, such as blind spots or flashing lights, occur prior to the headache pain— was substantially increased when there were several individuals in the family with seizure disorders. EPGP study participants with epilepsy who had three or more additional close relatives with a seizure disorder were more than twice as likely to experience MA than patients from families with fewer individuals with seizures. In other words, the stronger the genetic effect on epilepsy in the family, the higher the rates of MA. This result provides evidence that a gene or genes exist that cause both epilepsy and migraine.

Identification of genetic contributions to the comorbidity of epilepsy with other disorders, like migraine, has implications for epilepsy patients. Prior research has shown that coexisting conditions impact the quality of life, treatment success, and mortality of epilepsy patients, with some experts suggesting that these comorbidities may have a greater impact on patients than the seizures themselves. In fact, comorbid conditions are emphasized in the National Institutes of Health Epilepsy Research Benchmarks and in a recent report on epilepsy from the Institute of Medicine.

"Our study demonstrates a strong genetic basis for migraine and epilepsy, because the rate of migraine is increased only in people who have close (rather than distant) relatives with epilepsy and only when three or more family members are affected," concludes Dr. Winawer. "Further investigation of the genetics of groups of comorbid disorders and epilepsy will help to improve the diagnosis and treatment of these comorbidities, and enhance the quality of life for those with epilepsy."

(Source: eurekalert.org)

Filed under epilepsy migraine genetic cause genetics neuroscience science

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