Neuroscience

July 18, 2012

Sleep deprivation in the first few hours after exposure to a significantly stressful threat actually reduces the risk of Post-Traumatic Stress Disorder (PTSD), according to a study by researchers from Ben-Gurion University of the Negev (BGU) and Tel Aviv University.

The new study was published in the international scientific journal, Neuropsychopharmacology. It revealed in a series of experiments that sleep deprivation of approximately six hours immediately after exposure to a traumatic event reduces the development of post trauma-like behavioral responses. As a result, sleep deprivation the first hours after stress exposure might represent a simple, yet effective, intervention for PTSD.

The research was conducted by Prof. Hagit Cohen, director of the Anxiety and Stress Research Unit at BGU’s Faculty of Health Sciences, in collaboration with Prof. Joseph Zohar of Tel Aviv University.

Approximately 20 percent of people exposed to a severe traumatic event, such as a car or work accident, terrorist attack or war, cannot normally carry on their lives. These people retain the memory of the event for many years. It causes considerable difficulties in the person’s functioning in daily life and, in extreme cases, may render the individual completely dysfunctional.

"Often those close to someone exposed to a traumatic event, including medical teams, seek to relieve the distress and assume that it would be best if they could rest and "sleep on it," says Prof. Cohen. "Since memory is a significant component in the development of post-traumatic symptoms, we decided to examine the various effects of sleep deprivation immediately after exposure to trauma."

In the experiments, rats that underwent sleep deprivation after exposure to trauma (predator scent stress exposure), later did not exhibit behavior indicating memory of the event, while a control group of rats that was allowed to sleep after the stress exposure did remember, as shown by their post trauma-like behavior.

"As is the case for human populations exposed to severe stress, 15 to 20 percent of the animals develop long-term disruptions in their behavior," says Cohen. "Our research method for this study is, we believe, a breakthrough in biomedical research."

A pilot study in humans is currently being planned. The studies were funded by a Israel Academy of Science and Humanities grant and the Israel Ministry of Health.

Provided by American Associates, Ben-Gurion University of the Negev

Source: medicalxpress.com

July 18, 2012

(Phys.org) — New research at the Hebrew University of Jerusalem sheds light on pluripotency—the ability of embryonic stem cells to renew themselves indefinitely and to differentiate into all types of mature cells. Solving this problem, which is a major challenge in modern biology, could expedite the use of embryonic stem cells in cell therapy and regenerative medicine. If scientists can replicate the mechanisms that make pluripotency possible, they could create cells in the laboratory which could be implanted in humans to cure diseases characterized by cell death, such as Alzheimer’s, Parkinson’s, diabetes and other degenerative diseases.

To shed light on these processes, researchers in the lab of Dr. Eran Meshorer, in the Department of Genetics at the Hebrew University’s Alexander Silberman Institute of Life Sciences, are combining molecular, microscopic and genomic approaches. Meshorer’s team is focusing on epigenetic pathways—which cause biological changes without a corresponding change in the DNA sequence—that are specific to embryonic stem cells.

The molecular basis for epigenetic mechanisms is chromatin, which is comprised of a cell’s DNA and structural and regulatory proteins. In groundbreaking research performed by Shai Melcer, a PhD student in the Meshorer lab, the mechanisms which support an “open” chromatin conformation in embryonic stem cells were examined. The researchers found that chromatin is less condensed in embryonic stem cells, allowing them the flexibility or “functional plasticity” to turn into any kind of cell.

A distinct pattern of chemical modifications of chromatin structural proteins (referred to as the acetylation and methylation of histones) enables a looser chromatin configuration in embryonic stem cells. During the early stages of differentiation, this pattern changes to facilitate chromatin compaction.

But even more interestingly, the authors found that a nuclear lamina protein, lamin A, is also a part of the secret. In all differentiated cell types, lamin A binds compacted domains of chromatin and anchors them to the cell’s nuclear envelope. Lamin A is absent from embryonic stem cells and this may enable the freer, more dynamic chromatin state in the cell nucleus. The authors believe that chromatin plasticity is tantamount to functional plasticity since chromatin is made up of DNA that includes all genes and codes for all proteins in any living cell. Understanding the mechanisms that regulate chromatin function will enable intelligent manipulations of embryonic stem cells in the future.

"If we can apply this new understanding about the mechanisms that give embryonic stem cells their plasticity, then we can increase or decrease the dynamics of the proteins that bind DNA and thereby increase or decrease the cells’ differentiation potential," concludes Dr. Meshorer. “This could expedite the use of embryonic stem cells in cell therapy and regenerative medicine, by enabling the creation of cells in the laboratory which could be implanted in humans to cure diseases characterized by cell death, such as Alzheimer’s, Parkinson’s, diabetes and other degenerative diseases.”

Source: PHYS.ORG

ScienceDaily (July 17, 2012) — The ability of infants to recognize speech is more sophisticated than previously known, researchers in New York University’s Department of Psychology have found. Their study, which appears in the journal Developmental Psychology, showed that infants, as early as nine months old, could make distinctions between speech and non-speech sounds in both humans and animals.

A new study shows that infants, as early as nine months old, could make distinctions between speech and non-speech sounds in both humans and animals. (Credit: © ChantalS / Fotolia)

"Our results show that infant speech perception is resilient and flexible," explained Athena Vouloumanos, an assistant professor at NYU and the study’s lead author. "This means that our recognition of speech is more refined at an earlier age than we’d thought."

It is well-known that adults’ speech perception is fine-tuned — they can detect speech among a range of ambiguous sounds. But much less is known about the capability of infants to make similar assessments. Understanding when these abilities become instilled would shed new light on how early in life we develop the ability to recognize speech.

In order to gauge the aptitude to perceive speech at any early age, the researchers examined the responses of infants, approximately nine months in age, to recorded human and parrot speech and non-speech sounds. Human (an adult female voice) and parrot speech sounds included the words “truck,” “treat,” “dinner,” and “two.” The adult non-speech sounds were whistles and a clearing of the throat while the parrot non-speech sounds were squawks and chirps. The recorded parrot speech sounds were those of Alex, an African Gray parrot that had the ability to talk and reason and whose behaviors were studied by psychology researcher Irene Pepperberg.

Since infants cannot verbally communicate their recognition of speech, the researchers employed a commonly used method to measure this process: looking longer at what they find either interesting or unusual. Under this method, looking longer at a visual paired with a sound may be interpreted as a reflection of recognition. In this study, sounds were paired with a series of visuals: a checkerboard-like image, adult female faces, and a cup.

The results showed that infants listened longer to human speech compared to human non-speech sounds regardless of the visual stimulus, revealing the ability recognize human speech independent of the context.

Their findings on non-human speech were more nuanced. When paired with human-face visuals or human artifacts like cups, the infants listened to parrot speech longer than they did non-speech, such that their preference for parrot speech was similar to their preference for human speech sounds. However, this did not occur in the presence of other visual stimuli. In other words, infants were able to distinguish animal speech from non-speech, but only in some contexts.

"Parrot speech is unlike human speech, so the results show infants have the ability to detect different types of speech, even if they need visual cues to assist in this process," explained Vouloumanos.

Source: Science Daily

ScienceDaily (July 17, 2012) — Johns Hopkins researchers say they have discovered a cause-and-effect relationship between two well-established biological risk factors for schizophrenia previously believed to be independent of one another.

The findings could eventually lead researchers to develop better drugs to treat the cognitive dysfunction associated with schizophrenia and possibly other mental illnesses.

Researchers have long studied the role played in the brain’s neurons by the Disrupted-in-Schizophrenia 1 (DISC1) gene, a mutation with one of the strongest links to an increased risk of developing the debilitating psychiatric illness.

In a study published in the journal Molecular Psychiatry, the laboratory of Mikhail V. Pletnikov, M.D., Ph.D., in collaboration with the laboratory of Solomon H. Snyder, M.D., D.Sc., instead looked at the role the DISC1 gene plays in glia cells known as astrocytes, a kind of support cell in the brain that helps neurons communicate with one another.

"Abnormalities in glia cells could be as important as abnormalities in neuronal cells themselves," says Pletnikov, an associate professor of psychiatry and behavioral sciences at the Johns Hopkins University School of Medicine, and the study’s leader. "Most gene work has been done with neurons. But we also need to understand a lot more about the role that genetic mutations in glia cells play because neuron-glia interaction appears crucial in ensuring the brain operates normally."

Besides the paranoia and hallucinations that characterize the disease, schizophrenics have cognitive deficits, leaving them unable to think clearly or organize their thoughts and behavior.

Previous studies found that one of the roles of astrocytes is to secrete the neurotransmitter D-serine, which helps promote the transmission of glutamate in the brain, believed to be a key to cognitive function. Schizophrenics have decreased glutamate transmission. It appears, Pletnikov says, that people with DISC1 mutations associated with the psychiatric illness are faster to metabolize D-serine, which leads to a decrease in the apparently crucial transmitter.

In clinical trials, other researchers are trying to boost D-serine levels in people with schizophrenia to see if they can boost cognitive function.

In the new study, the Johns Hopkins researchers found that DISC1 is directly involved in regulating the production of D-serine by the enzyme known as serine racemase.

The researchers found that DISC1 normally binds to serine racemase and stabilizes it. The mutant DISC1 in patients with schizophrenia cannot bind with serine racemase, and instead destabilizes and destroys it. The result is a deficiency of D-serine.

The Hopkins researchers bred mice with the mutant DISC1 protein expressed only in astrocytes and, as predicted, the animals had decreased levels of D-serine. These mice also showed abnormal behavior “consistent with schizophrenia,” Pletnikov says. For example, the rodents showed sensitivity to psycho-stimulants that target glutamate transmission. By treating the mice with D-serine, the scientists were able to ameliorate the schizophrenic-like symptoms. Mice without the DISC1 mutation in astrocytes had normal D-serine levels.

Pletnikov says that in the future, researchers hope that they can target the unstable junction between the abnormal DISC1 and serine racemase. If drugs, for example, can be found to increase glutamate transmission in humans, doctors may be able to improve cognitive function in schizophrenics. He says a DISC1 mutation may also be an important risk factor in other psychiatric disorders.

"Abnormal glutamate transmission is believed to be present in patients with bipolar disorder, major depression and possibly anxiety disorders, so our findings could apply to other psychiatric diseases," he says.

Source: Science Daily

ScienceDaily (July 17, 2012) — Scientists have discovered two genetic variants associated with the substantial, rapid weight gain occurring in nearly half the patients treated with antipsychotic medications, according to two studies involving the Centre for Addiction and Mental Health (CAMH).

These results could eventually be used to identify which patients have the variations, enabling clinicians to choose strategies to prevent this serious side-effect and offer more personalized treatment.

"Weight gain occurs in up to 40 per cent of patients taking medications called second-generation or atypical antipsychotics, which are used because they’re effective in controlling the major symptoms of schizophrenia," says CAMH Scientist Dr. James Kennedy, senior author on the most recent study published online in the Archives of General Psychiatry.

This weight gain can lead to obesity, type 2 diabetes, heart problems and a shortened life span. “Identifying genetic risks leading to these side-effects will help us prescribe more effectively,” says Dr. Kennedy, head of the new Tanenbaum Centre for Pharmacogenetics, which is part of CAMH’s Campbell Family Mental Health Research Institute. Currently, CAMH screens for two other genetic variations that affect patients’ responses to psychiatric medications.

Each study identified a different variation near the melanocortin-4 receptor (MC4R) gene, which is known to be linked to obesity.

In the Archives of General Psychiatry study, people carrying two copies of a variant gained about three times as much weight as those with one or no copies, after six to 12 weeks of treatment with atypical antipsychotics. (The difference was approximately 6 kg versus 2 kg.) The study had four patient groups: two from the U.S., one in Germany and one from a larger European study.

"The weight gain was associated with this genetic variation in all these groups, which included pediatric patients with severe behaviour or mood problems, and patients with schizophrenia experiencing a first episode or who did not respond to other antipsychotic treatments," says CAMH Scientist Dr. Daniel Müller. "The results from our genetic analysis combined with this diverse set of patients provide compelling evidence for the role of this MC4R variant. Our research group has discovered other gene variants associated with antipsychotic-induced weight gain in the past, but this one appears to be the most compelling finding thus far."

Three of the four groups had never previously taken atypical antipsychotics. Different groups were treated with drugs such as olanzapine, risperidone, aripiprazole or quetiapine, and compliance was monitored to ensure the treatment regime was followed. Weight and other metabolic-related measures were taken at the start and during treatment.

A genome-wide association study was conducted on pediatric patients by the study’s lead researcher, Dr. Anil Malhotra, at the Zucker Hillside Hospital in Glen Oaks, NY. In this type of study, variations are sought across a person’s entire set of genes to identify those associated with a particular trait. The result pointed to the MC4R gene.

This gene’s role in antipsychotic-induced weight gain had been identified in a CAMH study published earlier this year in The Pharmacogenomics Journal, involving Drs. Müller and Kennedy, and conducted by PhD student Nabilah Chowdhury. They found a different variation on MC4R that was linked to the side-effect.

For both studies, CAMH researchers did genotyping experiments to identify the single changes to the sequence of the MC4R gene — known as single nucleotide polymorphisms (SNPs) — related to the drug-induced weight gain side-effect.

The MC4R gene encodes a receptor involved in the brain pathways regulating weight, appetite and satiety. “We don’t know exactly how the atypical antipsychotics disrupt this pathway, or how this variation affects the receptor,” says Dr. Müller. “We need further studies to validate this result and eventually turn this into a clinical application.”

Source: Science Daily

ScienceDaily (July 17, 2012) — Researchers at the University of Colorado School of Medicine have found a drug that boosts memory function in those with Down syndrome, a major milestone in the treatment of this genetic disorder that could significantly improve quality of life.

"Before now there had never been any positive results in attempts to improve cognitive abilities in persons with Down syndrome through medication," said Alberto Costa, MD, Ph.D., who led the four- year study at the CU School of Medicine. "This is the first time we have been able to move the needle at all and that means improvement is possible."

The study was published July 17 in the journal Translational Psychiatry.

Costa, an associate professor of medicine, and his colleagues studied 38 adolescents and young adults with Down syndrome. Half took the drug memantine, used to treat Alzheimer’s disease, and the others took a placebo.

Costa’s research team hypothesized that memantine, which improved memory in mice with Down syndrome, could increase test scores of young adults with the disorder in the area of spatial and episodic memory, functions associated with the hippocampus region of the brain.

Participants underwent a 16-week course of either memantine or a placebo while scientists compared the adaptive and cognitive function of the two groups.

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ScienceDaily (July 17, 2012) — A buildup of sodium in the brain detected by magnetic resonance imaging (MRI) may be a biomarker for the degeneration of nerve cells that occurs in patients with multiple sclerosis (MS), according to a new study published online in the journal Radiology.

The study found that patients with early-stage MS showed sodium accumulation in specific brain regions, while patients with more advanced disease showed sodium accumulation throughout the whole brain. Sodium buildup in motor areas of the brain correlated directly to the degree of disability seen in the advanced-stage patients.

"A major challenge with multiple sclerosis is providing patients with a prognosis of disease progression," said Patrick Cozzone, Ph.D., director emeritus of the Center for Magnetic Resonance in Biology and Medicine, a joint unit of National Center for Scientific Research (CNRS) and Aix-Marseille University in Marseille, France. "It’s very hard to predict the course of the disease."

In MS, the body’s immune system attacks the protective sheath (called myelin) that covers nerve cells, or neurons, in the brain and spinal cord. The scarring affects the neurons’ ability to conduct signals, causing neurological and physical disability. The type and severity of MS symptoms, as well as the progression of the disease, vary from one patient to another.

Dr. Cozzone, along with Wafaa Zaaraoui, Ph.D., research officer at CNRS, Jean-Philippe Ranjeva, Ph.D., professor in neuroscience at Aix-Marseille University and a European team of interdisciplinary researchers used 3 Tesla (3T) sodium MRI to study relapsing-remitting multiple sclerosis (RRMS), the most common form of the disease in which clearly defined attacks of worsening neurologic function are followed by periods of recovery. Sodium MRI produces images and information on the sodium content of cells in the body.

"We collaborated for two years with chemists and physicists to develop techniques to perform 3T sodium MRI on patients," Dr. Zaaraoui said. "To better understand this disease, we need to probe new molecules. The time has come for probing brain sodium concentrations."

Using specially developed hardware and software, the researchers conducted sodium MRI on 26 MS patients, including 14 with early-stage RRMS (less than five years in duration) and 12 with advanced disease (longer than five years), and 15 age- and sex-matched control participants.

In the early-stage RRMS patients, sodium MRI revealed abnormally high concentrations of sodium in specific brain regions, including the brainstem, cerebellum and temporal pole. In the advanced-stage RRMS patients, abnormally high sodium accumulation was widespread throughout the whole brain, including normal appearing brain tissue.

"In RRMS patients, the amount of sodium accumulation in gray matter associated with the motor system was directly correlated to the degree of patient disability," Dr. Zaaraoui said.

Current treatments for MS are only able to slow the progress of the disease. The use of sodium accumulation as a biomarker of neuron degeneration may assist pharmaceutical companies in developing and assessing potential treatments.

"Brain sodium MR imaging can help us to better understand the disease and to monitor the occurrence of neuronal injury in MS patients and possibly in patients with other brain disorders," Dr. Ranjeva said.

Source: Science Daily

ScienceDaily (July 17, 2012) — Using adult stem cells, Johns Hopkins researchers and a consortium of colleagues nationwide say they have generated the type of human neuron specifically damaged by Parkinson’s disease (PD) and used various drugs to stop the damage.

Their experiments on cells in the laboratory, reported in the July 4 issue of the journal Science Translational Medicine, could speed the search for new drugs to treat the incurable neurodegenerative disease, but also, they say, may lead them back to better ways of using medications that previously failed in clinical trials.

"Our study suggests that some failed drugs should actually work if they were used earlier, and especially if we could diagnose PD before tremors and other symptoms first appear," says one of the study’s leaders, Ted M. Dawson, M.D., Ph.D., a professor of neurology at the Johns Hopkins University School of Medicine.

Dawson and his colleagues, working as part of a National Institute of Neurological Disorders and Stroke consortium, created three lines of induced pluripotent stem (iPS) cells derived from the skin cells of adults with PD. Two of the cell lines had the mutated LRKK2 gene, a hallmark of the most common genetic cause of PD. Induced pluripotent stem cells are adult cells that have been genetically reprogrammed to their most primitive state. Under the right circumstances, they can develop into most or all of the 200 cell types in the human body.

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ScienceDaily (July 17, 2012) — A stroke can weaken one side of the body, raising the dangerous possibility of unstable walking and debilitating falls. Physical therapy can help patients learn to shift their body weight slightly to the weaker, stroke-affected side to help regain balance, but for some patients, the weakness returns after their therapy ends.

University of Illinois at Chicago physical therapy professor Alexander Aruin has developed an inexpensive, simple way to deal with the problem, training the brain to rebalance body weight using a simple shoe insole he calls a “compelled body weight shift.” It slightly lifts and tilts the body toward the stroke-affected side, restoring balance without the patient having to think about it.

Aruin along with colleagues at UIC and Marianjoy Rehabilitation Hospital in Wheaton, Ill., studied two patient groups: one group at UIC who just had strokes, and one at Marianjoy who had strokes over a year ago.

"We tried a purely biomechanical approach," Aruin said. "We mechanically lifted the healthy side so the patient cannot resist. The mechanics force body weight to where it is distributed almost 50/50. When patients ambulate in such a condition, they learn how to bear weight equally through both extremities. It’s quite simple."

The two test groups followed slightly different protocols and were tested for various lengths of time. Their results were measured against those of control groups, who did not get the small therapeutic shoe insole, which measures less than half an inch thick. patients in all groups also received standard post-stroke physical therapy.

After the testing period ended, patients stopped using the insole. About three months afterward they were tested again to see if they retained the ability to keep their balance. Aruin and his colleagues found that physical therapy helped both the insole-user and control groups, but the insole group got an added boost.

"They showed more symmetrical body weight distribution and bore more weight on their affected side, and their gait velocity improved," he said. "The outcome looks promising. The technique is very simple and inexpensive and has potential, which is exciting."

Aruin hopes other physical therapists use the simple devices on stroke patients to see if they too benefit from it. His associates are also considering ways to use the insole to improve posture in post-stroke patients.

Source: Science Daily

ScienceDaily (July 17, 2012) — Scientists at the California Institute of Technology (Caltech) pioneered the study of the link between irregularities in the immune system and neurodevelopmental disorders such as autism a decade ago. Since then, studies of postmortem brains and of individuals with autism, as well as epidemiological studies, have supported the correlation between alterations in the immune system and autism spectrum disorder.

Scientists at Caltech pioneered the study of the link between irregularities in the immune system and neurodevelopmental disorders such as autism a decade ago. Since then, studies of postmortem brains and of individuals with autism, as well as epidemiological studies, have supported the correlation between alterations in the immune system and autism spectrum disorder. (Credit: Elaine Hsiao)

What has remained unanswered, however, is whether the immune changes play a causative role in the development of the disease or are merely a side effect. Now a new Caltech study suggests that specific changes in an overactive immune system can indeed contribute to autism-like behaviors in mice, and that in some cases, this activation can be related to what a developing fetus experiences in the womb.

The results appear in a paper this week in the Proceedings of the National Academy of Sciences (PNAS).

"We have long suspected that the immune system plays a role in the development of autism spectrum disorder," says Paul Patterson, the Anne P. and Benjamin F. Biaggini Professor of Biological Sciences at Caltech, who led the work. "In our studies of a mouse model based on an environmental risk factor for autism, we find that the immune system of the mother is a key factor in the eventual abnormal behaviors in the offspring."

The first step in the work was establishing a mouse model that tied the autism-related behaviors together with immune changes. Several large epidemiological studies — including one that involved tracking the medical history of every person born in Denmark between 1980 and 2005 — have found a correlation between viral infection during the first trimester of a mother’s pregnancy and a higher risk for autism spectrum disorder in her child. To model this in mice, the researchers injected pregnant mothers with a viral mimic that triggered the same type of immune response a viral infection would.

"In mice, this single insult to the mother translates into autism-related behavioral abnormalities and neuropathologies in the offspring," says Elaine Hsiao, a graduate student in Patterson’s lab and lead author of the PNAS paper.

The team found that the offspring exhibit the core behavioral symptoms associated with autism spectrum disorder — repetitive or stereotyped behaviors, decreased social interactions, and impaired communication. In mice, this translates to such behaviors as compulsively burying marbles placed in their cage, excessively self grooming, choosing to spend time alone or with a toy rather than interacting with a new mouse, or vocalizing ultrasonically less often or in an altered way compared to typical mice.

Next, the researchers characterized the immune system of the offspring of mothers that had been infected and found that the offspring display a number of immune changes. Some of those changes parallel those seen in people with autism, including decreased levels of regulatory T cells, which play a key role in suppressing the immune response. Taken together, the observed immune alterations add up to an immune system in overdrive — one that promotes inflammation.

"Remarkably, we saw these immune abnormalities in both young and adult offspring of immune-activated mothers," Hsiao says. "This tells us that a prenatal challenge can result in long-term consequences for health and development."

With the mouse model established, the group was then able to test whether the offspring’s immune problems contribute to their autism-related behaviors. In the most revealing test of this hypothesis, the researchers were able to correct many of the autism-like behaviors in the offspring of immune-activated mothers by giving the offspring a bone-marrow transplant from typical mice. The normal stem cells in the transplanted bone marrow not only replenished the immune system of the host animals but altered their autism-like behavioral impairments.

The researchers emphasize that because the work was conducted in mice, the results cannot be readily extrapolated to humans, and they certainly do not suggest that bone-marrow transplants should be considered as a treatment for autism. They also have yet to establish whether it was the infusion of stem cells or the bone-marrow transplant procedure itself — complete with irradiation — that corrected the behaviors.

However, Patterson says, the results do suggest that immune irregularities in children could be an important target for innovative immune manipulations in addressing the behaviors associated with autism spectrum disorder. By correcting these immune problems, he says, it might be possible to ameliorate some of the classic developmental delays seen in autism.

In future studies, the researchers plan to examine the effects of highly targeted anti-inflammatory treatments on mice that display autism-related behaviors and immune changes. They are also interested in considering the gastrointestinal (GI) bacteria, or microbiota, of such mice. Coauthor Sarkis Mazmanian, a professor of biology at Caltech, has shown that gut bacteria are intimately tied to the function of the immune system. He and Patterson are investigating whether changes to the microbiota of these mice might also influence their autism-related behaviors.

Source: Science Daily

July 17, 2012

(Medical Xpress) — You’re headed out the door and you realize you don’t have your car keys. After a few minutes of rifling through pockets, checking the seat cushions and scanning the coffee table, you find the familiar key ring and off you go. Easy enough, right? What you might not know is that the task that took you a couple seconds to complete is a task that computers — despite decades of advancement and intricate calculations — still can’t perform as efficiently as humans: the visual search.

Pictured is part of the research team in front of the magnetic resonance imaging device at the UCSB Brain Imaging Center. From left to right: researcher Tim Preston; associate professor of psychological and brain sciences Barry Giesbrecht; and professor of psychological and brain sciences Miguel P. Eckstein. Not pictured: Koel Das, now a faculty member at the Indian Institute of Science in Bangalore, Karnatka, India; and lead author Fei Guo, now in the software industry. Credit: UCSB

"Our daily lives are comprised of little searches that are constantly changing, depending on what we need to do," said Miguel Eckstein, UC Santa Barbara professor of psychological and brain sciences and co-author of the recently released paper "Feature-Independent Neural Coding of Target Detection during Search of Natural Scenes," published in the Journal of Neuroscience. "So the idea is, where does that take place in the brain?"

A large part of the human brain is dedicated to vision, with different parts involved in processing the many visual properties of the world. Some parts are stimulated by color, others by motion, yet others by shape.

However, those parts of the brain tell only a part of the story. What Eckstein and co-authors wanted to determine was how we decide whether the target object we are looking for is actually in the scene, how difficult the search is, and how we know we’ve found what we wanted.

They found their answers in the dorsal frontoparietal network, a region of the brain that roughly corresponds to the top of one’s head, and is also associated with properties such as attention and eye movements. In the parts of the human brain used earlier in the processing stream, regions stimulated by specific features like color, motion, and direction are a major part of the search. However, in the dorsal frontoparietal network, activity is not confined to any specific features of the object.

"It’s flexible," said Eckstein. Using 18 observers, an MRI machine, and hundreds of photos of scenes flashed before the observers with instructions to look for certain items, the scientists monitored their subjects’ brain activity. By watching the intraparietal sulcus (IPS), located within the dorsal frontoparietal network, the researchers were able to note not only whether their subjects found the objects, but also how confident they were in their finds.

The IPS region would be stimulated even if the object was not there, said Eckstein, but the pattern of activity would not be the same as it would had the object actually existed in the scene. The pattern of activity was consistent, even though the 368 different objects the subjects searched for were defined by very different visual features. This, Eckstein said, indicates that IPS did not rely on the presence of any fixed feature to determine the presence or absence of various objects. Other visual regions did not show this consistent pattern of activity across objects.

"As you go further up in processing, the neurons are less interested in a specific feature, but they’re more interested in whatever is behaviorally relevant to you at the moment," said Eckstein. Thus, a search for an apple, for instance, would make red, green, and rounded shapes relevant. If the search was for your car keys, the interparietal sulcus would now be interested in gold, silver, and key-type shapes and not interested in green, red, and rounded shapes.

"For visual search to be efficient, we want those visual features related to what we are looking for to elicit strong responses in our brain and not others that are not related to our search, and are distracting," Eckstein added. "Our results suggest that this is what is achieved in the intraparietal sulcus, and allows for efficient visual search."

For Eckstein and colleagues, these findings are just the tip of the iceberg. Future research will dig more deeply into the seemingly simple yet essential ability of humans to do a visual search and how they can use the layout of a scene to guide their search.

"What we’re trying to really understand is what other mechanisms or strategies the brain has to make searches efficient and easy," said Eckstein. "What part of the brain is doing that?"

Provided by University of California - Santa Barbara

Source: medicalxpress.com

July 16, 2012 By Maureen Salamon

(HealthDay) — Evidence is building that poor sleep patterns may do more than make you cranky: The amount and quality of shuteye you get could be linked to mental deterioration and Alzheimer’s disease, four new studies suggest.

Inadequate shuteye associated with mental decline in four new studies.

Too little or too much sleep was equated with two years’ brain aging in one study. A separate study concluded that people with sleep apnea — disrupted breathing during sleep — were more than twice as likely to develop mild thinking problems or dementia compared to problem-free sleepers. Yet another suggests excessive daytime sleepiness may predict diminished memory and thinking skills, known as cognitive decline, in older people.

"Whether sleep changes, such as sleep apnea or disturbances, are signs of a decline to come or the cause of decline is something we don’t know, but these four studies … shed further light that this is an area we need to look into more," said Heather Snyder, senior associate director of medical and scientific relations for the Alzheimer’s Association in Chicago, who was not involved in the studies.

The studies are scheduled for presentation Monday at the Alzheimer’s Association annual meeting in Vancouver.

The largest of the studies, which examined data on more than 15,000 women in the U.S. Nurses’ Health Study, suggested that those who slept five hours a day or less, or nine hours a day or more, had lower average mental functioning than participants who slept seven hours per day. Too much or too little sleep was cognitively equivalent to aging by two years, according to the research, which followed the women over 14 years beginning in middle age.

The study also observed that women whose sleep duration changed by two hours or more a day from mid- to later life had worse brain function than participants with no change in sleep duration — a finding that held true regardless of how long they usually slept at the beginning of the study.

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ScienceDaily (July 16, 2012) — Post-traumatic stress disorder (PTSD) is more treatable than previously thought. A novel method has shown to be remarkably effective. The method, called Narrative Exposure Therapy (NET), is an intervention aimed at reducing symptoms of post-traumatic stress.

In an on-going Norwegian study, exposure therapy has been used with asylum seekers and refugees who have survived the ordeal of torture.

"According to previous studies, these patients do not benefit from traditional psychological therapy. In our study, however, 60 per cent show a marked improvement, and approximately 20 per cent show no symptoms of PTSD after treatment," says Håkon Stenmark, a PhD candidate at the Norwegian University of Science and Technology’s Department of Neuroscience, and has conducted the study in collaboration with colleague and fellow PhD candidate Joar Øverås Halvorsen.

Describing traumatic events

"Narrative" simply means telling a story. In exposure therapy the patient constructs a narration of his life while focusing on a detailed report of traumatic experiences. In a typical therapy session, the patient is given a rope to symbolize his or her life, from early childhood up to the present date.

The patient then describes the events in his life, good and bad, in chronological order. For every good memory the patient places a flower on the rope, and for every bad memory, a stone.

"I was blindfolded and seated in the prison’s interrogation room. I received multiple blows all over my body, and had no way of anticipating where I would be beaten next, the patient recalls with great difficulty."

The therapist is sitting at the opposite end of the table, listening attentively. Everything is written down, as it might prove useful later. The written account may be used in an application for asylum, or even as documentation for Amnesty International.

"Electrodes were fastened to my toes, and I was told I would be given electric shocks. The next thing I knew, a skinny man with a cigarette in his mouth turned the nob. The pain was excruciating, and my whole body tensed up."

"This is just one example. Although the patients are of different nationalities, and have been subjected to different kinds of torture, they share similar stories," Stenmark says.

Flashbacks and learning problems

Torture can result in a range of symptoms, depending on the method of torture as well as the duration of the ordeal. Nonetheless, symptoms typically fall into three main categories: ‘Reliving’ the event, avoidance and arousal. “A patients who is reliving torture may have flashbacks of the event, or episodes of repeated nightmares. Avoidance reactions are typically displayed as an extreme fear of the police or anybody who might resemble the abuser. People with these symptoms will try to isolate themselves and avoid people in general. Symptoms of arousal may result in difficulties concentrating, irritability, or having trouble falling or staying asleep,” Stenmark explains.

The classic symptom of PTSD is an inability to concentrate. As a consequence, sufferers often have learning difficulties and end up losing their jobs.

The brain’s “alarm system”

Existing trials are showing promising results with regards to exposure therapy. But why the method works in the first place, and the exact mechanisms behind it, have yet to be verified.

The most prominent theory is that exposure therapy changes the way fear is ‘wired’ in the memory. Simply stated, there is a part of the brain known as the brain’s ‘alarm system’, which enables us to respond to dangerous stimuli.

"During therapy the patient describes the traumatic event in a safe setting, while re-experiencing his or her emotions. In the process, the patient learns that the memories are not dangerous in themselves. The event was threatening when it occurred, but the memory the patient has today is not," Stenmark explains.

The goal of exposure therapy is to reduce the overall symptoms of PTSD, thereby increasing levels of functioning. Stenmark stresses that this is especially important for asylum seekers and refugees, as they often face additional challenges in Norwegian society.

Narrative exposure therapy was developed by trauma specialists working in refugee camps in Africa and Asia. To date, exposure therapy is not widely used in other parts of the world, which makes Øverås Halvorsen and Stenmark’s study the largest of its kind in the western world.

Source: Science Daily

ScienceDaily (July 16, 2012) — While Spider-Man is capturing the imagination of theatergoers, real-life spider men in Upstate New York are working intently to save a young boy’s life.

UB researchers are developing a treatment for muscular dystrophy using a peptide found in the venom of a Chilean rose tarantula. (Credit: Image courtesy of University at Buffalo)

It all began in 2009, when Jeff Harvey, a stockbroker from the Buffalo suburbs, discovered that his grandson, JB, had Duchenne muscular dystrophy. The disease is fatal. It strikes only boys, causing their muscles to waste away.

Hoping to help his grandson, Harvey searched Google for promising muscular dystrophy treatments and, in a moment of serendipity, stumbled upon University at Buffalo scientist Frederick Sachs, PhD.

Sachs was a professor of physiology and biophysics who had been studying the medical benefits of venom. In the venom of the Chilean rose tarantula, he and his colleagues discovered a protein that held promise for keeping muscular dystrophy at bay. Specifically, the protein helped stop muscle cells from deteriorating.

Within months of getting in touch, Harvey and Sachs co-founded Tonus Therapeutics, a pharmaceutical company devoted to developing the protein as a drug. Though the treatment has yet to be tested in humans, it has helped dystrophic mice gain strength in preliminary experiments.

The therapy is not a cure. But if it works in humans, it could extend the lives of children like JB for years — maybe even decades.

Success can’t come quickly enough.

JB, now four, can’t walk down the stairs alone. When he runs, he waddles. He receives physical therapy and takes steroids as a treatment. While playing tee ball one recent day, he confided to his grandfather, “When I grow up, I want to be a baseball player.” It was a heartbreaking moment.

"Oh, I would be thrilled if you could be a baseball player," Harvey remembers replying. He’s doing everything he can to make sure that JB — and other boys like him — can live out their dreams.

Source: Science Daily

July 16th, 2012

Spinal Muscular Atrophy affects one in 6,000 children and has no known cure.

A team of University of Missouri researchers has found that introducing a missing gene into the central nervous system could help extend the lives of patients with Spinal Muscular Atrophy (SMA) – the leading genetic cause of infantile death in the world.

SMA is a rare genetic disease that is inherited by one in 6,000 children who often die young because there is no cure. Children who inherit SMA are missing a gene that produces a protein which directs nerves in the spine to give commands to muscles.

The MU team, led by Christian Lorson, professor in the Department of Veterinary Pathobiology and the Department of Molecular Microbiology and Immunology, introduced the missing gene into mice born with SMA through two different methods: intravenously and directly into the mice’s central nervous systems. While both methods were effective in extending the lives of the mice, Lorson found that introducing the missing gene directly into the central nervous system extended the lives of the mice longer.

Mice born with spinal muscular atrophy typically only live five or six days. Researchers introduced the SMN gene into the mice’s central nervous systems and were able to extend their lives 10-25 days longer. The mice in the picture have spinal muscular atrophy.

“Typically, mice born with SMA only live five or six days, but by introducing the missing SMN gene into the mice’s central nervous systems, we were able to extend their lives 10-25 days longer than SMA mice who go untreated,” said Lorson, who works in the MU Bond Life Sciences Center and the College of Veterinary Medicine. “While this system is still not perfect, what our study did show is that the direct administration of the missing gene into the central nervous system provides some degree of rescue and a profound extension of survival.”

There are several different types of SMA that appear in humans, depending on the age that symptoms begin to appear. Lorson believes that introducing the missing gene through the central nervous system is a way to potentially treat humans regardless of what SMA type they have.

“This is a treatment method that is very close to being a reality for human patients,” Lorson said. “Clinical trials of SMA treatment using gene therapy are likely to begin in next 12-18 months, barring any unforeseen problems.”

Source: Neuroscience News

July 16, 2012

Can you teach an old dog (or human) new tricks? Yes, but it might take time, practice, and hard work before he or she gets it right, according to Hans Schroder and colleagues from Michigan State University in the US. Their work shows that when rules change, our attempts to control our actions are accompanied by a loss of attention to detail. Their work is published online in the Springer journal Cognitive, Affective, & Behavioral Neuroscience.

In order to adapt to changing conditions, humans need to be able to modify their behavior successfully. Overriding the rules we adhere to on a daily basis requires substantial attention and effort, and we do not always get it right the first time. When we switch between two or more tasks, we are slower and more likely to commit errors, which suggests switching tasks is a costly process. This may explain why it is so hard to learn from our mistakes when rules change.

The authors explain: “Switching the rules we use to perform a task makes us less aware of our mistakes. We therefore have a harder time learning from them. That’s because switching tasks is mentally taxing and costly, which leads us to pay less attention to the detail and therefore make more mistakes.”

A total of 67 undergraduates took part in the study. They were asked to wear a cap, which recorded electrical activity in the brain. They then performed a computer task that is easy to make mistakes on. Specifically, the participants were shown letter strings like “MMMMM” or “NNMNN” and were told to follow a simple rule: if ‘M’ is in the middle, press the left button; if ‘N’ is in the middle, press the right button. After they had followed this rule for almost 50 trials, they were instructed to perform the same task, but with the rules reversed i.e. now if ‘M’ is in the middle, press the right button; and if ‘N’ is in the middle, press the left button.

When the rules were reversed, participants made more consecutive errors. They were more likely to get it wrong twice in a row. This showed they were less apt to bounce back and learn from their mistakes. Reversing the rules also produced greater control-related and less error-awareness brain activity.

These results suggest that when rules are reversed, our brain works harder to juggle the two rules - the new rule and the old rule - and stay focused on the new rule. When we spend brain energy juggling these two rules, we have less brain power available for recognizing our mistakes.

Provided by Springer

Source: medicalxpress.com

ScienceDaily (July 16, 2012) — Far from processing every word we read or hear, our brains often do not even notice key words that can change the whole meaning of a sentence, according to new research from the Economic and Social Research Council (ESRC).

After a plane crash, where should the survivors be buried?

If you are considering where the most appropriate burial place should be, you are not alone. Scientists have found that around half the people asked this question, answer it as if they were being asked about the victims not the survivors.

Similarly, when asked “Can a man marry his widow’s sister?” most people answer “yes” — effectively answering that it would indeed be possible for a dead man to marry his bereaved wife’s sister.

What makes researchers particularly interested in people’s failure to notice words that actually don’t make sense, so called semantic illusions, is that these illusions challenge traditional models of language processing which assume that we build understanding of a sentence by deeply analysing the meaning of each word in turn.

Instead semantic illusions provide a strong line of evidence that the way we process language is often shallow and incomplete.

Professor Leuthold at University of Glasgow led a study using electroencephalography (EEG) to explore what is happening in our brains when we process sentences containing semantic illusions.

By analysing the patterns of brain activity when volunteers read or listened to sentences containing hard-to-detect semantic anomalies — words that fit the general context even though they do not actually make sense — the researchers found that when a volunteer was tricked by the semantic illusion, their brain had not even noticed the anomalous word.

Analyses of brain activity also revealed that we are more likely to use this type of shallow processing under conditions of higher cognitive load — that is, when the task we are faced with is more difficult or when we are dealing with more than one task at a time.

The research findings not only provide a better understanding of the processes involved in language comprehension but, according to Professor Leuthold, knowing what is happening in the brain when mistakes occur can help us to avoid the pitfalls,such as missing critical information in textbooks or legal documents, and communicate more effectively.

There are a number of tricks we can use to make sure we get the correct message across: “We know that we process a word more deeply if it is emphasised in some way. So, for example in a news story, a newsreader can stress important words that may otherwise be missed and these words can be italicised to make sure we notice them when reading,” said Professor Leuthold.

The way we construct sentences can also help reduce misunderstandings, he explained: “It’s a good idea to put important information first because we are more likely to miss unusual words when they are near the end of a sentence. Also, we often use an active sentence construction such as ‘Bob ate the apple’ because we make far more mistakes answering questions about a sentence with a passive construction — for example ‘The apple was eaten by Bob’.”

The study findings also suggest that we should avoid multi-tasking when we are reading or listening to an important message: “For example, talking to someone on the phone while driving on a busy motorway or in town, or doing some homework while listening to the newsmight lead to more shallow processing,” said Professor Leuthold.

Source: Science Daily

July 16, 2012

A nationwide consortium of scientists at 20 institutions, led by a principal faculty member at the Harvard Stem Cell Institute (HSCI), has used stem cells to take a major step toward developing personalized medicine to treat Parkinson’s disease.

This study points the way to screening patients with Parkinson’s for their particular variation of the disease, and then treating them with drugs shown effective to work on that variation, rather than trying to treat all patients with the same drugs, as is generally done now, notes Ole Isacson, a leader of the study. Credit: B. D. Colen/Harvard Staff

In part supported by the Harvard Miller Consortium for the Development of Nervous System Therapies, the team of scientists created induced pluripotent stem cells (iPS cells) from the skin cells of patients and at-risk individuals carrying genetic mutations implicated in Parkinson’s disease, and used those cells to derive neural cells, providing a platform for studying the disease in human cells outside of patients.

In a paper published in the journal Science Translational Medicine, the researchers report that although approximately 15 genetic mutations are linked to forms of Parkinson’s, many seem to affect the mitochondria, the cell unit that produces most of its energy.

“This is the first comprehensive study of how human neuronal cells can be models of Parkinson’s, and how it might be treated,” said Ole Isacson, a leader of the study, an HSCI principal faculty member, and a Harvard Medical School professor of neurology, based at McLean Hospital’s Neuroregeneration Laboratory.

The researchers determined that certain compounds or drugs could reverse some signs of disease in the cultured cells with specific genetic mutations, and not in cells with other types of mutations, making real the concept of developing drugs that would be prescribed to patients or individuals at risk for Parkinson’s.

The study was launched with federal stimulus funding provided by the National Institutes of Health (NIH) and was continued with funding from HSCI.

“These findings suggest new opportunities for clinical trials of Parkinson’s disease, wherein cell reprogramming technology could be used to identify the patients most likely to respond to a particular intervention,” said Margaret Sutherland, a program director at NIH’s National Institute of Neurological Disorders and Stroke, in a press release.

The new research indicates that compounds that previously have shown promise in treating Parkinson’s in animal studies, including the antioxidant coenzyme Q10, together with the immunosuppressant rapamycin, have differing levels of effectiveness on various genetic forms of Parkinson’s.

Researchers hope that such findings can provide the basis for more specific drugs for individuals with sporadic forms of Parkinson’s.

As Isacson explained in an interview, this study points the way to screening patients with Parkinson’s for their particular variation of the disease, and then treating them with drugs shown effective to work on that variation, rather than trying to treat all patients with the same drugs, as is generally done now.

“We believe that using human stem cells to study the disease is the correct way to go,” Isacson said. “We have the cell type most vulnerable to the disease in a dish. We can study the most vulnerable cells and compare them to the least vulnerable cells. Traditionally, in neurology,” he said, “all patients with the same disease get the same drugs. But they may have the disease for different reasons. This gives us a way to tease out those different reasons, and find different ways to treat them.”

Provided by Harvard University

Source: medicalxpress.com

July 16, 2012

For more than 20 years, doctors have been using cells from blood that remains in the placenta and umbilical cord after childbirth to treat a variety of illnesses, from cancer and immune disorders to blood and metabolic diseases.

This microscope image shows a colony of neurons derived from cord-blood cells using stem cell reprogramming technology. The green and red glow indicates that the cells are producing protein makers found in neurons, evidence that the cord-blood cells did in fact morph into neurons. The blue glow marks the nuclei of the neurons. Credit: Image: Courtesy of Alessandra Giorgetti

Now, scientists at the Salk Institute for Biological Studies have found a new way-using a single protein, known as a transcription factor-to convert cord blood (CB) cells into neuron-like cells that may prove valuable for the treatment of a wide range of neurological conditions, including stroke, traumatic brain injury and spinal cord injury.

The researchers demonstrated that these CB cells, which come from the mesoderm, the middle layer of embryonic germ cells, can be switched to ectodermal cells, outer layer cells from which brain, spinal and nerve cells arise. “This study shows for the first time the direct conversion of a pure population of human cord blood cells into cells of neuronal lineage by the forced expression of a single transcription factor,” says Juan Carlos Izpisua Belmonte, a professor in Salk’s Gene Expression Laboratory, who led the research team. The study, a collaboration with Fred H. Gage, a professor in Salk’s Laboratory of Genetics, and his team, was published on July 16 in the Proceedings of the National Academy of Sciences.

"Unlike previous studies, where multiple transcription factors were necessary to convert skin cells into neurons, our method requires only one transcription factor to convert CB cells into functional neurons," says Gage.

The Salk researchers used a retrovirus to introduce Sox2, a transcription factor that acts as a switch in neuronal development, into CB cells. After culturing them in the laboratory, they discovered colonies of cells expressing neuronal markers. Using a variety of tests, they determined that the new cells, called induced neuronal-like cells (iNC), could transmit electrical impulses, signaling that the cells were mature and functional neurons. Additionally, they transferred the Sox2-infused CB cells to a mouse brain and found that they integrated into the existing mouse neuronal network and were capable of transmitting electrical signals like mature functional neurons.

"We also show that the CB-derived neuronal cells can be expanded under certain conditions and still retain the ability to differentiate into more mature neurons both in the lab and in a mouse brain," says Mo Li, a scientist in Belmonte’s lab and a co-first author on the paper with Alessandra Giorgetti, of the Center for Regenerative Medicine, in Barcelona, and Carol Marchetto of Gage’s lab. "Although the cells we developed were not for a specific lineage-for example, motor neurons or mid-brain neurons-we hope to generate clinically relevant neuronal subtypes in the future."

Importantly, says Marchetto, “We could use these cells in the future for modeling neurological diseases such as autism, schizophrenia, Parkinson’s or Alzheimer’s disease.”

Cord blood cells, says Giorgetti, offer a number of advantages over other types of stem cells. First, they are not embryonic stem cells and thus they are not controversial. They are more plastic, or flexible, than adult stem cells from sources like bone marrow, which may make them easier to convert into specific cell lineages. The collection of CB cells is safe and painless and poses no risk to the donor, and they can be stored in blood banks for later use.

"If our protocol is developed into a clinical application, it could aid in future cell-replacement therapies," says Li. "You could search all the cord blood banks in the country to look for a suitable match."

Provided by Salk Institute

Source: medicalxpress.com

ScienceDaily (July 16, 2012) — A team of scientists at The New York Stem Cell Foundation (NYSCF) Laboratory led by Scott Noggle, PhD, NYSCF-Charles Evans Senior Research Fellow for Alzheimer’s Disease, has developed the first cell-based model of Alzheimer’s disease (AD) by reprogramming skin cells of Alzheimer’s patients to become brain cells that are affected in Alzheimer’s. This will allow researchers to work directly on living brain cells suffering from Alzheimer’s, which until now had not been possible. Andrew Sproul, PhD, a postdoctoral associate in Dr. Noggle’s laboratory, will present this work on July 19 at the Alzheimer’s Association International Conference (AAIC) held in Vancouver.

Dr. Noggle and his team reprogrammed skin cell samples taken from twelve patients diagnosed with early-onset Alzheimer’s and from healthy, genetically related individuals into induced pluripotent stem (iPS) cells, which can differentiate into any cell type. The team of scientists used these iPS cells to create cholinergic basal forebrain neurons, the brain cells that are affected in Alzheimer’s. These cells recapitulate the features and cellular-level functions of patients suffering from Alzheimer’s, a devastating disease that affects millions of people globally but for which there is currently no effective treatment.

NYSCF has pioneered the creation of disease models based on the derivation of human cells. Four years ago, a NYSCF-funded team created a cell-based model for ALS, or motor neuron disease, the first patient-specific stem cells created for any disease. The cell-based model for Alzheimer’s builds on this earlier work.

"Patient derived AD cells will prove invaluable for future research advances, as they already have with patient-derived ALS cells," said NYSCF CEO Susan Solomon. "They will be a critical tool in the drug discovery process, as potential drugs could be tested directly on these cells. Although research on animals has provided valuable insight into AD, we aren’t mice, and animals don’t properly reflect the features of the disease we are trying to cure. As we work to find new drugs and treatments our research should focus on actual human sufferers of Alzheimer’s disease," emphasized Ms. Solomon

This cell-based model has already led to important findings. Preliminary results of this NYSCF research, done in collaboration with Sam Gandy, MD, PhD, an international expert in the pathology of Alzheimer’s at Mount Sinai School of Medicine, demonstrated differences in cellular function in Alzheimer’s patients. Specifically, Alzheimer’s neurons produce more of the toxic form of beta amyloid, the protein fragment that makes up amyloid plaques, than in disease-free neurons.

"iPS cell technology, along with whole genome sequencing, provide our best chance at unravelling the causes of common forms of Alzheimer’s disease," noted Dr. Gandy.

"This collaboration is a great example of how NYSCF is bringing together experts in stem cell technology and clinicians to save and enhance lives by finding better treatments," Ms. Solomon explained.

The research to be reported at the AAIC by Andrew Sproul focused on stem cell models of individuals with presenilin-1 (PSEN1) mutations, a genetic cause of AD. As Dr. Sproul has said, this cell-based model could “revolutionize how we discover drugs to potentially cure Alzheimer’s disease.”

Source: Science Daily

July 16, 2012

Activity lingers longer in certain areas of the brain in those with Alzheimer’s than it does in healthy people, Mayo Clinic researchers who created a map of the brain found. The results suggest varying brain activity may reduce the risk of Alzheimer’s disease. The study, “Non-stationarity in the “Resting Brain’s” Modular Architecture,” was presented at the Alzheimer’s Association International Conference and recently published in the journal PLoS One.

Researchers compared brain activity to a complex network, with multiple objects sharing information along pathways.

"Our understanding of those objects and pathways is limited," says lead author David T. Jones, M.D. "There are regions in the brain that correspond to those objects, and we are not really clear exactly what those are. We need a good mapping or atlas of those regions that make up the network in the brain, which is part of what we were doing in this study."

Researchers examined 892 cognitively normal people taking part in the Mayo Clinic Study of Aging, and set out to create an active map of their brains while the people were “at rest,” not engaged in a specific task. To do this, they employed task-free, functional magnetic resonance imaging to construct an atlas of 68 functional regions of the brain, which correspond to the cities on the road map.

Researchers filled in the roads between these regions by creating dynamic graphic representations of brain connectivity within a sliding time window.

This analysis revealed that there were many roads that could be used to exchange information in the brain, and the brain uses different roads at different times. The question to answer then, said Dr. Jones, is whether or not Alzheimer’s patients used this map and these roads in a different way than their healthy peers.

"What we found in this study was that Alzheimer’s patients tended to spend more time using some roads and less time using other roads, biasing one over the other," he says.

While more research is needed, the researchers say one implication is that how we use our brains may protect us from Alzheimer’s. Dr. Jones says exercise, education, and social contacts may help balance activity in the brain.

"Diversifying the mental space that you explore may actually decrease your risk for Alzheimer’s," he says.

Provided by Mayo Clinic

Source: medicalxpress.com

July 16, 2012

One of the marvels of brain development is the mass migration of nerve cells to their functional position. European research has investigated the molecules required for their successful navigation.

Credit: Thinkstock

Formation of the cerebral cortex during embryonic development requires the migration of billions of cells from their birth position to their final destination. A motile nerve cell must have internal polarity to move in the specified direction. What is more, neurons then have to extend neurites or projections from the cell body to communicate with each other.

The key to this extraordinary feat of organisation lies in cell signalling pathways. The EU-funded Neuronal Polarity project aimed to characterise these cascades important in cerebral cortex development. At a later stage, defective cortical architecture can be responsible for brain pathologies including microcephaly, epilepsy and schizophrenia.

Project scientists showed that in vivo the guanine triphosphatase GTPase Ras-proximate-1 (Rap 1) caused an accumulation of neurons halfway to their destination. The team used time-lapse video microscopy and immunostaining to show that the problem does not lie with motility of the neurons but in a defect in their polarity. Other evidence from motility tests in vitro and the fact that some neurons do actually make it to their destination, albeit slowly, suggest Rap 1 is important for initial polarisation of the neurons.

The transmembrane receptor N-cadherin (Ncad) also has an important function in polarising cortical neurons. Experimental data confirmed that this receptor is involved downstream from Rap 1. Overall, inhibition of Rap 1 reduces Ncad presence.

Neuronal Polarity scientists suggest that Rap 1 activity is important in migrating neurons to maintain a high level of Ncad at the plasma membrane for nerve cells to polarise correctly.

Exactly how Ncad interacts with molecular cascades for neuron polarisation is still under investigation. The Neuronal Polarity project accumulated data on which to base a concrete research path for future investigation.

Provided by CORDIS

Source: medicalxpress.com

ScienceDaily (July 16, 2012) — Mayo Clinic researchers have found a novel way to monitor real-time chemical changes in the brains of patients undergoing deep brain stimulation (DBS). The groundbreaking insight will help physicians more effectively use DBS to treat brain disorders such as Parkinson’s disease, depression and Tourette syndrome.

The findings are published in the journal Mayo Clinic Proceedings.

Researchers hope to use the discovery to create a DBS system that can instantly respond to chemical changes in the brain. Parkinson’s, Tourette syndrome and depression all involve a surplus or deficiency of neurochemicals in the brain. The idea is to monitor those neurochemicals and adjust them to appropriate levels.

"We can learn what neurochemicals can be released by DBS, neurochemical stimulation, or other stimulation. We can basically learn how the brain works," says author Su-Youne Chang, Ph.D., of the Mayo Clinic Neurosurgery Department. As researchers better understand how the brain works, they can predict changes, and respond before those changes disrupt brain functioning.

Researchers observed the real-time changes of the neurotransmitter adenosine in the brains of tremor patients undergoing deep brain stimulation. Neurotransmitters such as dopamine and serotonin are chemicals that transmit signals from a neuron to a target cell across a synapse.

The team used fast scan cyclic voltammetry (FSCV) to quantify concentrations of adenosine released in patients during deep brain stimulation. The data was recorded using Wireless Instantaneous Neurotransmitter Concentration Sensing, a small wireless neurochemical sensor implanted in the patient’s brain. The sensor, combined with FSCV, scans for the neurotransmitter and translates that information onto a laptop in the operating room. The sensor has previously identified neurotransmitters serotonin and dopamine in tests in brain tissue. This was the first time researchers used this technique in patients.

Tremors are a visual cue that the technique is working; researchers suspect adenosine plays a role in reducing tremors.

Researchers also hope to learn more about conditions without such external manifestations.

"We can’t watch pain as we do tremors," says Kendall Lee, M.D., Ph.D., a Mayo Clinic neurosurgeon. "What is exciting about this electrochemical feedback is that we can monitor the brain without external feedback. So now, we can monitor neurochemicals in the brain and learn about brain processes like pain."

DBS has been used successfully worldwide to treat patients with tremors. However, physicians do not fully understand why DBS works in patients. They know that when DBS electrodes are inserted before electrical stimulation, there is an immediate tremor reduction. Known as the microthalamotomy effect, it is reported in up to 53 percent of patients and known to last as long as a year.

Researchers hope to use the study findings to create a self-contained “smart” DBS system.

"With the stimulator and detection, we can create algorithms and then raise neurotransmitters to a specified level," says Kevin Bennet, a Mayo Clinic engineer who helped create the system. "We can raise these chemicals to appropriate levels, rising and falling with each person throughout their life. Within milliseconds, we can measure, calculate and respond. From the patient’s perspective, this would be essentially instantaneous."

Source: Science Daily

FRIDAY, July 13 (HealthDay News) — Movies often stereotype people with schizophrenia as being violent and unpredictable, says a researcher who claims Hollywood dispenses misinformation about symptoms, causes and treatment of this mental illness.

Hollywood portrayals are often inaccurate, misleading, study shows.

For the study, published in the July issue of Psychiatric Services, Patricia Owen of the psychology department at St. Mary’s University in San Antonio, Texas, reviewed 41 English-language films released between 1990 and 2010 that featured at least one main character with schizophrenia.

Owen found that 83 percent of those characters were portrayed as dangerous or violent to others or themselves. Almost one-third engaged in homicidal behavior, and one-quarter committed suicide, the researcher said.

According to the U.S. National Institute of Mental Health, the risk of violence is small among people with schizophrenia. But suicide risk is higher than average. About 10 percent, mostly young men, do kill themselves, the agency notes.

Delusions, auditory and visual hallucinations, and disorganized speech or thought were displayed by most of the characters, the study author pointed out in a news release from the American Psychiatric Association.

But much more common symptoms of schizophrenia — such as flat affect, lack of speech and lack of motivation — were seen much less frequently.

Although schizophrenia incidence is nearly equal among women and men, almost 80 percent of the characters with schizophrenia were male, the study found.

The review noted, however, the movies did get some characterizations of schizophrenia right. Specifically, about half of the characters had low socioeconomic status, which is consistent with data on the illness. Moreover, about half of the movies depicted or alluded to the use of medication to treat the mental illness. Psychotherapy and group therapy were not portrayed often.

Owen suggested that more research is needed to understand how films influence public perceptions about schizophrenia, and to determine how to increase empathy and understanding.

Films featuring a character with schizophrenia include A Beautiful Mind and Donnie Darko.

Source: DoctorsLounge

ScienceDaily (July 13, 2012) — A new study by University of North Carolina School of Medicine researchers found that 31 percent of children identified as at risk for autism spectrum disorders (ASD) at 12 months received a confirmed diagnosis of ASD by age 3 years.

In addition, 85 percent of the children found to be at risk for ASD based on results from the First Year Inventory (FYI), a 63-item questionnaire filled out by their parents, had some other developmental disability or concern by age three, said Grace Baranek, PhD, senior author of the study and an autism researcher with the Program for Early Autism, Research, Leadership and Service (PEARLS) in the Department of Allied Health Sciences at the UNC School of Medicine.

"These results indicate that an overwhelming majority of children who screen positive on the FYI indeed experience some delay in development by age three that may warrant early intervention," she said.

Lead author of the study, Lauren Turner-Brown, PhD, also a researcher with PEARLS and the Carolina Institute for Developmental Disabilities said, “Identification of children at risk for ASD at 12 months could provide a substantial number of children and their families with access to intervention services months or years before they would otherwise receive a traditional diagnosis.”

The First Year Inventory was developed by Grace Baranek, PhD, Linda Watson, EdD, Elizabeth Crais, PhD and J. Steven Reznick, PhD, who are all researchers with PEARLS. All are also co-authors of the study with Turner-Brown, published online ahead of print on July 10, 2012 by Autism: The International Journal of Research & Practice.

In the study, parents of 699 children who had completed the FYI when their child was 12 months old completed additional screening questionnaires when their child reached age 3. In addition, children who were found to be at risk for ASD based on these measures were invited for in-person diagnostic evaluations.

"These findings are encouraging and suggest promise in the approach of using parent report of infant behaviors as a tool for identifying 12-month-olds who are at risk for an eventual diagnosis of ASD," Turner-Brown said.

Source: Science Daily

ScienceDaily (July 12, 2012) — Millions of people suffering from multiple sclerosis, Parkinson’s, muscular dystrophy, spinal cord injuries or amputees could soon interact with their computers and surroundings using just their eyes, thanks to a new device that costs less than £40.

Researchers from Imperial College London demonstrated the functionality of the new system by getting a group of people to play the classic computer game Pong without any kind of handset. (Credit: Image courtesy of Institute of Physics (IOP))

Composed from off-the-shelf materials, the new device can work out exactly where a person is looking by tracking their eye movements, allowing them to control a cursor on a screen just like a normal computer mouse.

The technology comprises an eye-tracking device and “smart” software that have been presented July 13, in IOP Publishing’s Journal of Neural Engineering. Researchers from Imperial College London demonstrated its functionality by getting a group of people to play the classic computer game Pong without any kind of handset. In addition users were able to browse the web and write emails “hands-off.”

A video of somebody using the device to play Pong can be viewed here (https://www.youtube.com/watch?v=zapK5wvYU84)

The GT3D device is made up of two fast video game console cameras, costing less than £20 each, that are attached, outside of the line of vision, to a pair of glasses that cost just £3. The cameras constantly take pictures of the eye, working out where the pupil is pointing, and from this the researchers can use a set of calibrations to work out exactly where a person is looking on the screen.

Even more impressively, the researchers are also able to use more detailed calibrations to work out the 3D gaze of the subjects — in other words, how far into the distance they were looking. It is believed that this could allow people to control an electronic wheelchair simply by looking where they want to go or control a robotic prosthetic arm.

To demonstrate the effectiveness of the eye-tracker, the researchers got subjects to play the video game Pong. In this game, the subject used his or her eyes to move a bat to hit a ball that was bouncing around the screen — a feat that is difficult to accomplish with other read-out mechanisms such as brain waves (EEG).

Dr Aldo Faisal, Lecturer in Neurotechnology at Imperial’s Department of Bioengineering and the Department of Computing, is confident in the ability to utilise eye movements given that six of the subjects, who had never used their eyes as a control input before, could still register a respectable score within 20 per cent of the able bodied users after just 10 minutes of using the device for the first time.

The commercially viable device uses just one watt of power and can transmit data wirelessly over Wi-Fi or via USB into any Windows or Linux computer.

The GT3D system has also solved the ‘Midas touch problem’, allowing users to click on an item on the screen using their eyes, instead of a mouse button.

This problem has previously been resolved by staring at an icon for a prolonged period or blinking; however, the latter is part of our natural behaviour and happens unintentionally. Instead, the researchers calibrated the system so that a simple wink would represent a mouse click, which only occurs voluntarily unlike the blink.

Dr Faisal said: “Crucially, we have achieved two things: we have built a 3D eye tracking system hundreds of times cheaper than commercial systems and used it to build a real-time brain machine interface that allows patients to interact more smoothly and more quickly than existing invasive technologies that are tens of thousands of times more expensive.

"This is frugal innovation; developing smarter software and piggy-backing existing hardware to create devices that can help people worldwide independent of their healthcare circumstances."

Source: Science Daily

ScienceDaily (July 12, 2012) — Negative suggestion can induce symptoms of illness. Nocebo effects are the adverse events that occur during sham treatment and/or as a result of negative expectations. While the positive counterpart — the placebo effect — has been intensively studied in recent years, the scientific literature contains few studies on nocebo phenomena. In the latest issue of Deutsches Ärzteblatt International, Winfried Häuser of the Technical University of Munich and his co-authors present the underlying neurobiological mechanisms and highlight the relevance of the nocebo effect in everyday clinical practice.

Nocebo responses can, for instance, be brought about by unintended negative suggestion on the part of doctors or nurses, e.g., when informing the patient about the possible complications of a proposed treatment. It is also assumed that a certain proportion of the undesired effects of drugs can be attributed to nocebo effects. The mechanisms behind this phenomenon are — as with placebo effects — learning by Pavlovian conditioning and reaction to induced expectations.

What are the consequences for clinical practice? Doctors find themselves in an ethical dilemma between their obligation to tell the patient about the possible side effects of a treatment and their duty to minimize the risk of a medical intervention and thus to avoid triggering nocebo effects. As one possible strategy to solve this dilemma, Häuser et al. suggest emphasizing the tolerability of therapeutic measures. Another option, with the patient’s permission, would be to desist from discussing undesired effects during the patient briefing.

Source: Science Daily

ScienceDaily (July 12, 2012) — University of Kansas researchers have found larger resting pupil size and lower levels of a salivary enzyme associated with the neurotransmitter norepinephrine in children with autism spectrum disorder.

However, even though the levels of the enzyme, salivary alpha-amylase (sAA), were lower than those of typically-developing children in samples taken in the afternoon in the lab, samples taken at home throughout the day showed that sAA levels were higher in general across the day and much less variable for children with ASD.

"What this says is that the autonomic system of children with ASD is always on the same level," Christa Anderson, assistant research professor, said. "They are in overdrive."

The sAA levels of typically-developing children gradually rise and fall over the day, said Anderson, who co-directed the study with John Colombo, professor of psychology.

Norepinephrine (NE) has been found in the blood plasma levels of individuals with ASD but some researchers have questioned whether these levels were just related to the stress from blood draws.

The KU study addressed this by collecting salivary measures by simply placing a highly absorbent sponge swab under the child’s tongue and confirmed that this method of collection did not stress the children by assessing their stress levels through cortisol, another hormone.

Collecting sAA levels has the potential for physicians to screen children for ASD much earlier, noninvasively and relatively inexpensively, said Anderson.

But Anderson and Colombo also see pupil size and sAA levels as biomarkers that could be the physiological signatures of a possible dysfunction in the autonomic nervous system.

"Many theories of autism propose that the disorder is due to deficits in higher-order brain areas," said Colombo. "Our findings, however, suggest that the core deficits may lie in areas of the brain typically associated with more fundamental, vital functions."

The study, published online in the May 29, 2012 Developmental Psychobiology compared children between the ages of 20 and 72 months of age diagnosed with ASD to a group of typically developing children and a third group of children with Down Syndrome.

Both findings address the Centers for Disease Control’s urgent public health priority goals for ASD: to find biological indicators that can both help screen children earlier and lead to better understanding of how the nervous system develops and functions in the disorder.

Source: Science Daily

ScienceDaily (July 12, 2012) — Researchers at Emory University School of Medicine have identified five rare mutations in a single gene that appear to increase the chances that a boy will develop an autism spectrum disorder (ASD).

Mutations in the AFF2 gene, and other genes like it on the X chromosome, may explain why autism spectrum disorders affect four times as many boys as girls.

The mutations in AFF2 appeared in 2.5 percent (5 out of 202) boys with an ASD. Mutations in X chromosome genes only affect boys, who have one X chromosome. Girls have a second copy of the gene that can compensate.

The results were published July 5 in the journal Human Molecular Genetics.

"Our data suggest that AFF2 could be one of the major X-linked risk factors for ASD’s," says senior author Michael Zwick, PhD, assistant professor of human genetics at Emory University School of Medicine.

The finding bolsters a growing consensus among geneticists that rare variants in many different genes contribute significantly to risk for autism spectrum disorders.

The mutations in the AFF2 gene probably do not cause ASDs all by themselves, Zwick says.

"We do not think that the variants we have identified are monogenic causes of autism," he says. "Our data does support the idea that this is an autism susceptibility gene."

In some situations, mutations in a single gene are enough by themselves to lead to a neurodevelopmental disorder with autistic features, such as fragile X syndrome or tuberous sclerosis complex. But these types of mutations are thought to account for a small number of ASD cases.

Recent large-scale genetic studies of autism spectrum disorders have identified several “rare variants” that sharply increase ASD risk. Scientists believe rare variants could explain up to 15 or 20 percent of ASD cases. However, until now no single variant has been found in more than one percent of ASD cases.

Working with Zwick, postdoctoral fellow Kajari Mondal and her colleagues read the sequence of the AFF2 gene in DNA from 202 boys diagnosed with autism spectrum disorders. The patient samples came from the Autism Genetic Resource Exchange and the Simons Simplex Collection.

Tests showed that in four cases, the affected boys had inherited the risk-conferring mutations from their mothers. One boy had a “de novo” (not coming from the parents) mutation. Compared with X-linked genes in unaffected people, mutations in AFF2 were five times more abundant in the boys with ASDs.

The AFF2 gene had already been identified as responsible for a rare inherited form of intellectual disability with autistic features. This effect is seen when the AFF2 gene is deleted or silenced completely.

AFF2 has some similarity to FMR1, the gene responsible for fragile X syndrome. Like FMR1, it can be silenced by a triplet repeat. In these cases, the presence of the triplet repeat (three genetic bases repeated dozens of times) triggers a change in chromosomal structure that prevents the gene from being turned on.

In contrast, the mutations Zwick’s team found are more subtle, slightly changing the sequence of the protein AFF2 encodes. Little is known about the precise function of the AFF2 protein. A related gene in fruit flies called lilliputian also appears to regulate the development of neurons.

Zwick says one of his laboratory’s projects is to learn more about the function of the AFF2 gene, and to probe how the mutations identified by his team affect the function. His team is also working on gauging the extent to which other genes on the X chromosome contribute to autism risk.

Source: Science Daily

ScienceDaily (July 12, 2012) — Diagnosing multiple sclerosis (MS) is a challenge even for experienced neurologists. This autoimmune disease has many symptoms and rarely presents a uniform clinical picture. New scientific findings on the immune response involved in MS could now help improve the diagnosis of this illness. Scientists analyzing the blood of MS patients have discovered antibodies that attack a specific potassium channel in the cell membrane. Potassium channels play an important role in transmitting impulses to muscle and nerve cells and it is exactly these processes that are inhibited in MS patients.

Right: The autoantibody can be seen binding to the membrane of glial cells in the MS serum. By comparison, the image on the left shows a blood sample from a patient with another neurological disease. (Credit: KKNMS)

The results are published in the current issue of the New England Journal of Medicine.

For the first time, scientists in Germany’s multiple sclerosis competence network have been able to identify an antibody that bonds with the potassium channel KIR4.1. “We found this autoantibody in almost half of the MS patients in our study,” explains Bernhard Hemmer, Professor of Neurology at the Klinikum rechts der Isar hospital at Technische Universität München (TUM). The biomarker was not present in healthy patients. The findings could therefore indicate that KIR4.1 is one of the targets of the autoimmune response in MS. Humans and animals without the KIR4.1 channel experience neurological failure and cannot coordinate their movements properly. Furthermore, their bodies do not create sufficient amounts of myelin, a layer of insulation that protects the nerve cells.

KIR4.1 is primarily present in the membrane of glial cells, which are responsible for controlling metabolism in the brain and forming myelin. The neurologists will now be conducting follow-up studies into how KIR4.1 antibodies influence the development of MS. This autoantibody is extremely rare in people with other neurological diseases, making it an important potential diagnostic marker for MS in the future. “This autoantibody could improve diagnosis of MS and help us differentiate it more clearly from other neurological diseases,” continues Hemmer. This will also be the focus of further research.

Source: Science Daily

July 12, 2012

(HealthDay) — A supplement mixture (Souvenaid) containing dietary precursors and specific nutrients can improve memory in drug-naive patients with mild Alzheimer’s disease (AD), according to a study published in the July issue of the Journal of Alzheimer’s Disease.

Philip Scheltens, M.D., from the VU University Medical Center in Amsterdam, and colleagues conducted a 24-week, randomized, controlled trial in which drug-naive patients with mild AD were randomized in a 1:1 ratio to receive Souvenaid or an iso-caloric control product once daily. Memory function was assessed using the domain z-score of the Neuropsychological Test Battery (NTB).

The researchers found that, over the intervention period, the NTB memory domain z-score was significantly increased in patients taking Souvenaid versus the control group (P = 0.023), with a trend toward improvement in the NTB total composite z- score (P = 0.053). Functional connectivity in the delta band, as measured by an electroencephalography, was significantly different between the study groups in favor of the active group. There was very high adherence to the intervention (96.6 percent for the control and 97.1 percent for the active group). Both products were well tolerated and there was no between-group difference in the occurrence of serious adverse events.

"In conclusion, this study confirms that Souvenaid is well tolerated and improves memory performance,” the authors write. “Our results warrant further investigation of the clinical potential of Souvenaid in preclinical or clinical conditions characterized by synaptic loss, in particular AD.”

Several authors disclosed financial ties to Danone Research BV and Nutricia Advanced Medical Nutrition, which sponsored the study and manufacture Souvenaid.

Source: medicalxpress.com

ScienceDaily (July 12, 2012) — Obesity is not to blame for poor educational performance, according to early findings from research funded by the Economic and Social Research Council (ESRC). In a study that combines statistical methods with genetic information, researchers dispel the false idea that being overweight has damaging educational consequences.

Previous studies have shown that children who are heavier are less likely to do well at school. However, Dr Stephanie von Hinke Kessler Scholder from University of York argues it’s vital to understand what drives this association. “We sought to test whether obesity ‘directly’ hinders performance due to bullying or health problems, or whether kids who are obese do less well because of other factors that are associated with both obesity and lower exam results, such as coming from a disadvantaged family,” Dr Scholder explains.

Researchers examined data on almost 4,000 members of the Children of the 90s Birth Cohort Study. These data include the children’s DNA. It is well known that genes are randomly allocated within a population, irrespective of factors such as socio-economic position. The researchers combined the latest developments from genetic epidemiology with statistical methodologies in economic and econometric research. Using two carefully chosen ‘genetic markers’, the research team was able to identify children with a slightly higher genetic pre-disposition to obesity.

“Based on a simple correlation between children’s obesity as measured by their fat mass and their exam results, we found that heavier children did do slightly worse in school,” Dr Scholder points out. “But, when we used children’s genetic markers to account for potentially other factors, we found no evidence that obesity causally affects exam results. So, we conclude that obesity is not a major factor affecting children’s educational outcomes.”

These findings suggest that the previously found negative relationship between weight and educational performance is driven by factors that affect both weight and educational attainment. Future research should focus on other determinants of poor educational outcomes, such as social class or a family’s socio-economic circumstances, Dr Scholder points out.

The finding that obesity is not a cause of poorer educational performance is, the researchers suggest, a positive thing. “Clearly there are reasons why there are differences in educational outcomes, but our research shows that obesity is not one of them,” Dr Scholder argues.

Source: Science Daily

July 12, 2012

Biologists at UC San Diego have discovered a chemical that offers a completely new and promising direction for the development of drugs to treat metabolic disorders such as type 2 diabetes—a major public health concern in the United States due to the current obesity epidemic.

Their discovery, detailed in a paper published July 13 in an advance online issue of the journal Science, initially came as a surprise because the chemical they isolated does not directly control glucose production in the liver, but instead affects the activity of a key protein that regulates the internal mechanisms of our daily night and day activities, which scientists call our circadian rhythm or biological clock.

Scientists had long suspected that diabetes and obesity could be linked to problems in the biological clock. Laboratory mice with altered biological clocks, for example, often become obese and develop diabetes. Two years ago, a team headed by Steve Kay, dean of the Division of Biological Sciences at UC San Diego, discovered the first biochemical link between the biological clock and diabetes. It found that a key protein, cryptochrome, that regulates the biological clocks of plants, insects and mammals also regulates glucose production in the liver and that altering the levels of this protein could improve the health of diabetic mice.

Now Kay and his team have discovered a small molecule—one that can be easily developed into a drug—that controls the intricate molecular cogs or timekeeping mechanisms of cryptochrome in such a manner that it can repress the production of glucose by the liver. Like mice and other animals, humans have evolved biochemical mechanisms to keep a steady supply of glucose flowing to the brain at night, when we’re not eating or otherwise active.

"At the end of the night, our hormones signal that we’re in a fasting state," said Kay. "And during the day, when we’re active, our biological clock shuts down those fasting signals that tell our liver to make more glucose because that’s when we’re eating."

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ScienceDaily (July 11, 2012) — Widely held beliefs about Neuro-Linguistic Programming and lying are unfounded.

Twenty portrait of a woman with different expressions. (Credit: © gemenacom / Fotolia)

Proponents of Neuro-Linguistic Programming (NLP) have long claimed that it is possible to tell whether a person is lying from their eye movements.  Research published July 11 in the journal PLoS ONE reveals that this claim is unfounded, with the authors calling on the public and organisations to abandon this approach to lie detection.

For decades many NLP practitioners have claimed that when a person looks up to their right they are likely to be lying, whilst a glance up to their left is indicative of telling the truth.

Professor Richard Wiseman (University of Hertfordshire, UK) and Dr Caroline Watt (University of Edinburgh, UK) tested this idea by filming volunteers as they either lied or told the truth, and then carefully coded their eye movements.  In a second study another group of participants was asked to watch the films and attempt to detect the lies on the basis of the volunteers’ eye movements.

"The results of the first study revealed no relationship between lying and eye movements, and the second showed that telling people about the claims made by NLP practitioners did not improve their lie detection skills,” noted Wiseman. 

A final study involved moving out of the laboratory and was conducted in collaboration with Dr Leanne ten Brinke and Professor Stephen Porter from the University of British Columbia, Canada.  The team analysed films of liars and truth tellers from high profile press conferences in which people were appealing for missing relatives or claimed to have been the victim of a crime. 

"Our previous research with these films suggests that there are significant differences in the behaviour of liars and truth tellers," noted Dr Leanne ten Brinke. "However, the alleged tell-tale pattern of eye movements failed to emerge."

"A large percentage of the public believes that certain eye movements are a sign of lying, and this idea is even taught in organisational training courses.  Our research provides no support for the idea and so suggests that it is time to abandon this approach to detecting deceit" remarked Watt.

Source: Science Daily