Neuroscience

Articles and news from the latest research reports.

Posts tagged neuroscience

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One gene influences recovery from traumatic brain injury

Researchers report that one tiny variation in the sequence of a gene may cause some people to be more impaired by traumatic brain injury (TBI) than others with comparable wounds.

The study, described in the journal PLOS ONE, measured general intelligence in a group of 156 Vietnam War veterans who suffered penetrating head injuries during the war. All of the study subjects had damage to the prefrontal cortex, a brain region behind the forehead that is important to cognitive tasks such as planning, problem-solving, self-restraint and complex thought.

The researchers controlled for the size and location of subjects’ brain injuries and other factors, such as intelligence prior to injury, which might have contributed to differences in cognitive function. (Prior to combat, the veterans had completed the Armed Forces Qualifications Test, which included measures of intelligence that provided a baseline for the new analysis.)

“We administered a large, cognitive battery of tests to investigate how they performed after their injury,” said study leader Aron Barbey, a professor of speech and hearing science, of psychology and of neuroscience at the University of Illinois. “And we had a team of neurologists who helped characterize the nature and scope of the patients’ brain injuries.”

The researchers also collected blood for a genetic analysis, focusing on a gene known as BDNF (brain-derived neurotrophic factor).

The team found that a single polymorphism (a difference in one “letter” of the sequence) in the BDNF gene accounted for significant differences in intelligence among those with similar injuries and comparable intelligence before being injured.

“BDNF is a basic growth factor and it’s related to neurogenesis, the production of new neurons,” Barbey said. “What we found is that if people have a specific polymorphism in the BDNF gene, they recovered to a greater extent than those with a different variant of the gene.”

The change in the gene alters the BDNF protein: The amino acid methionine (Met) is incorporated at a specific site in the protein instead of valine (Val). Since people inherit two versions of each gene, one from each parent, they have either Val/Val, Val/Met or Met/Met variants of the gene.

“The effects of this difference were large – very large,” Barbey said. “If an individual had the Val/Val combination, then their performance on a battery of cognitive tests (conducted long after the injury occurred) was remarkably lower than that of individuals who had the Val/Met or Met/Met combination.”

On average, those with the Val/Val polymorphism scored about eight IQ points lower on tests of general intelligence than those with the Val/Met or Met/Met variants, Barbey said. Those with the Val/Val variant also were significantly more impaired in “specific competencies for intelligence like verbal comprehension, perceptual organization, working memory and processing speed,” he said.

To test these results, the researchers did the analysis over again “in a subset of individuals who had very similar (brain injuries) to the other group,” Barbey said. “We found the same kind of effects, suggesting that lesion location isn’t a factor influencing the difference between the groups.”

The finding opens a new avenue of exploration for treatments to aid the process of recovery from TBI, Barbey said.

(Source: news.illinois.edu)

Filed under prefrontal cortex brain-derived neurotrophic factor TBI memory brain injury neuroscience science

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In one ear and out the other
Remember that sound bite you heard on the radio this morning? The grocery items your spouse asked you to pick up? Chances are, you won’t.
Researchers at the University of Iowa have found that when it comes to memory, we don’t remember things we hear nearly as well as things we see or touch.
“As it turns out, there is merit to the Chinese proverb ‘I hear, and I forget; I see, and I remember,” says lead author of the study and UI graduate student, James Bigelow.
“We tend to think that the parts of our brain wired for memory are integrated. But our findings indicate our brain may use separate pathways to process information. Even more, our study suggests the brain may process auditory information differently than visual and tactile information, and alternative strategies—such as increased mental repetition—may be needed when trying to improve memory,” says Amy Poremba, associate professor in the UI Department of Psychology and corresponding author on the paper, published this week in the journal PLoS One.
Bigelow and Poremba discovered that when more than 100 UI undergraduate students were exposed to a variety of sounds, visuals, and things that could be felt, the students were least apt to remember the sounds they had heard.
In an experiment testing short-term memory, participants were asked to listen to pure tones they heard through headphones, look at various shades of red squares, and feel low-intensity vibrations by gripping an aluminum bar. Each set of tones, squares and vibrations was separated by time delays ranging from one to 32 seconds.
Although students’ memory declined across the board when time delays grew longer, the decline was much greater for sounds, and began as early as four to eight seconds after being exposed to them.
While this seems like a short time span, it’s akin to forgetting a phone number that wasn’t written down, notes Poremba. “If someone gives you a number, and you dial it right away, you are usually fine. But do anything in between, and the odds are you will have forgotten it,” she says.
In a second experiment, Bigelow and Poremba tested participants’ memory using things they might encounter on an everyday basis. Students listened to audio recordings of dogs barking, watched silent videos of a basketball game, and touched and held common objects blocked from view, such as a coffee mug. The researchers found that between an hour and a week later, students were worse at remembering the sounds they had heard, but their memory for visual scenes and tactile objects was about the same.
Both experiments suggest that the way your mind processes and stores sound may be different from the way it process and stores other types of memories. And that could have big implications for educators, design engineers, and advertisers alike.
“As teachers, we want to assume students will remember everything we say. But if you really want something to be memorable you may need to include a visual or hands-on experience, in addition to auditory information,” says Poremba.
Previous research has suggested that humans may have superior visual memory, and that hearing words associated with sounds—rather than hearing the sounds alone—may aid memory. Bigelow and Poremba’s study builds upon those findings by confirming that, indeed, we remember less of what we hear, regardless of whether sounds are linked to words.
The study also is the first to show that our ability to remember what we touch is roughly equal to our ability to remember what we see. The finding is important, because experiments with nonhuman primates such as monkeys and chimpanzees have shown that they similarly excel at visual and tactile memory tasks, but struggle with auditory tasks. Based on these observations, the authors believe humans’ weakness for remembering sounds likely has its roots in the evolution of the primate brain.

In one ear and out the other

Remember that sound bite you heard on the radio this morning? The grocery items your spouse asked you to pick up? Chances are, you won’t.

Researchers at the University of Iowa have found that when it comes to memory, we don’t remember things we hear nearly as well as things we see or touch.

“As it turns out, there is merit to the Chinese proverb ‘I hear, and I forget; I see, and I remember,” says lead author of the study and UI graduate student, James Bigelow.

“We tend to think that the parts of our brain wired for memory are integrated. But our findings indicate our brain may use separate pathways to process information. Even more, our study suggests the brain may process auditory information differently than visual and tactile information, and alternative strategies—such as increased mental repetition—may be needed when trying to improve memory,” says Amy Poremba, associate professor in the UI Department of Psychology and corresponding author on the paper, published this week in the journal PLoS One.

Bigelow and Poremba discovered that when more than 100 UI undergraduate students were exposed to a variety of sounds, visuals, and things that could be felt, the students were least apt to remember the sounds they had heard.

In an experiment testing short-term memory, participants were asked to listen to pure tones they heard through headphones, look at various shades of red squares, and feel low-intensity vibrations by gripping an aluminum bar. Each set of tones, squares and vibrations was separated by time delays ranging from one to 32 seconds.

Although students’ memory declined across the board when time delays grew longer, the decline was much greater for sounds, and began as early as four to eight seconds after being exposed to them.

While this seems like a short time span, it’s akin to forgetting a phone number that wasn’t written down, notes Poremba. “If someone gives you a number, and you dial it right away, you are usually fine. But do anything in between, and the odds are you will have forgotten it,” she says.

In a second experiment, Bigelow and Poremba tested participants’ memory using things they might encounter on an everyday basis. Students listened to audio recordings of dogs barking, watched silent videos of a basketball game, and touched and held common objects blocked from view, such as a coffee mug. The researchers found that between an hour and a week later, students were worse at remembering the sounds they had heard, but their memory for visual scenes and tactile objects was about the same.

Both experiments suggest that the way your mind processes and stores sound may be different from the way it process and stores other types of memories. And that could have big implications for educators, design engineers, and advertisers alike.

“As teachers, we want to assume students will remember everything we say. But if you really want something to be memorable you may need to include a visual or hands-on experience, in addition to auditory information,” says Poremba.

Previous research has suggested that humans may have superior visual memory, and that hearing words associated with sounds—rather than hearing the sounds alone—may aid memory. Bigelow and Poremba’s study builds upon those findings by confirming that, indeed, we remember less of what we hear, regardless of whether sounds are linked to words.

The study also is the first to show that our ability to remember what we touch is roughly equal to our ability to remember what we see. The finding is important, because experiments with nonhuman primates such as monkeys and chimpanzees have shown that they similarly excel at visual and tactile memory tasks, but struggle with auditory tasks. Based on these observations, the authors believe humans’ weakness for remembering sounds likely has its roots in the evolution of the primate brain.

Filed under sound sound processing memory visual memory neuroscience science

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Phantom limb pain relieved when amputated arm is put back to work
Max Ortiz Catalan has developed a new method for the treatment of phantom limb pain (PLP) after an amputation. The method is based on a unique combination of several technologies, and has been initially tested on a patient who has suffered from severe phantom limb pain for 48 years. A case study shows a drastic reduction of pain.
People who lose an arm or a leg often experience phantom sensations, as if the missing limb were still there. Seventy per cent of amputees experience pain in the amputated limb despite that it no longer exists. Phantom limb pain can be a serious chronic and deteriorating condition that reduces the quality of the person´s life considerably. The exact cause of phantom limb pain and other phantom sensations is yet unknown.
Phantom limb pain is currently treated with several different methods. Examples include mirror therapy, different types of medication, acupuncture and hypnosis. In many cases, however, nothing helps. This was the case for the patient that Chalmers researcher Max Ortiz Catalan selected for a case study of the new treatment method he has envisaged as a potential solution.
The patient lost his arm 48 years ago, and had since that time suffered from phantom pain varying from moderate to unbearable. He was never entirely free of pain.
The patient´s pain was drastically reduced after a period of treatment with the new method. He now has periods where he is entirely free of pain, and he is no longer awakened by intense periods of pain at night like he was previously. The new method uses muscle signals from the patient´s arm stump to drive a system known as augmented reality. The electrical signals in the muscles are sensed by electrodes on the skin. The signals are then translated into arm movements by complex algorithms. The patient can see himself on a screen with a superimposed virtual arm, which is controlled using his own neural command in real time.
”There are several features of this system which combined might be the cause of pain relief” says Max Ortiz Catalan. “The motor areas in the brain needed for movement of the amputated arm are reactivated, and the patient obtains visual feedback that tricks the brain into believing there is an arm executing such motor commands. He experiences himself as a whole, with the amputated arm back in place.”
Modern therapies that use conventional mirrors or virtual reality are based on visual feedback via the opposite arm or leg. For this reason, people who have lost both arms or both legs cannot be helped using these methods.
”Our method differs from previous treatment because the control signals are retrieved from the arm stump, and thus the affected arm is in charge” says Max Ortiz Catalan. ”The promotion of motor execution and the vivid sensation of completion provided by augmented reality may be the reason for the patient improvement, while mirror therapy and medicaments did not help previously.”
A clinical study will now be conducted of the new treatment, which has been developed in a collaboration between Chalmers University of Technology, Sahlgrenska University Hospital, the University of Gothenburg and Integrum. Three Swedish hospitals and other European clinics will cooperate during the study which will target patients with conditions resembling the one in the case study – that is, people who suffer from phantom pain and who have not responded to other currently available treatments.
The research group has also developed a system that can be used at home. Patients will be able to apply this therapy on their own, once it has been approved. An extension of the treatment is that it can be used by other patient groups that need to rehabilitate their mobility, such as stroke victims or some patients with spinal cord injuries.

Phantom limb pain relieved when amputated arm is put back to work

Max Ortiz Catalan has developed a new method for the treatment of phantom limb pain (PLP) after an amputation. The method is based on a unique combination of several technologies, and has been initially tested on a patient who has suffered from severe phantom limb pain for 48 years. A case study shows a drastic reduction of pain.

People who lose an arm or a leg often experience phantom sensations, as if the missing limb were still there. Seventy per cent of amputees experience pain in the amputated limb despite that it no longer exists. Phantom limb pain can be a serious chronic and deteriorating condition that reduces the quality of the person´s life considerably. The exact cause of phantom limb pain and other phantom sensations is yet unknown.

Phantom limb pain is currently treated with several different methods. Examples include mirror therapy, different types of medication, acupuncture and hypnosis. In many cases, however, nothing helps. This was the case for the patient that Chalmers researcher Max Ortiz Catalan selected for a case study of the new treatment method he has envisaged as a potential solution.

The patient lost his arm 48 years ago, and had since that time suffered from phantom pain varying from moderate to unbearable. He was never entirely free of pain.

The patient´s pain was drastically reduced after a period of treatment with the new method. He now has periods where he is entirely free of pain, and he is no longer awakened by intense periods of pain at night like he was previously.
The new method uses muscle signals from the patient´s arm stump to drive a system known as augmented reality. The electrical signals in the muscles are sensed by electrodes on the skin. The signals are then translated into arm movements by complex algorithms. The patient can see himself on a screen with a superimposed virtual arm, which is controlled using his own neural command in real time.

”There are several features of this system which combined might be the cause of pain relief” says Max Ortiz Catalan. “The motor areas in the brain needed for movement of the amputated arm are reactivated, and the patient obtains visual feedback that tricks the brain into believing there is an arm executing such motor commands. He experiences himself as a whole, with the amputated arm back in place.”

Modern therapies that use conventional mirrors or virtual reality are based on visual feedback via the opposite arm or leg. For this reason, people who have lost both arms or both legs cannot be helped using these methods.

”Our method differs from previous treatment because the control signals are retrieved from the arm stump, and thus the affected arm is in charge” says Max Ortiz Catalan. ”The promotion of motor execution and the vivid sensation of completion provided by augmented reality may be the reason for the patient improvement, while mirror therapy and medicaments did not help previously.”

A clinical study will now be conducted of the new treatment, which has been developed in a collaboration between Chalmers University of Technology, Sahlgrenska University Hospital, the University of Gothenburg and Integrum. Three Swedish hospitals and other European clinics will cooperate during the study which will target patients with conditions resembling the one in the case study – that is, people who suffer from phantom pain and who have not responded to other currently available treatments.

The research group has also developed a system that can be used at home. Patients will be able to apply this therapy on their own, once it has been approved. An extension of the treatment is that it can be used by other patient groups that need to rehabilitate their mobility, such as stroke victims or some patients with spinal cord injuries.

Filed under amputation phantom limb phantom limb pain prosthetics virtual reality technology neuroscience science

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Researchers generate new neurons in brains, spinal cords of living adult mammals
UT Southwestern Medical Center researchers created new nerve cells in the brains and spinal cords of living mammals without the need for stem cell transplants to replenish lost cells.
Although the research indicates it may someday be possible to regenerate neurons from the body’s own cells to repair traumatic brain injury or spinal cord damage or to treat conditions such as Alzheimer’s disease, the researchers stressed that it is too soon to know whether the neurons created in these initial studies resulted in any functional improvements, a goal for future research.
Spinal cord injuries can lead to an irreversible loss of neurons, and along with scarring, can ultimately lead to impaired motor and sensory functions. Scientists are hopeful that regenerating cells can be an avenue to repair damage, but adult spinal cords have limited ability to produce new neurons. Biomedical scientists have transplanted stem cells to replace neurons, but have faced other hurdles, underscoring the need for new methods of replenishing lost cells.
Scientists in UT Southwestern’s Department of Molecular Biology first successfully turned astrocytes – the most common non-neuronal brain cells – into neurons that formed networks in mice. They now successfully turned scar-forming astrocytes in the spinal cords of adult mice into neurons. The latest findings are published today in Nature Communications and follow previous findings published in Nature Cell Biology.
“Our earlier work was the first to clearly show in vivo (in a living animal) that mature astrocytes can be reprogrammed to become functional neurons without the need of cell transplantation. The current study did something similar in the spine, turning scar-forming astrocytes into progenitor cells called neuroblasts that regenerated into neurons,” said Dr. Chun-Li Zhang, assistant professor of molecular biology at UT Southwestern and senior author of both studies.
“Astrocytes are abundant and widely distributed both in the brain and in the spinal cord. In response to injury, these cells proliferate and contribute to scar formation. Once a scar has formed, it seals the injured area and creates a mechanical and biochemical barrier to neural regeneration,” Dr. Zhang explained. “Our results indicate that the astrocytes may be ideal targets for in vivo reprogramming.”
The scientists’ two-step approach first introduces a biological substance that regulates the expression of genes, called a transcription factor, into areas of the brain or spinal cord where that factor is not highly expressed in adult mice. Of 12 transcription factors tested, only SOX2 switched fully differentiated, adult astrocytes to an earlier neuronal precursor, or neuroblast, stage of development, Dr. Zhang said.
In the second step, the researchers gave the mice a drug called valproic acid (VPA) that encouraged the survival of the neuroblasts and their maturation (differentiation) into neurons. VPA has been used to treat epilepsy for more than half a century and also is prescribed to treat bipolar disorder and to prevent migraine headaches, he said.
The current study reports neurogenesis (neuron creation) occurred in the spinal cords of both adult and aged (over one-year old) mice of both sexes, although the response was much weaker in the aged mice, Dr. Zhang said. Researchers now are searching for ways to boost the number and speed of neuron creation. Neuroblasts took four weeks to form and eight weeks to mature into neurons, slower than neurogenesis reported in lab dish experiments, so researchers plan to conduct experiments to determine if the slower pace helps the newly generated neurons properly integrate into their environment.
In the spinal cord study, SOX2-induced mature neurons created from reprogramming of astrocytes persisted for 210 days after the start of the experiment, the longest time the researchers examined, he added.
Because tumor growth is a concern when cells are reprogrammed to an earlier stage of development, the researchers followed the mice in the Nature Cell Biology study for nearly a year to look for signs of tumor formation and reported finding none.
(Image: Shutterstock)

Researchers generate new neurons in brains, spinal cords of living adult mammals

UT Southwestern Medical Center researchers created new nerve cells in the brains and spinal cords of living mammals without the need for stem cell transplants to replenish lost cells.

Although the research indicates it may someday be possible to regenerate neurons from the body’s own cells to repair traumatic brain injury or spinal cord damage or to treat conditions such as Alzheimer’s disease, the researchers stressed that it is too soon to know whether the neurons created in these initial studies resulted in any functional improvements, a goal for future research.

Spinal cord injuries can lead to an irreversible loss of neurons, and along with scarring, can ultimately lead to impaired motor and sensory functions. Scientists are hopeful that regenerating cells can be an avenue to repair damage, but adult spinal cords have limited ability to produce new neurons. Biomedical scientists have transplanted stem cells to replace neurons, but have faced other hurdles, underscoring the need for new methods of replenishing lost cells.

Scientists in UT Southwestern’s Department of Molecular Biology first successfully turned astrocytes – the most common non-neuronal brain cells – into neurons that formed networks in mice. They now successfully turned scar-forming astrocytes in the spinal cords of adult mice into neurons. The latest findings are published today in Nature Communications and follow previous findings published in Nature Cell Biology.

“Our earlier work was the first to clearly show in vivo (in a living animal) that mature astrocytes can be reprogrammed to become functional neurons without the need of cell transplantation. The current study did something similar in the spine, turning scar-forming astrocytes into progenitor cells called neuroblasts that regenerated into neurons,” said Dr. Chun-Li Zhang, assistant professor of molecular biology at UT Southwestern and senior author of both studies.

“Astrocytes are abundant and widely distributed both in the brain and in the spinal cord. In response to injury, these cells proliferate and contribute to scar formation. Once a scar has formed, it seals the injured area and creates a mechanical and biochemical barrier to neural regeneration,” Dr. Zhang explained. “Our results indicate that the astrocytes may be ideal targets for in vivo reprogramming.”

The scientists’ two-step approach first introduces a biological substance that regulates the expression of genes, called a transcription factor, into areas of the brain or spinal cord where that factor is not highly expressed in adult mice. Of 12 transcription factors tested, only SOX2 switched fully differentiated, adult astrocytes to an earlier neuronal precursor, or neuroblast, stage of development, Dr. Zhang said.

In the second step, the researchers gave the mice a drug called valproic acid (VPA) that encouraged the survival of the neuroblasts and their maturation (differentiation) into neurons. VPA has been used to treat epilepsy for more than half a century and also is prescribed to treat bipolar disorder and to prevent migraine headaches, he said.

The current study reports neurogenesis (neuron creation) occurred in the spinal cords of both adult and aged (over one-year old) mice of both sexes, although the response was much weaker in the aged mice, Dr. Zhang said. Researchers now are searching for ways to boost the number and speed of neuron creation. Neuroblasts took four weeks to form and eight weeks to mature into neurons, slower than neurogenesis reported in lab dish experiments, so researchers plan to conduct experiments to determine if the slower pace helps the newly generated neurons properly integrate into their environment.

In the spinal cord study, SOX2-induced mature neurons created from reprogramming of astrocytes persisted for 210 days after the start of the experiment, the longest time the researchers examined, he added.

Because tumor growth is a concern when cells are reprogrammed to an earlier stage of development, the researchers followed the mice in the Nature Cell Biology study for nearly a year to look for signs of tumor formation and reported finding none.

(Image: Shutterstock)

Filed under valproic acid spinal cord astrocytes neurons neurodegeneration genetics neuroscience science

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New risk gene illuminates Alzheimer’s disease

A team of international scientists, including a researcher from Simon Fraser University, has isolated a gene thought to play a causal role in the development of Alzheimer’s disease. The Proceedings of the National Academy of Sciences recently published the team’s study.

The newly identified gene affects accumulation of amyloid-beta, a protein believed to be one of the main causes of the damage that underpins this brain disease in humans.

The gene encodes a protein that is important for intracellular transportation. Each brain cell relies on an internal highway system that transports molecular signals needed for the development, communication, and survival of the cell. 

This system’s impairment can disrupt amyloid-beta processing, causing its eventual accumulation. This contributes to the development of amyloid plaques, which are a key hallmark of Alzheimer’s disease.

Teasing out contributing disease factors, whether genetic or environmental, has long posed a challenge for Alzheimer’s researchers.

“Alzheimer’s is a multifactorial disease where a build-up of subtle problems develop in the nervous system over a span of decades,” says Michael Silverman, an SFU biology associate professor. He worked on the study with a team of Japanese scientists led by Dr. Takashi Morihara at Osaka University.   

Identifying these subtle, yet perhaps critical genetic contributions is challenging. “Alzheimer’s, like many human disorders, has a genetic component, yet many environmental and lifestyle factors contribute to the disease as well,” says Silverman. “In a sense, it is like looking for a needle in a complex genetic haystack.”

Only a small fraction of cases have a strong hereditary component, for example early-onset Alzheimer’s.

This breakthrough in Alzheimer’s research could open new avenues for the design of therapeutics and pave the way for early detection by helping healthcare professionals identify those who are predisposed to the disease.

“One possibility is that a genetic test for a particular variant of this newly discovered gene, along with other variants of genes that contribute to Alzheimer’s, will help to give a person their overall risk for the disease.  

“Lifestyle changes, such as improved diet, exercise, and an increase in cognitive stimulation may then help to slow the progression of Alzheimer’s,” says Silverman.

(Source: sfu.ca)

Filed under alzheimer's disease neurodegenerative diseases genetics neurons neuroscience science

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An Amazing Village Designed Just For People With Dementia
Centuries after Shakespeare wrote about King Lear’s symptoms, there’s still no perfect way to care for sufferers of dementia and Alzheimer’s. In the Netherlands, however, a radical idea is being tested: Self-contained “villages” where people with dementia shop, cook, and live together—safely.
We, as a population, are aging rapidly. According to the Alzheimer’s Association, one in three seniors today dies with dementia. The process of finding—and paying for—long-term care can be very confusing, unfortunately, and difficult for both loved ones and patients. Most caretakers are underpaid, overworked, and must drive far distances to their jobs—giving away some 17 billion unpaid hours of care a year. And it’s just going to get worse: Alzheimer’s has increased by an incredible 68 percent since 2000, and the cost of caring for sufferers will increase from $203 billion last year to $1.2 trillion by 2050.
In short, we’re not prepared for the future that awaits us—financially, infrastructurally, or even socially. But in the small town of Weesp, in Holland—that bastion of social progressivism—at a dementia-focused living center called De Hogeweyk, aka Dementiavillage, the relationship between patients and their care is serving as a model for the rest of the world.
Read more

An Amazing Village Designed Just For People With Dementia

Centuries after Shakespeare wrote about King Lear’s symptoms, there’s still no perfect way to care for sufferers of dementia and Alzheimer’s. In the Netherlands, however, a radical idea is being tested: Self-contained “villages” where people with dementia shop, cook, and live together—safely.

We, as a population, are aging rapidly. According to the Alzheimer’s Association, one in three seniors today dies with dementia. The process of finding—and paying for—long-term care can be very confusing, unfortunately, and difficult for both loved ones and patients. Most caretakers are underpaid, overworked, and must drive far distances to their jobs—giving away some 17 billion unpaid hours of care a year. And it’s just going to get worse: Alzheimer’s has increased by an incredible 68 percent since 2000, and the cost of caring for sufferers will increase from $203 billion last year to $1.2 trillion by 2050.

In short, we’re not prepared for the future that awaits us—financially, infrastructurally, or even socially. But in the small town of Weesp, in Holland—that bastion of social progressivism—at a dementia-focused living center called De Hogeweyk, aka Dementiavillage, the relationship between patients and their care is serving as a model for the rest of the world.

Read more

Filed under alzheimer's disease dementia dementia village de hogeweyk psychology neuroscience science

757 notes

New ideas change your brain cells
A new University of British Columbia study identifies an important molecular change that occurs in the brain when we learn and remember.
Published this month in Nature Neuroscience, the research shows that learning stimulates our brain cells in a manner that causes a small fatty acid to attach to delta-catenin, a protein in the brain. This biochemical modification is essential in producing the changes in brain cell connectivity associated with learning, the study finds.
In animal models, the scientists found almost twice the amount of modified delta-catenin in the brain after learning about new environments. While delta-catenin has previously been linked to learning, this study is the first to describe the protein’s role in the molecular mechanism behind memory formation.
“More work is needed, but this discovery gives us a much better understanding of the tools our brains use to learn and remember, and provides insight into how these processes become disrupted in neurological diseases,” says co-author Shernaz Bamji, an associate professor in UBC’s Life Sciences Institute.
It may also provide an explanation for some mental disabilities, the researchers say. People born without the gene have a severe form of mental retardation called Cri-du-chat syndrome, a rare genetic disorder named for the high-pitched cat-like cry of affected infants. Disruption of the delta-catenin gene has also been observed in some patients with schizophrenia.
“Brain activity can change both the structure of this protein, as well as its function,” says Stefano Brigidi, first author of the article and a PhD candidate Bamji’s laboratory. “When we introduced a mutation that blocked the biochemical modification that occurs in healthy subjects, we abolished the structural changes in brain’s cells that are known to be important for memory formation.”
Background 
According to the researchers, more work is needed to fully establish the importance of delta-catenin in building the brain connectivity behind learning and memory. Disruptions to these nerve cell connections are also believed to cause neurodegenerative diseases such as Alzheimer’s and Huntington disease. Understanding the biochemical processes that are important for maintaining these connections may help address the abnormalities in nerve cells that occur in these disease states.
(Image: Shutterstock)

New ideas change your brain cells

A new University of British Columbia study identifies an important molecular change that occurs in the brain when we learn and remember.

Published this month in Nature Neuroscience, the research shows that learning stimulates our brain cells in a manner that causes a small fatty acid to attach to delta-catenin, a protein in the brain. This biochemical modification is essential in producing the changes in brain cell connectivity associated with learning, the study finds.

In animal models, the scientists found almost twice the amount of modified delta-catenin in the brain after learning about new environments. While delta-catenin has previously been linked to learning, this study is the first to describe the protein’s role in the molecular mechanism behind memory formation.

“More work is needed, but this discovery gives us a much better understanding of the tools our brains use to learn and remember, and provides insight into how these processes become disrupted in neurological diseases,” says co-author Shernaz Bamji, an associate professor in UBC’s Life Sciences Institute.

It may also provide an explanation for some mental disabilities, the researchers say. People born without the gene have a severe form of mental retardation called Cri-du-chat syndrome, a rare genetic disorder named for the high-pitched cat-like cry of affected infants. Disruption of the delta-catenin gene has also been observed in some patients with schizophrenia.

“Brain activity can change both the structure of this protein, as well as its function,” says Stefano Brigidi, first author of the article and a PhD candidate Bamji’s laboratory. “When we introduced a mutation that blocked the biochemical modification that occurs in healthy subjects, we abolished the structural changes in brain’s cells that are known to be important for memory formation.”

Background

According to the researchers, more work is needed to fully establish the importance of delta-catenin in building the brain connectivity behind learning and memory. Disruptions to these nerve cell connections are also believed to cause neurodegenerative diseases such as Alzheimer’s and Huntington disease. Understanding the biochemical processes that are important for maintaining these connections may help address the abnormalities in nerve cells that occur in these disease states.

(Image: Shutterstock)

Filed under delta-catenin synaptic plasticity learning memory synapses genetic disorders neuroscience science

114 notes

Watching how the brain works

University of Miami researchers develop a method to visualize protein interactions in a living organism’s brain

There are more than a trillion cells called neurons that form a labyrinth of connections in our brains. Each of these neurons contains millions of proteins that perform different functions. Exactly how individual proteins interact to form the complex networks of the brain still remains as a mystery that is just beginning to unravel.

For the first time, a group of scientists has been able to observe intact interactions between proteins, directly in the brain of a live animal. The new live imaging approach was developed by a team of researchers at the University of Miami (UM).

image

(Image caption: Photonic resonance energy transfer described by Förster, or FRET, occurs when two small proteins come within a very small distance of each other — eight nanometers or less. The fluorescence lifetime of the donor molecule will become shorter — from 3 nanosecond to, perhaps, 2.5 nanoseconds. We then interpret this as evidence that the two proteins of interest are physically interacting with each other — a molecular signaling event. Credit: Akira Chiba/University of Miami)

"Our ultimate goal is to create the systematic survey of protein interactions in the brain," says Akira Chiba, professor of Biology in the College of Arts and Sciences at UM and lead investigator of the project. "Now that the genome project is complete, the next step is to understand what the proteins coded by our genes do in our body."

The new technique will allow scientists to visualize the interactions of proteins in the brain of an animal, along different points throughout its development, explains Chiba, who likens protein interactions to the way organisms associate with each other.

"We know that proteins are one billionth of a human in size. Nevertheless, proteins make networks and interact with each other, like social networking humans do," Chiba says. "The scale is very different, but it’s the same behavior happening among the basic units of a given network."

The researchers chose embryos of the fruit fly (Drosophila melanogaster) as an ideal model for the study. Because of its compact and transparent body, it is possible to visualize processes inside the Drosophila cells using a fluorescence lifetime imaging microscope (FLIM). The results of the observations are applicable to other animal brains, including the human brain.

The Drosophila embryos in the study contained a pair of fluorescent labeled proteins: a developmentally essential and ubiquitously present protein called Rho GTPase Cdc42 (cell division control protein 42), labeled with green fluorescent tag and its alleged signaling partner, the regulatory protein WASp (Wiskot-Aldrich Syndrome protein), labeled with red fluorescent tag. Together, these specialized proteins are believed to help neurons grow during brain development. The proteins were selected because the same (homolog) proteins exist in the human brain as well.

Previous methods required chemical or physical treatments that most likely disturb or even kill the cells. That made it impossible to study the protein interactions in their natural environment.

image

(Image caption: FRET (Förster resonance energy transfer) between the two interacting protein partners occurs, Cdc42 and WASp, within neurons, during the time and space that coincides with the formation of new synapses in the brain of the baby insect. Synapses connect individual neurons in the brain. Credit: Akira Chiba / University of Miami)

The current study addresses these challenges by using the occurrence of a phenomenon called Förster resonance energy transfer, or FRET. It occurs when two small proteins come within a very small distance of each other, (eight nanometers). The event is interpreted as the time and place where the particular protein interaction occurs within the living animal.

image

(Image caption: Proteins are one billionth of a human in size. Nevertheless, proteins make networks and interact with each other, like social networking humans do,” says Akira Chiba, professor of Biology in the College of Arts and Sciences at the University of Miami. “The scale is very different, but it’s the same behavior happening among the basic units of a given network.” Credit: Akira Chiba / University of Miami)

The findings show that FRET between the two interacting protein partners occurs within neurons, during the time and space that coincides with the formation of new synapses in the brain of the baby insect. Synapses connect individual neurons in the brain.

"Previous studies have demonstrated that Cdc42 and WASp can directly bind to each other in a test-tube, but this is the first direct demonstration that these two proteins are interacting within the brain," Chiba says.

(Source: eurekalert.org)

Filed under proteins protein interactions neurons CNS fruit flies FLIM FRET neuroscience science

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Researchers Pinpoint Brain Region Essential for Social Memory

Columbia University Medical Center (CUMC) researchers have determined that a small region of the hippocampus known as CA2 is essential for social memory, the ability of an animal to recognize another of the same species. A better grasp of the function of CA2 could prove useful in understanding and treating disorders characterized by altered social behaviors, such as autism, schizophrenia, and bipolar disorder. The findings, made in mice, were published on Feb. 23, 2014, in the online edition of Nature.
Scientists have long understood that the hippocampus—a pair of seahorse-shaped structures in the brain’s temporal lobes—plays a critical role in our ability to remember the who, what, where, and when of our daily lives. Recent studies have shown that different subregions of the hippocampus have different functions. For instance, the dentate gyrus is critical for distinguishing between similar environments, while CA3 enables us to recall a memory from partial cues (e.g., Proust’s famous madeleine). The CA1 region is critical for all forms of memory.
“However, the role of CA2, a relatively small region of the hippocampus sandwiched between CA3 and CA1, has remained largely unknown,” said senior author Steven A. Siegelbaum, PhD, professor of neuroscience and pharmacology, chair of the Department of Neuroscience, a member of the Mortimer B. Zuckerman Mind Brain Behavior Institute and Kavli Institute for Brain Science, and a Howard Hughes Medical Institute Investigator. A few studies have suggested that CA2 might be involved in social memory, as this region has a high level of expression of a receptor for vasopressin, a hormone linked to sexual motivation, bonding, and other social behaviors.
To learn more about this part of the hippocampus, the researchers created a transgenic mouse in which CA2 neurons could be selectively inhibited in adult animals. Once the neurons were inhibited, the mice were given a series of behavioral tests. “The mice looked quite normal until we looked at social memory,” said first author Frederick L. Hitti, an MD-PhD student in Dr. Siegelbaum’s laboratory, who developed the transgenic mouse. “Normally, mice are naturally curious about a mouse they’ve never met; they spend more time investigating an unfamiliar mouse than a familiar one. In our experiment, however, mice with an inactivated CA2 region showed no preference for a novel mouse versus a previously encountered mouse, indicating a lack of social memory.”
In two separate novel-object recognition tests, the CA2-deficient mice showed a normal preference for an object they had not previously encountered, showing that the mice did not have a global lack of interest in novelty. In another experiment, the researchers tested whether the animals’ inability to form social memories might have to do with deficits in olfaction (sense of smell), which is crucial for normal social interaction. However, the mice showed no loss in ability to discriminate social or non-social odors.
In humans, the importance of the hippocampus for social memory was famously illustrated by the case of Henry Molaison, who had much of his hippocampus removed by surgeons in 1953 in an attempt to cure severe epilepsy. Molaison (often referred to as HM in the scientific literature) was subsequently unable to form new memories of people. Scientists have observed that lesions limited to the hippocampus also impair social memory in both rodents and humans.
“Because several neuropsychiatric disorders are associated with altered social behaviors, our findings raise the possibility that CA2 dysfunction may contribute to these behavioral changes,” said Dr. Siegelbaum. This possibility is supported by findings of a decreased number of CA2 inhibitory neurons in individuals with schizophrenia and bipolar disorder and altered vasopressin signaling in autism. Thus, CA2 may provide a new target for therapeutic approaches to the treatment of social disorders.
Researchers Pinpoint Brain Region Essential for Social Memory

Columbia University Medical Center (CUMC) researchers have determined that a small region of the hippocampus known as CA2 is essential for social memory, the ability of an animal to recognize another of the same species. A better grasp of the function of CA2 could prove useful in understanding and treating disorders characterized by altered social behaviors, such as autism, schizophrenia, and bipolar disorder. The findings, made in mice, were published on Feb. 23, 2014, in the online edition of Nature.

Scientists have long understood that the hippocampus—a pair of seahorse-shaped structures in the brain’s temporal lobes—plays a critical role in our ability to remember the who, what, where, and when of our daily lives. Recent studies have shown that different subregions of the hippocampus have different functions. For instance, the dentate gyrus is critical for distinguishing between similar environments, while CA3 enables us to recall a memory from partial cues (e.g., Proust’s famous madeleine). The CA1 region is critical for all forms of memory.

“However, the role of CA2, a relatively small region of the hippocampus sandwiched between CA3 and CA1, has remained largely unknown,” said senior author Steven A. Siegelbaum, PhD, professor of neuroscience and pharmacology, chair of the Department of Neuroscience, a member of the Mortimer B. Zuckerman Mind Brain Behavior Institute and Kavli Institute for Brain Science, and a Howard Hughes Medical Institute Investigator. A few studies have suggested that CA2 might be involved in social memory, as this region has a high level of expression of a receptor for vasopressin, a hormone linked to sexual motivation, bonding, and other social behaviors.

To learn more about this part of the hippocampus, the researchers created a transgenic mouse in which CA2 neurons could be selectively inhibited in adult animals. Once the neurons were inhibited, the mice were given a series of behavioral tests. “The mice looked quite normal until we looked at social memory,” said first author Frederick L. Hitti, an MD-PhD student in Dr. Siegelbaum’s laboratory, who developed the transgenic mouse. “Normally, mice are naturally curious about a mouse they’ve never met; they spend more time investigating an unfamiliar mouse than a familiar one. In our experiment, however, mice with an inactivated CA2 region showed no preference for a novel mouse versus a previously encountered mouse, indicating a lack of social memory.”

In two separate novel-object recognition tests, the CA2-deficient mice showed a normal preference for an object they had not previously encountered, showing that the mice did not have a global lack of interest in novelty. In another experiment, the researchers tested whether the animals’ inability to form social memories might have to do with deficits in olfaction (sense of smell), which is crucial for normal social interaction. However, the mice showed no loss in ability to discriminate social or non-social odors.

In humans, the importance of the hippocampus for social memory was famously illustrated by the case of Henry Molaison, who had much of his hippocampus removed by surgeons in 1953 in an attempt to cure severe epilepsy. Molaison (often referred to as HM in the scientific literature) was subsequently unable to form new memories of people. Scientists have observed that lesions limited to the hippocampus also impair social memory in both rodents and humans.

“Because several neuropsychiatric disorders are associated with altered social behaviors, our findings raise the possibility that CA2 dysfunction may contribute to these behavioral changes,” said Dr. Siegelbaum. This possibility is supported by findings of a decreased number of CA2 inhibitory neurons in individuals with schizophrenia and bipolar disorder and altered vasopressin signaling in autism. Thus, CA2 may provide a new target for therapeutic approaches to the treatment of social disorders.

Filed under hippocampus social memory schizophrenia autism social interaction dentate gyrus psychology neuroscience science

233 notes

New study settles how social understanding is performed by the brain
A new study settles an important question about how social understanding is performed in the brain. The findings may help us to attain a better understanding of why people with autism and schizophrenia have difficulties with social interaction.
In a study to be published in Psychological Science, researchers from Aarhus University and the University of Copenhagen demonstrate that brain cells in what is called the mirror system help people make sense of the actions they see other people perform in everyday life.
Using magnetic stimulation to temporarily disrupt normal processing of the areas of the human brain involved in the production of actions of human participants, it is demonstrated that these areas are also involved in the understanding of actions. The study is the first to demonstrate a clear causal effect, whereas earlier studies primarily have looked at correlations, which are difficult to interpret.
One of the researchers, John Michael, explains the process:
“There has been a great deal of hype about the mirror system, and now we have performed an experiment that finally provides clear and straightforward evidence that the mirror system serves to help people make sense of others’ actions,” says John Michael.
Understanding autism and schizophrenia
The study shows that there are areas of the brain that are involved in the production of actions. And the researchers found evidence that these areas contribute to understanding others’ actions. This means that the same areas are involved in producing actions and understanding others’ actions. This helps us in everyday life, but it also holds great potential when trying to understand why people with autism and schizophrenia have difficulties with social interaction.
“Attaining knowledge of the processes underlying social understanding in people in general is an important part of the process of attaining knowledge of the underlying causes of the difficulties that some people diagnosed with autism and schizophrenia experience in sustaining social understanding. But it is important to emphasise that this is just one piece of the puzzle.”
“The findings may be interesting to therapists and psychiatrists who work with patients with schizophrenia or autism, or even to educational researchers,” adds John Michael.
Facts about the empirical basis
The participants (20 adults) came to the lab three times. They were given brain scans on the first visit. On the second and third, they received stimulation to their motor system and then performed a typical psychological task in which they watched brief videos of actors pantomiming actions (about 250 videos each time). After each video they had to choose a picture of an object that matched the pantomimed video. For example, a hammer was the correct answer for the video of an actor pretending to hammer. This task was intended to gauge their understanding of the observed actions. The researchers found that the stimulation interfered with their performance of this task.
Innovative method
The researchers used an innovative technique for magnetically stimulating highly specific brain areas in order to temporarily disrupt normal processing in those areas. The reason for using this technique (called continuous theta-burst stimulation) in general is that it makes it possible to determine which brain areas perform which functions. For example, if you stimulate (and thus temporarily impair) area A, and the participants subsequently have difficulty with some specific task (task T), then you can infer that area A usually performs task T. The effect goes away after 20 minutes, so this is a harmless and widely applicable way to identify which tasks are performed by which areas.
With continuous theta-burst stimulation, you can actually determine that the activation of A contributes as a cause to people performing T. This method thus promises to be of great use to neuroscientists in the coming years.

New study settles how social understanding is performed by the brain

A new study settles an important question about how social understanding is performed in the brain. The findings may help us to attain a better understanding of why people with autism and schizophrenia have difficulties with social interaction.

In a study to be published in Psychological Science, researchers from Aarhus University and the University of Copenhagen demonstrate that brain cells in what is called the mirror system help people make sense of the actions they see other people perform in everyday life.

Using magnetic stimulation to temporarily disrupt normal processing of the areas of the human brain involved in the production of actions of human participants, it is demonstrated that these areas are also involved in the understanding of actions. The study is the first to demonstrate a clear causal effect, whereas earlier studies primarily have looked at correlations, which are difficult to interpret.

One of the researchers, John Michael, explains the process:

“There has been a great deal of hype about the mirror system, and now we have performed an experiment that finally provides clear and straightforward evidence that the mirror system serves to help people make sense of others’ actions,” says John Michael.

Understanding autism and schizophrenia

The study shows that there are areas of the brain that are involved in the production of actions. And the researchers found evidence that these areas contribute to understanding others’ actions. This means that the same areas are involved in producing actions and understanding others’ actions. This helps us in everyday life, but it also holds great potential when trying to understand why people with autism and schizophrenia have difficulties with social interaction.

“Attaining knowledge of the processes underlying social understanding in people in general is an important part of the process of attaining knowledge of the underlying causes of the difficulties that some people diagnosed with autism and schizophrenia experience in sustaining social understanding. But it is important to emphasise that this is just one piece of the puzzle.”

“The findings may be interesting to therapists and psychiatrists who work with patients with schizophrenia or autism, or even to educational researchers,” adds John Michael.

Facts about the empirical basis

The participants (20 adults) came to the lab three times. They were given brain scans on the first visit. On the second and third, they received stimulation to their motor system and then performed a typical psychological task in which they watched brief videos of actors pantomiming actions (about 250 videos each time). After each video they had to choose a picture of an object that matched the pantomimed video. For example, a hammer was the correct answer for the video of an actor pretending to hammer. This task was intended to gauge their understanding of the observed actions. The researchers found that the stimulation interfered with their performance of this task.

Innovative method

The researchers used an innovative technique for magnetically stimulating highly specific brain areas in order to temporarily disrupt normal processing in those areas. The reason for using this technique (called continuous theta-burst stimulation) in general is that it makes it possible to determine which brain areas perform which functions. For example, if you stimulate (and thus temporarily impair) area A, and the participants subsequently have difficulty with some specific task (task T), then you can infer that area A usually performs task T. The effect goes away after 20 minutes, so this is a harmless and widely applicable way to identify which tasks are performed by which areas.

With continuous theta-burst stimulation, you can actually determine that the activation of A contributes as a cause to people performing T. This method thus promises to be of great use to neuroscientists in the coming years.

Filed under social interaction autism schizophrenia mirror-neuron system theory of mind social cognition psychology neuroscience science

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