Neuroscience

Articles and news from the latest research reports.

Posts tagged science

132 notes

Smell and eye tests show potential to detect Alzheimer’s early
A decreased ability to identify odors might indicate the development of cognitive impairment and Alzheimer’s disease, while examinations of the eye could indicate the build-up of beta-amyloid, a protein associated with Alzheimer’s, in the brain, according to the results of four research trials reported today at the Alzheimer’s Association International Conference® 2014 (AAIC® 2014) in Copenhagen.
In two of the studies, the decreased ability to identify odors was significantly associated with loss of brain cell function and progression to Alzheimer’s disease. In two other studies, the level of beta-amyloid detected in the eye (a) was significantly correlated with the burden of beta-amyloid in the brain and (b) allowed researchers to accurately identify the people with Alzheimer’s in the studies.
Beta-amyloid protein is the primary material found in the sticky brain “plaques” characteristic of Alzheimer’s disease. It is known to build up in the brain many years before typical Alzheimer’s symptoms of memory loss and other cognitive problems.
"In the face of the growing worldwide Alzheimer’s disease epidemic, there is a pressing need for simple, less invasive diagnostic tests that will identify the risk of Alzheimer’s much earlier in the disease process," said Heather Snyder, Ph.D., Alzheimer’s Association director of Medical and Scientific Operations. "This is especially true as Alzheimer’s researchers move treatment and prevention trials earlier in the course of the disease."
"More research is needed in the very promising area of Alzheimer’s biomarkers because early detection is essential for early intervention and prevention, when new treatments become available. For now, these four studies reported at AAIC point to possible methods of early detection in a research setting to choose study populations for clinical trials of Alzheimer’s treatments and preventions," Snyder said.
With the support of the Alzheimer’s Association and the Alzheimer’s community, the United States created its first National Plan to Address Alzheimer’s Disease in 2012. The plan includes the critical goal, which was adopted by the G8 at the Dementia Summit in 2013, of preventing and effectively treating Alzheimer’s by 2025. It is only through strong implementation and adequate funding of the plan, including an additional $200 million in fiscal year 2015 for Alzheimer’s research, that we’ll meet that goal. For more information and to get involved, visit http://www.alz.org.
Clinically, at this time it is only possible to detect Alzheimer’s late in its development, when significant brain damage has already occurred. Biological markers of Alzheimer’s disease may be able to detect it at an earlier stage. For example, using brain PET imaging in conjunction with a specialized chemical that binds to beta-amyloid protein, the buildup of the protein as plaques in the brain can be revealed years before symptoms appear. These scans can be expensive and are not available everywhere. Amyloid can also be detected in cerebrospinal fluid through a lumbar puncture where a needle is inserted between two bones (vertebrae) in your lower back to remove a sample of the fluid that surrounds your brain and spinal cord.
Read more
(Image: Getty Images)

Smell and eye tests show potential to detect Alzheimer’s early

A decreased ability to identify odors might indicate the development of cognitive impairment and Alzheimer’s disease, while examinations of the eye could indicate the build-up of beta-amyloid, a protein associated with Alzheimer’s, in the brain, according to the results of four research trials reported today at the Alzheimer’s Association International Conference® 2014 (AAIC® 2014) in Copenhagen.

In two of the studies, the decreased ability to identify odors was significantly associated with loss of brain cell function and progression to Alzheimer’s disease. In two other studies, the level of beta-amyloid detected in the eye (a) was significantly correlated with the burden of beta-amyloid in the brain and (b) allowed researchers to accurately identify the people with Alzheimer’s in the studies.

Beta-amyloid protein is the primary material found in the sticky brain “plaques” characteristic of Alzheimer’s disease. It is known to build up in the brain many years before typical Alzheimer’s symptoms of memory loss and other cognitive problems.

"In the face of the growing worldwide Alzheimer’s disease epidemic, there is a pressing need for simple, less invasive diagnostic tests that will identify the risk of Alzheimer’s much earlier in the disease process," said Heather Snyder, Ph.D., Alzheimer’s Association director of Medical and Scientific Operations. "This is especially true as Alzheimer’s researchers move treatment and prevention trials earlier in the course of the disease."

"More research is needed in the very promising area of Alzheimer’s biomarkers because early detection is essential for early intervention and prevention, when new treatments become available. For now, these four studies reported at AAIC point to possible methods of early detection in a research setting to choose study populations for clinical trials of Alzheimer’s treatments and preventions," Snyder said.

With the support of the Alzheimer’s Association and the Alzheimer’s community, the United States created its first National Plan to Address Alzheimer’s Disease in 2012. The plan includes the critical goal, which was adopted by the G8 at the Dementia Summit in 2013, of preventing and effectively treating Alzheimer’s by 2025. It is only through strong implementation and adequate funding of the plan, including an additional $200 million in fiscal year 2015 for Alzheimer’s research, that we’ll meet that goal. For more information and to get involved, visit http://www.alz.org.

Clinically, at this time it is only possible to detect Alzheimer’s late in its development, when significant brain damage has already occurred. Biological markers of Alzheimer’s disease may be able to detect it at an earlier stage. For example, using brain PET imaging in conjunction with a specialized chemical that binds to beta-amyloid protein, the buildup of the protein as plaques in the brain can be revealed years before symptoms appear. These scans can be expensive and are not available everywhere. Amyloid can also be detected in cerebrospinal fluid through a lumbar puncture where a needle is inserted between two bones (vertebrae) in your lower back to remove a sample of the fluid that surrounds your brain and spinal cord.

Read more

(Image: Getty Images)

Filed under alzheimer's disease dementia biomarkers beta amyloid smell vision neuroscience science

157 notes

Molecular imbalance linked to brain tumour seizures
Researchers in France may have discovered why some patients with a type of brain tumour have epileptic seizures.
“This small study is interesting and shows that glioma-linked epilepsy may be connected to certain channels found in the membranes of nerve cells” - Dr Robin Grant, Edinburgh Cancer Research UK Centre
Their study, published in Science Translational Medicine, suggests that seizures in patients with glioma may be linked to an imbalance of chloride – which is involved in nerve activity – in certain brain cells.
Whether a patient has seizures is linked to how aggressive their tumour is – with less aggressive cases being more prone to epilepsy as tumour cells slowly progress and alter brain tissue.
It is hoped that further research could explore treatments for glioma-linked epilepsy by controlling chloride levels in the brain.
Glioma develops from specialised brain cells known as ‘glial cells’ that usually help to keep brain nerve cells in place, providing support and protection to ensure correct brain function.
In the latest study, scientists from Sorbonne University studied brain tissue samples from 47 glioma patients and found that nerve tissue infiltrated by glioma cells behaves in similar ways to other forms of epilepsy.
Looking at the patient samples, the team found that a particular type of nerve cell – called a pyramidal cell – released excessive amounts of chloride from inside the cells when exposed to a molecule called GABA, which is also involved in transmitting nerve signals.
GABA was released by other neighbouring nerve cells called ‘interneurons’. And the researchers believe that the release of chloride through specialised molecular channels in the membrane of nerve cells, may be responsible for the seizures experienced in some glioma patients.
Dr Robin Grant, an expert in epilepsy and glioma from the Edinburgh Cancer Research UK Centre, who was not involved in the research, said that the channels may make good drug targets for further investigation, but a finer understanding of the involvement of other processes is still needed.
“This small study is interesting and shows that glioma-linked epilepsy, as with other types of epilepsy, may be connected to certain channels found in the membranes of nerve cells.
“More research will be needed to understand the finer details of this process in glioma and whether these channels, along with other similar channels found in nerve cells, could be good targets for drugs to help control the condition.”

Molecular imbalance linked to brain tumour seizures

Researchers in France may have discovered why some patients with a type of brain tumour have epileptic seizures.

“This small study is interesting and shows that glioma-linked epilepsy may be connected to certain channels found in the membranes of nerve cells” - Dr Robin Grant, Edinburgh Cancer Research UK Centre

Their study, published in Science Translational Medicine, suggests that seizures in patients with glioma may be linked to an imbalance of chloride – which is involved in nerve activity – in certain brain cells.

Whether a patient has seizures is linked to how aggressive their tumour is – with less aggressive cases being more prone to epilepsy as tumour cells slowly progress and alter brain tissue.

It is hoped that further research could explore treatments for glioma-linked epilepsy by controlling chloride levels in the brain.

Glioma develops from specialised brain cells known as ‘glial cells’ that usually help to keep brain nerve cells in place, providing support and protection to ensure correct brain function.

In the latest study, scientists from Sorbonne University studied brain tissue samples from 47 glioma patients and found that nerve tissue infiltrated by glioma cells behaves in similar ways to other forms of epilepsy.

Looking at the patient samples, the team found that a particular type of nerve cell – called a pyramidal cell – released excessive amounts of chloride from inside the cells when exposed to a molecule called GABA, which is also involved in transmitting nerve signals.

GABA was released by other neighbouring nerve cells called ‘interneurons’. And the researchers believe that the release of chloride through specialised molecular channels in the membrane of nerve cells, may be responsible for the seizures experienced in some glioma patients.

Dr Robin Grant, an expert in epilepsy and glioma from the Edinburgh Cancer Research UK Centre, who was not involved in the research, said that the channels may make good drug targets for further investigation, but a finer understanding of the involvement of other processes is still needed.

“This small study is interesting and shows that glioma-linked epilepsy, as with other types of epilepsy, may be connected to certain channels found in the membranes of nerve cells.

“More research will be needed to understand the finer details of this process in glioma and whether these channels, along with other similar channels found in nerve cells, could be good targets for drugs to help control the condition.”

Filed under brain tumours epileptic seizures epilepsy glioma glial cells nerve cells neuroscience science

112 notes

Virtual Finger Enables Scientists to Navigate and Analyze 3D Images of Complex Biological Structures
Researchers have pioneered a revolutionary new way to digitally navigate three-dimensional images. The new technology, called Virtual Finger, allows scientists to move through digital images of small structures like neurons and synapses using the flat surface of their computer screens. Virtual Finger’s unique technology makes 3D imaging studies orders of magnitude more efficient, saving time, money and resources at an unprecedented level across many areas of experimental biology. The software and its applications are profiled in this week’s issue of the journal Nature Communications.
Most other image analysis software works by dividing a three-dimensional image into a series of thin slices, each of which can be viewed like a flat image on a computer screen. To study three-dimensional structures, scientists sift through the slices one at a time: a technique that is increasingly challenging with the advent of big data. “Looking through 3D image data one flat slice at a time is simply not efficient, especially when we are dealing with terabytes of data,” explains Hanchuan Peng, Associate Investigator at the Allen Institute for Brain Science. “This is similar to looking through a glass window and seeing objects outside, but not being able to manipulate them because of the physical barrier.”
In sharp contrast, Virtual Finger allows scientists to digitally reach into three-dimensional images of small objects like single cells to access the information they need much more quickly and intuitively. “When you move your cursor along the flat screen of your computer, our software recognizes whether you are pointing to an object that is near, far, or somewhere in between, and allows you to analyze it in depth without having to sift through many two-dimensional images to reach it,” explains Peng.
Scientists at the Allen Institute are already using Virtual Finger to improve their detection of spikes from individual cells, and to better model the morphological structures of neurons. But Virtual Finger promises to be a game-changer for many biological experiments and methods of data analysis, even beyond neuroscience. In their Nature Communications article, the collaborative group of scientists describes how the technology has already been applied to perform three-dimensional microsurgery in order to knock out single cells, study the developing lung, and create a map of all the neural connections in the fly brain.
“Using Virtual Finger could make data collection and analysis ten to 100 times faster, depending on the experiment,” says Peng. “The software allows us to navigate large amounts of biological data in the same way that Google Earth allows you to navigate the world. It truly is a revolutionary technology for many different applications within biological science,” says Peng.
Hanchuan Peng began developing Virtual Finger while at the Howard Hughes Medical Institute’s Janelia Research Campus and continued development at the Allen Institute for Brain Science.

Virtual Finger Enables Scientists to Navigate and Analyze 3D Images of Complex Biological Structures

Researchers have pioneered a revolutionary new way to digitally navigate three-dimensional images. The new technology, called Virtual Finger, allows scientists to move through digital images of small structures like neurons and synapses using the flat surface of their computer screens. Virtual Finger’s unique technology makes 3D imaging studies orders of magnitude more efficient, saving time, money and resources at an unprecedented level across many areas of experimental biology. The software and its applications are profiled in this week’s issue of the journal Nature Communications.

Most other image analysis software works by dividing a three-dimensional image into a series of thin slices, each of which can be viewed like a flat image on a computer screen. To study three-dimensional structures, scientists sift through the slices one at a time: a technique that is increasingly challenging with the advent of big data. “Looking through 3D image data one flat slice at a time is simply not efficient, especially when we are dealing with terabytes of data,” explains Hanchuan Peng, Associate Investigator at the Allen Institute for Brain Science. “This is similar to looking through a glass window and seeing objects outside, but not being able to manipulate them because of the physical barrier.”

In sharp contrast, Virtual Finger allows scientists to digitally reach into three-dimensional images of small objects like single cells to access the information they need much more quickly and intuitively. “When you move your cursor along the flat screen of your computer, our software recognizes whether you are pointing to an object that is near, far, or somewhere in between, and allows you to analyze it in depth without having to sift through many two-dimensional images to reach it,” explains Peng.

Scientists at the Allen Institute are already using Virtual Finger to improve their detection of spikes from individual cells, and to better model the morphological structures of neurons. But Virtual Finger promises to be a game-changer for many biological experiments and methods of data analysis, even beyond neuroscience. In their Nature Communications article, the collaborative group of scientists describes how the technology has already been applied to perform three-dimensional microsurgery in order to knock out single cells, study the developing lung, and create a map of all the neural connections in the fly brain.

“Using Virtual Finger could make data collection and analysis ten to 100 times faster, depending on the experiment,” says Peng. “The software allows us to navigate large amounts of biological data in the same way that Google Earth allows you to navigate the world. It truly is a revolutionary technology for many different applications within biological science,” says Peng.

Hanchuan Peng began developing Virtual Finger while at the Howard Hughes Medical Institute’s Janelia Research Campus and continued development at the Allen Institute for Brain Science.

Filed under virtual finger 3D imaging neurons neuroscience science

85 notes

Sublime Microglia: Expanding Roles for the Guardians of the CNS
Recent findings challenge the concept that microglia solely function in disease states in the central nervous system (CNS). Rather than simply reacting to CNS injury, infection, or pathology, emerging lines of evidence indicate that microglia sculpt the structure of the CNS, refine neuronal circuitry and network connectivity, and contribute to plasticity. These physiological functions of microglia in the normal CNS begin during development and persist into maturity. Here, we develop a conceptual framework for functions of microglia beyond neuroinflammation and discuss the rich repertoire of signaling and communication motifs in microglia that are critical both in pathology and for the normal physiology of the CNS.
Full Article

Sublime Microglia: Expanding Roles for the Guardians of the CNS

Recent findings challenge the concept that microglia solely function in disease states in the central nervous system (CNS). Rather than simply reacting to CNS injury, infection, or pathology, emerging lines of evidence indicate that microglia sculpt the structure of the CNS, refine neuronal circuitry and network connectivity, and contribute to plasticity. These physiological functions of microglia in the normal CNS begin during development and persist into maturity. Here, we develop a conceptual framework for functions of microglia beyond neuroinflammation and discuss the rich repertoire of signaling and communication motifs in microglia that are critical both in pathology and for the normal physiology of the CNS.

Full Article

Filed under microglia CNS inflammation immune cells neuroscience science

490 notes

Virtual humans inspire patients to open up
When we feel down and find ourselves at the doctor’s office for help, the best person to get us to open up about our problems isn’t a person at all. It’s a computer.
A new USC study suggests that patients are more willing to disclose personal information to virtual humans than actual ones, in large part because computers lack the proclivity to look down on people the way another human might.
The research, which was funded by the Defense Advanced Research Projects Agency and the U.S. Army, is promising for people suffering from post-traumatic stress and other mental anguish, said Gale Lucas, a social psychologist at USC’s Institute for Creative Technologies, who led the study. In intake interviews, people were more honest about their symptoms, no matter how potentially embarrassing, when they believed that a human observer wasn’t in on the conversation.
“In any given topic, there’s a difference between what a person is willing to admit in person versus anonymously,” Lucas said.
The study, which will be published in the journal Computers in Human Behavior, provides the first empirical evidence that virtual humans can increase a patient’s willingness to disclose personal information in a clinical setting, researchers said. It also presents compelling reasons for doctors to start using virtual humans as medical screeners. The honest answers acquired by a virtual human could help doctors diagnose and treat their patients more appropriately.
The recruitment process
Researchers recruited 239 adults through Craigslist to participate in the study. The adults, whose ages ranged from 18 to 65, were invited to a laboratory to interact with a virtual human as if they were being admitted to a clinic or hospital.
Subjects were interviewed as part of an evaluation of SimSensei, a virtual human application that can be used to identify signals of depression and other mental health issues through real-time sensing and recognition of nonverbal behaviors. It is a research project designed to assess the potential of such technology and is based on more than 10 years of virtual human research and development at ICT.
Some participants were told the virtual human’s responses were fully automated, others were told that the responses were remotely controlled, puppet-like, by a human observer in another room. In reality, all participants were randomly assigned a fully or semi-automated virtual human, regardless of what they were told, and their video interviews were later analyzed by a (human) researcher.
The mere belief that participants were interacting with only a computer made them more open and honest, researchers found, even when the virtual human asked personal questions such as, “What’s something you feel guilty about?” or “Tell me about an event, or something that you wish you could erase from your memory.”
In addition, video analysis of the study subjects’ facial expressions showed that they were also more likely to show more intense signs of sadness — perhaps the most vulnerable of expressions — when they thought only pixels were present.
Opening up to a virtual human
One participant who thought the virtual human was automated said the experience was “way better than talking to a person. I don’t really feel comfortable talking about personal stuff to other people.”
In contrast, a participant who thought the conversation was being observed told researchers, “I wish you hadn’t told me that other people were in the other room listening in. It was weird, like, I don’t even know these people. I would have said a lot more stuff if they weren’t there.”
The virtual human named Ellie opened the conversation with questions such as “Where are you from originally?” and incorporated feedback (“I’m sorry to hear that”) and empathetic listening through facial expressions and nodding. Secondly, “her” virtual nature gave participants a sense of anonymity, making them more willing to disclose personal information in a private setting without fear of criticism.
“We know that developing a rapport and feeling free of judgment are two important factors that affect a person’s willingness to disclose personal information,” said co-author Jonathan Gratch, director of virtual humans research at ICT and a professor in USC’s Department of Computer Science. “The virtual character delivered on both these fronts and that is what makes this a particularly valuable tool for obtaining information people might feel sensitive about sharing.”
The researchers were careful to emphasize that the virtual human could supplement — not replace — trained clinicians. Still, the implications of the findings are plentiful both in terms of reducing costs and improving care, and several are being explored in projects being developed at ICT, including virtual humans to help detect signs of depression, provide screening services for patients in remote areas or act as role-playing partners for training health professionals.
In an age where people are increasingly interacting with computers over real people for everything from banking to grocery shopping, the researchers hope that opening up to a virtual character will open the door for people to get the care they need in a variety of health care settings as well.

Virtual humans inspire patients to open up

When we feel down and find ourselves at the doctor’s office for help, the best person to get us to open up about our problems isn’t a person at all. It’s a computer.

A new USC study suggests that patients are more willing to disclose personal information to virtual humans than actual ones, in large part because computers lack the proclivity to look down on people the way another human might.

The research, which was funded by the Defense Advanced Research Projects Agency and the U.S. Army, is promising for people suffering from post-traumatic stress and other mental anguish, said Gale Lucas, a social psychologist at USC’s Institute for Creative Technologies, who led the study. In intake interviews, people were more honest about their symptoms, no matter how potentially embarrassing, when they believed that a human observer wasn’t in on the conversation.

“In any given topic, there’s a difference between what a person is willing to admit in person versus anonymously,” Lucas said.

The study, which will be published in the journal Computers in Human Behavior, provides the first empirical evidence that virtual humans can increase a patient’s willingness to disclose personal information in a clinical setting, researchers said. It also presents compelling reasons for doctors to start using virtual humans as medical screeners. The honest answers acquired by a virtual human could help doctors diagnose and treat their patients more appropriately.

The recruitment process

Researchers recruited 239 adults through Craigslist to participate in the study. The adults, whose ages ranged from 18 to 65, were invited to a laboratory to interact with a virtual human as if they were being admitted to a clinic or hospital.

Subjects were interviewed as part of an evaluation of SimSensei, a virtual human application that can be used to identify signals of depression and other mental health issues through real-time sensing and recognition of nonverbal behaviors. It is a research project designed to assess the potential of such technology and is based on more than 10 years of virtual human research and development at ICT.

Some participants were told the virtual human’s responses were fully automated, others were told that the responses were remotely controlled, puppet-like, by a human observer in another room. In reality, all participants were randomly assigned a fully or semi-automated virtual human, regardless of what they were told, and their video interviews were later analyzed by a (human) researcher.

The mere belief that participants were interacting with only a computer made them more open and honest, researchers found, even when the virtual human asked personal questions such as, “What’s something you feel guilty about?” or “Tell me about an event, or something that you wish you could erase from your memory.”

In addition, video analysis of the study subjects’ facial expressions showed that they were also more likely to show more intense signs of sadness — perhaps the most vulnerable of expressions — when they thought only pixels were present.

Opening up to a virtual human

One participant who thought the virtual human was automated said the experience was “way better than talking to a person. I don’t really feel comfortable talking about personal stuff to other people.”

In contrast, a participant who thought the conversation was being observed told researchers, “I wish you hadn’t told me that other people were in the other room listening in. It was weird, like, I don’t even know these people. I would have said a lot more stuff if they weren’t there.”

The virtual human named Ellie opened the conversation with questions such as “Where are you from originally?” and incorporated feedback (“I’m sorry to hear that”) and empathetic listening through facial expressions and nodding. Secondly, “her” virtual nature gave participants a sense of anonymity, making them more willing to disclose personal information in a private setting without fear of criticism.

“We know that developing a rapport and feeling free of judgment are two important factors that affect a person’s willingness to disclose personal information,” said co-author Jonathan Gratch, director of virtual humans research at ICT and a professor in USC’s Department of Computer Science. “The virtual character delivered on both these fronts and that is what makes this a particularly valuable tool for obtaining information people might feel sensitive about sharing.”

The researchers were careful to emphasize that the virtual human could supplement — not replace — trained clinicians. Still, the implications of the findings are plentiful both in terms of reducing costs and improving care, and several are being explored in projects being developed at ICT, including virtual humans to help detect signs of depression, provide screening services for patients in remote areas or act as role-playing partners for training health professionals.

In an age where people are increasingly interacting with computers over real people for everything from banking to grocery shopping, the researchers hope that opening up to a virtual character will open the door for people to get the care they need in a variety of health care settings as well.

Filed under virtual reality virtual humans self-disclosure simsensei psychology neuroscience science

97 notes

Sleep Disturbances, Common in Parkinson’s Disease, Can Be Early Indicator of Disease Onset

Up to 70% of Parkinson’s disease (PD) patients experience sleep problems that negatively impact their quality of life. Some patients have disturbed sleep/wake patterns such as difficulty falling asleep or staying asleep, while other patients may be subject to sudden and involuntary daytime sleep “attacks.” In the extreme, PD patients may exhibit REM-sleep behavior disorder (RBD), characterized by vivid, violent dreams or dream re-enactment, even before motor symptoms appear. A review in the Journal of Parkinson’s Disease discusses the underlying causes of sleep problems in PD, as well as medications, disease pathology, and comorbidities, and describes the most appropriate diagnostic tools and treatment options.

Sleep problems in PD patients can have wide-ranging adverse effects and can worsen in later stages of the disease. Sleepiness socially isolates patients and excessive sleepiness can put patients at risk of falls or injury, and can mean patients must give up driving. Sleepiness can impair cognition and concentration, exacerbate depression, and interfere with employment. Wakefulness at night impairs daytime wakefulness and may also cause mood instabilities and can exhaust caregivers.

“Diagnosis and effective treatment and management of these problems are essential for improving the quality of life and reducing institutionalization of these patients,” says lead author Wiebke Schrempf, MD, Technische Universität Dresden, Faculty of Medicine Carl Gustav Carus, Department of Neurology, Division of Neurodegenerative Diseases, Dresden, Germany.

Dr. Schrempf and colleagues describe some of the complexities associated with treating sleep problems in PD patients, such as the worsening of sleep problems by dopaminergic medications used to treat motor symptoms. Lower doses of levodopa or dopamine agonists are able to improve sleep quality partly by reducing motor symptoms such as nighttime hypokinesia (decreased body movement), dyskinesia (abnormal voluntary movements), or tremor (involuntary shaking), which interfere with normal sleep. However, the same medications may also cause excessive daytime sleepiness. The report describes how changing medication, dose, duration of treatment, or timing of administration can improve outcomes.

The presence of other conditions common in PD patients such as depression, dementia, hallucinations, and psychosis may interfere with sleep. Unfortunately, some antidepressants can also impair sleep.

Sleep problems may also be harbingers of future neurodegenerative disease. Patients with RBD exhibit intermittent loss of normal muscle relaxation during REM sleep and engage in dream enactment behavior during which they may shout, laugh, or exhibit movements like kicking and boxing. “RBD seems to be a good clinical predictor of emerging neurodegenerative diseases with a high specificity and low sensitivity, whereas other early clinical features of PD, such as olfactory dysfunction and constipation, are less specific,” says Dr. Schrempf. “These early clues may help identify PD patients before motor symptoms appear, when disease-modifying therapies may be most beneficial.”

PD is the second most common neurodegenerative disorder in the United States, affecting approximately one million Americans and five million people worldwide. Its prevalence is projected to double by 2030. The most characteristic symptoms are movement-related, such as involuntary shaking and muscle stiffness. Non-motor symptoms, such as worsening depression, cognition, and anxiety, olfactory dysfunction, and sleep disturbances, can appear prior to the onset of motor symptoms.

(Source: alphagalileo.org)

Filed under parkinson's disease sleep sleep problems medication neuroscience science

109 notes

Team Sheds New Light on Nerve Cell Growth

Amidst the astounding complexity of the billions of nerve cells and trillions of synaptic connections in the brain, how do nerve cells decide how far to grow or how many connections to build? How do they coordinate these events within the developing brain?

In a new study, scientists from the Florida campus of The Scripps Research Institute (TSRI) have shed new light on these complex processes, showing that a particular protein plays a far more sophisticated role in neuron development than previously thought.

The study, published in the journal PLOS Genetics, focuses on the large, intracellular signaling protein RPM-1 that is expressed in the nervous system. TSRI Assistant Professor Brock Grill and his team show the surprising degree to which RPM-1 harnesses sophisticated mechanisms to regulate neuron development.

Specifically, the research sheds light on the role of RPM-1 in the development of axons or nerve fibers—the elongated projections of nerve cells that transmit electrical impulses away from the neuron via synapses. Some axons are quite long; in the sciatic nerve, axons run from the base of the spine to the big toe.

“Collectively, our recent work offers significant evidence that RPM-1 coordinates how long an axon grows with construction of synaptic connections,” said Grill. “Understanding how these two developmental processes are coordinated at the molecular level is extremely challenging. We’ve now made significant progress.”

Putting Together the Pieces

The study describes how RPM-1 regulates the activity of a single protein known as DLK-1, a protein that regulates neuron development and plays an essential role in axon regeneration. RPM-1 uses PPM-2, an enzyme that removes a phosphate group from a protein thereby altering its function, in combination with intrinsic ubiquitin ligase activity to directly inhibit DLK-1.

“Studies on RPM-1 have been critical to understanding how this conserved family of proteins works,” said Scott T. Baker, the first author of the study and a member of Grill’s research team. “Because RPM-1 plays multiple roles during neuronal development, you wouldn’t want to interfere with it. But exploring the role of PPM-2 in controlling DLK-1 and axon regeneration could be worthwhile—and could have implications in neurodegenerative diseases.”

The Grill lab has also explored other aspects of how RPM-1 regulates neuron development. A related study, also published in PLOS Genetics, shows that RPM-1 functions as a part of a novel pathway to control β-catenin activity—this is the first evidence that RPM-1 works in connection with extracellular signals, such as a family of protein growth factors known as Wnts, and is part of larger signaling networks that regulate development. A paper in the journal Neural Development shows that RPM-1 is localized at both the synapse and the mature axon tip, evidence that RPM-1 is positioned to potentially coordinate the construction of synapses with regulation of axon extension and termination.

(Source: scripps.edu)

Filed under nerve cells synapse formation RPM-1 DLK-1 neuron development neuroscience science

85 notes

(Image caption: On these images, the cerebral activation detected by ultrasound imaging is shown in red. During odor presentation, specific areas are activated in the olfactory bulb but not in the piriform cortex. Credit: © Mickael Tanter / Hirac Gurden)
Ultrasound tracks odor representation in the brain
A new ultrasound imaging technique has provided the first ever in vivo visualization of activity in the piriform cortex of rats during odor perception. This deep-seated brain structure plays an important role in olfaction, and was inaccessible to functional imaging until now. This work also sheds new light on the still poorly known functioning of the olfactory system, and notably how information is processed in the brain. This study is the result of a collaboration between the team led by Mickael Tanter at the Institut Langevin (CNRS/INSERM/ESPCI ParisTech/UPMC/Université Paris Diderot) and that led by Hirac Gurden in the Laboratoire Imagerie et Modélisation en Neurobiologie et Cancérologie (CNRS/Université Paris-Sud/Université Paris Diderot). Their findings are published in NeuroImage.
How can the perception of the senses help represent the external environment? How, for example, does the brain process food-or perfume-related olfactory data? Although the organization of the olfactory system is well known - it is similar in organisms ranging from insects to mammals - its functioning remains unclear. To answer these questions, the scientists focused on the two brain structures that act as major olfactory relays: the olfactory bulb and the piriform cortex. In the rat, the olfactory bulb is located between the eyes, just behind the nasal bone. The piriform cortex, meanwhile, is deep-seated in the brain of rodents, which made it impossible to obtain any functional images in a living animal until now.
Yet the neurofunctional ultrasound imaging technique developed by Mickael Tanter’s team, called fUS(functional Ultrasound), allows the monitoring of neuronal activity in the piriform cortex. It is based on the transmission of ultrasonic plane waves into the brain tissue. After data processing, the echoes returned by the structures crossed by these waves can provide images with unequalled spatial and temporal resolution: 80 micrometers and a few tens of milliseconds. The contrast on these images is due to variations in the brain’s blood flow. Indeed, the activity of nerve cells requires an input of energy: it is therefore coupled to an influx of blood into the zone concerned. By recording volume variations in the blood vessels irrigating the different brain structures, it is there fore possible to determine the location of activated neurons.
Several imaging techniques, such as MRI, are already based on the link between blood volume and neuronal activity. But fUS offers advantages in terms of cost, ease of use and resolution. Furthermore, it provides easier access to the deepest structures that are often located several centimeters beneath the cranium.
The recordings performed by Hirac Gurden’s team using this technique made it possible to observe the spatial distribution of activity within the olfactory bulb. When an odor was perceived, blood volume increased in clearly defined areas: each odor thus corresponded to a specific pattern of activated neurons. In addition to these findings, and for the first time, the images revealed an absence of spatial distribution in the piriform cortex. At this level, two different odors triggered the same activation throughout the region.
The cellular mechanisms responsible for the disappearance of a spatial signature are not yet clearly defined, but these findings lead to the formulation of several hypotheses. The piriform cortex could be a structure that serves not only to process olfactory stimuli but rather to integrate and memorize different types of data. By making abstraction of the strict odor-induced patterns, it would be possible to make associations and achieve a global concept. For example, based on the perception of the hundreds of odorant molecules found in coffee, the piriform cortex would be able to recognize a single odor, that ofcoffee.
This work opens new perspectives for both imaging and neurobiology. The researchers will now be focusing on the effects of learning on cortical activity in order to elucidate its role and the specificities of the olfactory system.

(Image caption: On these images, the cerebral activation detected by ultrasound imaging is shown in red. During odor presentation, specific areas are activated in the olfactory bulb but not in the piriform cortex. Credit: © Mickael Tanter / Hirac Gurden)

Ultrasound tracks odor representation in the brain

A new ultrasound imaging technique has provided the first ever in vivo visualization of activity in the piriform cortex of rats during odor perception. This deep-seated brain structure plays an important role in olfaction, and was inaccessible to functional imaging until now. This work also sheds new light on the still poorly known functioning of the olfactory system, and notably how information is processed in the brain. This study is the result of a collaboration between the team led by Mickael Tanter at the Institut Langevin (CNRS/INSERM/ESPCI ParisTech/UPMC/Université Paris Diderot) and that led by Hirac Gurden in the Laboratoire Imagerie et Modélisation en Neurobiologie et Cancérologie (CNRS/Université Paris-Sud/Université Paris Diderot). Their findings are published in NeuroImage.

How can the perception of the senses help represent the external environment? How, for example, does the brain process food-or perfume-related olfactory data? Although the organization of the olfactory system is well known - it is similar in organisms ranging from insects to mammals - its functioning remains unclear. To answer these questions, the scientists focused on the two brain structures that act as major olfactory relays: the olfactory bulb and the piriform cortex. In the rat, the olfactory bulb is located between the eyes, just behind the nasal bone. The piriform cortex, meanwhile, is deep-seated in the brain of rodents, which made it impossible to obtain any functional images in a living animal until now.

Yet the neurofunctional ultrasound imaging technique developed by Mickael Tanter’s team, called fUS(functional Ultrasound), allows the monitoring of neuronal activity in the piriform cortex. It is based on the transmission of ultrasonic plane waves into the brain tissue. After data processing, the echoes returned by the structures crossed by these waves can provide images with unequalled spatial and temporal resolution: 80 micrometers and a few tens of milliseconds. The contrast on these images is due to variations in the brain’s blood flow. Indeed, the activity of nerve cells requires an input of energy: it is therefore coupled to an influx of blood into the zone concerned. By recording volume variations in the blood vessels irrigating the different brain structures, it is there fore possible to determine the location of activated neurons.

Several imaging techniques, such as MRI, are already based on the link between blood volume and neuronal activity. But fUS offers advantages in terms of cost, ease of use and resolution. Furthermore, it provides easier access to the deepest structures that are often located several centimeters beneath the cranium.

The recordings performed by Hirac Gurden’s team using this technique made it possible to observe the spatial distribution of activity within the olfactory bulb. When an odor was perceived, blood volume increased in clearly defined areas: each odor thus corresponded to a specific pattern of activated neurons. In addition to these findings, and for the first time, the images revealed an absence of spatial distribution in the piriform cortex. At this level, two different odors triggered the same activation throughout the region.

The cellular mechanisms responsible for the disappearance of a spatial signature are not yet clearly defined, but these findings lead to the formulation of several hypotheses. The piriform cortex could be a structure that serves not only to process olfactory stimuli but rather to integrate and memorize different types of data. By making abstraction of the strict odor-induced patterns, it would be possible to make associations and achieve a global concept. For example, based on the perception of the hundreds of odorant molecules found in coffee, the piriform cortex would be able to recognize a single odor, that of
coffee.

This work opens new perspectives for both imaging and neurobiology. The researchers will now be focusing on the effects of learning on cortical activity in order to elucidate its role and the specificities of the olfactory system.

Filed under piriform cortex olfactory system olfactory bulb functional ultrasound imaging odor neuroscience science

207 notes

Blame it on the astrocytes
In the brains of all vertebrates, information is transmitted through synapses, a mechanism that allows an electric or chemical signal to be passed from one brain cell to another. Chemical synapses, which are the most abundant type of synapse, can be either excitatory or inhibitory. Synapse formation is crucial for learning, memory, perception and cognition, and the balance between excitatory and inhibitory synapses critical for brain function. For instance, every time we learn something, the new information is transformed into memory through synaptic plasticity, a process in which synapses are strengthened and become more responsive to different stimuli or environmental cues. Synapses may change their shape or function in a matter of seconds or over an entire lifetime. In humans, a number of disorders are associated with dysfunctional synapses, including autism, epilepsy, substance abuse and depression.
Astrocytes, named for their star-like shape, are ubiquitous brain cells known for regulating excitatory synapse formation through cells. Recent studies have shown that astrocytes also play a role in forming inhibitory synapses, but the key players and underlying mechanisms have remained unknown until now.
A new study just published in the journal Glia and available online on July 11th, details the newly discovered mechanism by which astrocytes are involved in inhibitory synapse formation and presents strong evidence that Transforming Growth Factor Beta 1 (TGF β1), a protein produced by many cell types (including astrocytes) is a key player in this process. The team led by Flávia Gomes of the Rio de Janeiro Institute of Biomedical Sciences at the Federal University of Rio de Janeiro investigated the process in both mouse and human tissues, first in test tubes, then in living brain cells.
Previous evidence has shown that TGF β1, a molecule associated with essential functions in nervous system development and repair, modulates other components responsible for normal brain function. In this study, the authors were able to show that TGF β1 triggers N-methyl-D-aspartate receptor (NMDA), a molecule controlling memory formation and maintenance through synaptic plasticity. In the study, the group also shows that TGF β1-induction of inhibitory synapses depends on activation of another molecule - Ca2+/calmodulin-dependent protein kinase II (CaMK2)-, which works as a mediator for learning and memory. “Our study is the first to associate this complex pathway of molecules, of which TGF β1 seems to be a key player, to astrocytes’ ability to modulate inhibitory synapses”, says Flávia Gomes.
The idea that the balance between excitatory and inhibitory inputs depends on astrocyte signals gains strong support with this new study and suggests a pivotal role for astrocytes in the development of neurological disorders involving impaired inhibitory synapse transmission. Knowing the players and mechanisms underlying inhibitory synapses may improve our understanding of synaptic plasticity and cognitive processes and may help develop new drugs for treating these diseases.
(Image credit)

Blame it on the astrocytes

In the brains of all vertebrates, information is transmitted through synapses, a mechanism that allows an electric or chemical signal to be passed from one brain cell to another. Chemical synapses, which are the most abundant type of synapse, can be either excitatory or inhibitory. Synapse formation is crucial for learning, memory, perception and cognition, and the balance between excitatory and inhibitory synapses critical for brain function. For instance, every time we learn something, the new information is transformed into memory through synaptic plasticity, a process in which synapses are strengthened and become more responsive to different stimuli or environmental cues. Synapses may change their shape or function in a matter of seconds or over an entire lifetime. In humans, a number of disorders are associated with dysfunctional synapses, including autism, epilepsy, substance abuse and depression.

Astrocytes, named for their star-like shape, are ubiquitous brain cells known for regulating excitatory synapse formation through cells. Recent studies have shown that astrocytes also play a role in forming inhibitory synapses, but the key players and underlying mechanisms have remained unknown until now.

A new study just published in the journal Glia and available online on July 11th, details the newly discovered mechanism by which astrocytes are involved in inhibitory synapse formation and presents strong evidence that Transforming Growth Factor Beta 1 (TGF β1), a protein produced by many cell types (including astrocytes) is a key player in this process. The team led by Flávia Gomes of the Rio de Janeiro Institute of Biomedical Sciences at the Federal University of Rio de Janeiro investigated the process in both mouse and human tissues, first in test tubes, then in living brain cells.

Previous evidence has shown that TGF β1, a molecule associated with essential functions in nervous system development and repair, modulates other components responsible for normal brain function. In this study, the authors were able to show that TGF β1 triggers N-methyl-D-aspartate receptor (NMDA), a molecule controlling memory formation and maintenance through synaptic plasticity. In the study, the group also shows that TGF β1-induction of inhibitory synapses depends on activation of another molecule - Ca2+/calmodulin-dependent protein kinase II (CaMK2)-, which works as a mediator for learning and memory. “Our study is the first to associate this complex pathway of molecules, of which TGF β1 seems to be a key player, to astrocytes’ ability to modulate inhibitory synapses”, says Flávia Gomes.

The idea that the balance between excitatory and inhibitory inputs depends on astrocyte signals gains strong support with this new study and suggests a pivotal role for astrocytes in the development of neurological disorders involving impaired inhibitory synapse transmission. Knowing the players and mechanisms underlying inhibitory synapses may improve our understanding of synaptic plasticity and cognitive processes and may help develop new drugs for treating these diseases.

(Image credit)

Filed under astrocytes synaptic plasticity synapses TGF β1 neuroscience science

184 notes

Brain activity in sex addiction mirrors that of drug addiction
Pornography triggers brain activity in people with compulsive sexual behaviour – known commonly as sex addiction – similar to that triggered by drugs in the brains of drug addicts, according to a University of Cambridge study published in the journal PLOS ONE. However, the researchers caution that this does not necessarily mean that pornography itself is addictive.
Although precise estimates are unknown, previous studies have suggested that as many as one in 25 adults is affected by compulsive sexual behaviour, an obsession with sexual thoughts, feelings or behaviour which they are unable to control. This can have an impact on a person’s personal life and work, leading to significant distress and feelings of shame. Excessive use of pornography is one of the main features identified in many people with compulsive sexual behaviour. However, there is currently no formally accepted definition of diagnosing the condition.
In a study funded by the Wellcome Trust, researchers from the Department of Psychiatry at the University of Cambridge looked at brain activity in nineteen male patients affected by compulsive sexual behaviour and compared them to the same number of healthy volunteers. The patients started watching pornography at earlier ages and in higher proportions relative to the healthy volunteers.
“The patients in our trial were all people who had substantial difficulties controlling their sexual behaviour and this was having significant consequences for them, affecting their lives and relationships,” explains Dr Valerie Voon, a Wellcome Trust Intermediate Clinical Fellow at the University of Cambridge. “In many ways, they show similarities in their behaviour to patients with drug addictions. We wanted to see if these similarities were reflected in brain activity, too.”
The study participants were shown a series of short videos featuring either sexually explicit content or sports whilst their brain activity was monitored using functional magnetic resonance imaging (fMRI), which uses a blood oxygen level dependent (BOLD) signal to measure brain activity.
The researchers found that three regions in particular were more active in the brains of the people with compulsive sexual behaviour compared with the healthy volunteers. Significantly, these regions – the ventral striatum, dorsal anterior cingulate and amygdala – were regions that are also particularly activated in drug addicts when shown drug stimuli. The ventral striatum is involved in processing reward and motivation, whilst the dorsal anterior cingulate is implicated in anticipating rewards and drug craving. The amygdala is involved in processing the significance of events and emotions.
The researchers also asked the participants to rate the level of sexual desire that they felt whilst watching the videos, and how much they liked the videos. Drug addicts are thought to be driven to seek their drug because they want – rather than enjoy – it. This abnormal process is known as incentive motivation, a compelling theory in addiction disorders.
As anticipated, patients with compulsive sexual behaviour showed higher levels of desire towards the sexually explicit videos, but did not necessarily rate them higher on liking scores. In the patients, desire was also correlated with higher interactions between regions within the network identified – with greater cross-talk between the dorsal cingulate, ventral striatum and amygdala – for explicit compared to sports videos.
Dr Voon and colleagues also found a correlation between brain activity and age – the younger the patient, the greater the level of activity in the ventral striatum in response to pornography. Importantly, this association was strongest in individuals with compulsive sexual behaviour. The frontal control regions of the brain – essentially, the ‘brakes’ on our compulsivity – continue to develop into the mid-twenties and this imbalance may account for greater impulsivity and risk taking behaviours in younger people. The age-related findings in individuals with compulsive sexual behaviours suggest that the ventral striatum may be important in developmental aspects of compulsive sexual behaviours in a similar fashion as it is in drug addictions, although direct testing of this possibility is needed.
“There are clear differences in brain activity between patients who have compulsive sexual behaviour and healthy volunteers. These differences mirror those of drug addicts,” adds Dr Voon. “Whilst these findings are interesting, it’s important to note, however, that they could not be used to diagnose the condition. Nor does our research necessarily provide evidence that these individuals are addicted to porn – or that porn is inherently addictive. Much more research is required to understand this relationship between compulsive sexual behaviour and drug addiction.”
Dr John Williams, Head of Neuroscience and Mental Health at the Wellcome Trust, says: “Compulsive behaviours, including watching porn to excess, over-eating and gambling, are increasingly common. This study takes us a step further to finding out why we carry on repeating behaviours that we know are potentially damaging to us. Whether we are tackling sex addiction, substance abuse or eating disorders, knowing how best, and when, to intervene in order to break the cycle is an important goal of this research.”

Brain activity in sex addiction mirrors that of drug addiction

Pornography triggers brain activity in people with compulsive sexual behaviour – known commonly as sex addiction – similar to that triggered by drugs in the brains of drug addicts, according to a University of Cambridge study published in the journal PLOS ONE. However, the researchers caution that this does not necessarily mean that pornography itself is addictive.

Although precise estimates are unknown, previous studies have suggested that as many as one in 25 adults is affected by compulsive sexual behaviour, an obsession with sexual thoughts, feelings or behaviour which they are unable to control. This can have an impact on a person’s personal life and work, leading to significant distress and feelings of shame. Excessive use of pornography is one of the main features identified in many people with compulsive sexual behaviour. However, there is currently no formally accepted definition of diagnosing the condition.

In a study funded by the Wellcome Trust, researchers from the Department of Psychiatry at the University of Cambridge looked at brain activity in nineteen male patients affected by compulsive sexual behaviour and compared them to the same number of healthy volunteers. The patients started watching pornography at earlier ages and in higher proportions relative to the healthy volunteers.

“The patients in our trial were all people who had substantial difficulties controlling their sexual behaviour and this was having significant consequences for them, affecting their lives and relationships,” explains Dr Valerie Voon, a Wellcome Trust Intermediate Clinical Fellow at the University of Cambridge. “In many ways, they show similarities in their behaviour to patients with drug addictions. We wanted to see if these similarities were reflected in brain activity, too.”

The study participants were shown a series of short videos featuring either sexually explicit content or sports whilst their brain activity was monitored using functional magnetic resonance imaging (fMRI), which uses a blood oxygen level dependent (BOLD) signal to measure brain activity.

The researchers found that three regions in particular were more active in the brains of the people with compulsive sexual behaviour compared with the healthy volunteers. Significantly, these regions – the ventral striatum, dorsal anterior cingulate and amygdala – were regions that are also particularly activated in drug addicts when shown drug stimuli. The ventral striatum is involved in processing reward and motivation, whilst the dorsal anterior cingulate is implicated in anticipating rewards and drug craving. The amygdala is involved in processing the significance of events and emotions.

The researchers also asked the participants to rate the level of sexual desire that they felt whilst watching the videos, and how much they liked the videos. Drug addicts are thought to be driven to seek their drug because they want – rather than enjoy – it. This abnormal process is known as incentive motivation, a compelling theory in addiction disorders.

As anticipated, patients with compulsive sexual behaviour showed higher levels of desire towards the sexually explicit videos, but did not necessarily rate them higher on liking scores. In the patients, desire was also correlated with higher interactions between regions within the network identified – with greater cross-talk between the dorsal cingulate, ventral striatum and amygdala – for explicit compared to sports videos.

Dr Voon and colleagues also found a correlation between brain activity and age – the younger the patient, the greater the level of activity in the ventral striatum in response to pornography. Importantly, this association was strongest in individuals with compulsive sexual behaviour. The frontal control regions of the brain – essentially, the ‘brakes’ on our compulsivity – continue to develop into the mid-twenties and this imbalance may account for greater impulsivity and risk taking behaviours in younger people. The age-related findings in individuals with compulsive sexual behaviours suggest that the ventral striatum may be important in developmental aspects of compulsive sexual behaviours in a similar fashion as it is in drug addictions, although direct testing of this possibility is needed.

“There are clear differences in brain activity between patients who have compulsive sexual behaviour and healthy volunteers. These differences mirror those of drug addicts,” adds Dr Voon. “Whilst these findings are interesting, it’s important to note, however, that they could not be used to diagnose the condition. Nor does our research necessarily provide evidence that these individuals are addicted to porn – or that porn is inherently addictive. Much more research is required to understand this relationship between compulsive sexual behaviour and drug addiction.”

Dr John Williams, Head of Neuroscience and Mental Health at the Wellcome Trust, says: “Compulsive behaviours, including watching porn to excess, over-eating and gambling, are increasingly common. This study takes us a step further to finding out why we carry on repeating behaviours that we know are potentially damaging to us. Whether we are tackling sex addiction, substance abuse or eating disorders, knowing how best, and when, to intervene in order to break the cycle is an important goal of this research.”

Filed under addiction compulsive sexual behavior brain activity amygdala motivation neuroscience science

free counters