Neuroscience

Articles and news from the latest research reports.

Posts tagged neuroscience

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“Simplified” brain lets the iCub robot learn language 
The iCub humanoid robot on which the team directed by Peter Ford Dominey, CNRS Director of Research at Inserm Unit 846 known as the “Institut pour les cellules souches et cerveau de Lyon” [Lyon Institute for Stem Cell and Brain Research] (Inserm, CNRS, Université Claude Bernard Lyon 1) has been working for many years will now be able to understand what is being said to it and even anticipate the end of a sentence. This technological prowess was made possible by the development of a “simplified artificial brain” that reproduces certain types of so-called “recurrent” connections observed in the human brain. The artificial brain system enables the robot to learn, and subsequently understand, new sentences containing a new grammatical structure. It can link two sentences together and even predict how a sentence will end before it is uttered. This research has been published in the Plos One journal.

“Simplified” brain lets the iCub robot learn language

The iCub humanoid robot on which the team directed by Peter Ford Dominey, CNRS Director of Research at Inserm Unit 846 known as the “Institut pour les cellules souches et cerveau de Lyon” [Lyon Institute for Stem Cell and Brain Research] (Inserm, CNRS, Université Claude Bernard Lyon 1) has been working for many years will now be able to understand what is being said to it and even anticipate the end of a sentence. This technological prowess was made possible by the development of a “simplified artificial brain” that reproduces certain types of so-called “recurrent” connections observed in the human brain. The artificial brain system enables the robot to learn, and subsequently understand, new sentences containing a new grammatical structure. It can link two sentences together and even predict how a sentence will end before it is uttered. This research has been published in the Plos One journal.

Filed under robots robotics humanoids iCub language language processing neural networks ANN neuroscience science

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Language Protein Differs in Males, Females
Male rat pups have more of a specific brain protein associated with language development than females, according to a study published February 20 in The Journal of Neuroscience. The study also found sex differences in the brain protein in a small group of children. The findings may shed light on sex differences in communication in animals and language acquisition in people.
Sex differences in early language acquisition and development in children are well documented — on average, girls tend to speak earlier and with greater complexity than boys of the same age. However, scientists continue to debate the origin and significance of such differences. Previous studies showed the Foxp2 protein plays an important role in speech and language development in humans and vocal communication in birds and other mammals.
In the current study, J. Michael Bowers, PhD, Margaret McCarthy, PhD, and colleagues at the University of Maryland School of Medicine examined whether sex differences in the expression of the Foxp2 protein in the developing brain might underlie communication differences between the sexes.
The researchers analyzed the levels of Foxp2 protein in the brains of four-day-old female and male rats and compared the ultrasonic distress calls made by the animals when separated from their mothers and siblings. Compared with females, males had more of the protein in brain areas associated with cognition, emotion, and vocalization. They also made more noise than females — producing nearly double the total vocalizations over the five-minute separation period — and were preferentially retrieved and returned to the nest first by the mother.
When the researchers reduced levels of the Foxp2 protein in the male pups and increased it in female pups, they reversed the sex difference in the distress calls, causing males to sound like females and the females like males. This change led the mother to reverse her behavior as well, preferentially retrieving the females over the males.
“This study is one of the first to report a sex difference in the expression of a language-associated protein in humans or animals,” McCarthy said. “The findings raise the possibility that sex differences in brain and behavior are more pervasive and established earlier than previously appreciated.”
The researchers extended their findings to humans in a preliminary study of Foxp2 protein in a small group of children. Unlike the rats, in which Foxp2 protein was elevated in males, they found that in humans, the girls had more of the Foxp2 protein in the cortex — a brain region associated with language — than age-matched boys.
“At first glance, one might conclude that the findings in rats don’t generalize to humans, but the higher levels of Foxp2 expression are found in the more communicative sex in each species,” noted Cheryl Sisk, who studies sex differences at Michigan State University and was not involved with the study.

Language Protein Differs in Males, Females

Male rat pups have more of a specific brain protein associated with language development than females, according to a study published February 20 in The Journal of Neuroscience. The study also found sex differences in the brain protein in a small group of children. The findings may shed light on sex differences in communication in animals and language acquisition in people.

Sex differences in early language acquisition and development in children are well documented — on average, girls tend to speak earlier and with greater complexity than boys of the same age. However, scientists continue to debate the origin and significance of such differences. Previous studies showed the Foxp2 protein plays an important role in speech and language development in humans and vocal communication in birds and other mammals.

In the current study, J. Michael Bowers, PhD, Margaret McCarthy, PhD, and colleagues at the University of Maryland School of Medicine examined whether sex differences in the expression of the Foxp2 protein in the developing brain might underlie communication differences between the sexes.

The researchers analyzed the levels of Foxp2 protein in the brains of four-day-old female and male rats and compared the ultrasonic distress calls made by the animals when separated from their mothers and siblings. Compared with females, males had more of the protein in brain areas associated with cognition, emotion, and vocalization. They also made more noise than females — producing nearly double the total vocalizations over the five-minute separation period — and were preferentially retrieved and returned to the nest first by the mother.

When the researchers reduced levels of the Foxp2 protein in the male pups and increased it in female pups, they reversed the sex difference in the distress calls, causing males to sound like females and the females like males. This change led the mother to reverse her behavior as well, preferentially retrieving the females over the males.

“This study is one of the first to report a sex difference in the expression of a language-associated protein in humans or animals,” McCarthy said. “The findings raise the possibility that sex differences in brain and behavior are more pervasive and established earlier than previously appreciated.”

The researchers extended their findings to humans in a preliminary study of Foxp2 protein in a small group of children. Unlike the rats, in which Foxp2 protein was elevated in males, they found that in humans, the girls had more of the Foxp2 protein in the cortex — a brain region associated with language — than age-matched boys.

“At first glance, one might conclude that the findings in rats don’t generalize to humans, but the higher levels of Foxp2 expression are found in the more communicative sex in each species,” noted Cheryl Sisk, who studies sex differences at Michigan State University and was not involved with the study.

Filed under language development brain protein sex differences vocal communication vocalization neuroscience science

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Researchers discover a biological marker of dyslexia
Though learning to read proceeds smoothly for most children, as many as one in 10 is estimated to suffer from dyslexia, a constellation of impairments unrelated to intelligence, hearing or vision that make learning to read a struggle. Now, Northwestern University researchers report they have found a biological mechanism that appears to play an important role in the reading process.
"We discovered a systematic relationship between reading ability and the consistency with which the brain encodes sounds," says Nina Kraus, Hugh Knowles Professor of Neurobiology, Physiology and Communication. "Unstable Representation of Sound: A Biological Marker of Dyslexia," co-authored by Jane Hornickel, will appear in the Feb. 20 issue of The Journal of Neuroscience.
Recording the automatic brain wave responses of 100 school-aged children to speech sounds, the Northwestern researchers found that the very best readers encoded the sound most consistently while the poorest readers encoded it with the greatest inconsistency. Presumably, the brain’s response to sound stabilizes when children learn to successfully connect sounds with their meanings.
Happily biology is not destiny. In prior work in Northwestern’s Auditory Neuroscience Laboratory, Kraus and her colleagues found that the inconsistency with which the poorest readers encode sound could be “fixed” through training.
In that study, children with reading impairments were fitted for a year with assistive listening devices that transmitted their teacher’s voice directly into their ears. After a year, the children showed improvement not only in reading but also in the consistency with which their brains encoded speech sounds, particularly consonants.
"Use of the devices focused youngsters’ brains on the "meaningful" sounds coming from their teacher, diminishing other, extraneous distractions," said Kraus. "After a year of use, the students had honed their auditory systems and no longer required the assistive devices to keep their reading and encoding advantage."
People rarely have difficulty encoding vowel sounds, which are relatively simple and long, according to Kraus. It is consonant sounds — sounds which are shorter and more acoustically complex — that are most likely to be incorrectly categorized by the brain.
"Understanding the biological mechanisms of reading puts us in a better position to both understand how normal reading works and to ameliorate it where it goes awry," says Kraus.
"Our results suggest that good readers profit from a stable neural representation of sound, and that children with inconsistent neural responses are likely at a disadvantage when learning to read," Kraus adds. "The good news is that response consistency can be improved with auditory training."
Decades of research from laboratories worldwide have shown that reading ability is associated with auditory skills, including auditory memory and attention, the ability to rhyme sounds and the ability to categorize rapidly occurring sounds.
(Image: Michael Pettigrew)

Researchers discover a biological marker of dyslexia

Though learning to read proceeds smoothly for most children, as many as one in 10 is estimated to suffer from dyslexia, a constellation of impairments unrelated to intelligence, hearing or vision that make learning to read a struggle. Now, Northwestern University researchers report they have found a biological mechanism that appears to play an important role in the reading process.

"We discovered a systematic relationship between reading ability and the consistency with which the brain encodes sounds," says Nina Kraus, Hugh Knowles Professor of Neurobiology, Physiology and Communication. "Unstable Representation of Sound: A Biological Marker of Dyslexia," co-authored by Jane Hornickel, will appear in the Feb. 20 issue of The Journal of Neuroscience.

Recording the automatic brain wave responses of 100 school-aged children to speech sounds, the Northwestern researchers found that the very best readers encoded the sound most consistently while the poorest readers encoded it with the greatest inconsistency. Presumably, the brain’s response to sound stabilizes when children learn to successfully connect sounds with their meanings.

Happily biology is not destiny. In prior work in Northwestern’s Auditory Neuroscience Laboratory, Kraus and her colleagues found that the inconsistency with which the poorest readers encode sound could be “fixed” through training.

In that study, children with reading impairments were fitted for a year with assistive listening devices that transmitted their teacher’s voice directly into their ears. After a year, the children showed improvement not only in reading but also in the consistency with which their brains encoded speech sounds, particularly consonants.

"Use of the devices focused youngsters’ brains on the "meaningful" sounds coming from their teacher, diminishing other, extraneous distractions," said Kraus. "After a year of use, the students had honed their auditory systems and no longer required the assistive devices to keep their reading and encoding advantage."

People rarely have difficulty encoding vowel sounds, which are relatively simple and long, according to Kraus. It is consonant sounds — sounds which are shorter and more acoustically complex — that are most likely to be incorrectly categorized by the brain.

"Understanding the biological mechanisms of reading puts us in a better position to both understand how normal reading works and to ameliorate it where it goes awry," says Kraus.

"Our results suggest that good readers profit from a stable neural representation of sound, and that children with inconsistent neural responses are likely at a disadvantage when learning to read," Kraus adds. "The good news is that response consistency can be improved with auditory training."

Decades of research from laboratories worldwide have shown that reading ability is associated with auditory skills, including auditory memory and attention, the ability to rhyme sounds and the ability to categorize rapidly occurring sounds.

(Image: Michael Pettigrew)

Filed under dyslexia brainwaves biological marker reading ability neuroscience science

78 notes

New therapy uses electricity to cancel out Parkinson tremors
A new therapy could help suppress tremors in people with Parkinson’s disease, an Oxford University study suggests.
The technique – called transcranial alternating current stimulation or TACS – cancels out the brain signal causing the tremors by applying a small, safe electric current across electrodes on the outside of a patient’s head.
The preliminary study, conducted with 15 people with Parkinson’s disease at Oxford’s John Radcliffe Hospital, is published in the journal Current Biology. The researchers showed a 50 per cent reduction in resting tremors among the patients.
Physical tremors are a significant and debilitating symptom of Parkinson’s disease, but do not respond well to existing drug treatments.
Tremors can be successfully treated with deep brain stimulation, a technique that involves surgery to insert electrodes deep into the brain itself to deliver electrical impulses. But this invasive therapy is expensive and carries some health risks, including bleeding in to the brain, which means it is not suitable for all patients.
In TACS in contrast, the electrode pads are placed on the outside of the patient’s head, so it does not carry the risks associated with deep brain stimulation.
Professor Peter Brown of the Nuffield Department of Clinical Neurosciences, who led the study, said: ‘Tremors experienced by Parkinson’s sufferers can be devastating and any therapy that can suppress or reduce those tremors significantly improves quality of life for patients.
'We are very hopeful this research may, in time, lead to a therapy that is both successful and carries reduced medical risks. We have proved the principle, now we have to optimise it and adapt it so it is able to be used in patients. Often that is the hardest part.'

New therapy uses electricity to cancel out Parkinson tremors

A new therapy could help suppress tremors in people with Parkinson’s disease, an Oxford University study suggests.

The technique – called transcranial alternating current stimulation or TACS – cancels out the brain signal causing the tremors by applying a small, safe electric current across electrodes on the outside of a patient’s head.

The preliminary study, conducted with 15 people with Parkinson’s disease at Oxford’s John Radcliffe Hospital, is published in the journal Current Biology. The researchers showed a 50 per cent reduction in resting tremors among the patients.

Physical tremors are a significant and debilitating symptom of Parkinson’s disease, but do not respond well to existing drug treatments.

Tremors can be successfully treated with deep brain stimulation, a technique that involves surgery to insert electrodes deep into the brain itself to deliver electrical impulses. But this invasive therapy is expensive and carries some health risks, including bleeding in to the brain, which means it is not suitable for all patients.

In TACS in contrast, the electrode pads are placed on the outside of the patient’s head, so it does not carry the risks associated with deep brain stimulation.

Professor Peter Brown of the Nuffield Department of Clinical Neurosciences, who led the study, said: ‘Tremors experienced by Parkinson’s sufferers can be devastating and any therapy that can suppress or reduce those tremors significantly improves quality of life for patients.

'We are very hopeful this research may, in time, lead to a therapy that is both successful and carries reduced medical risks. We have proved the principle, now we have to optimise it and adapt it so it is able to be used in patients. Often that is the hardest part.'

Filed under parkinson's disease tremors TACS electric current neuroscience science

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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

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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.

image

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.

image

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.”

image

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

21 notes

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

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