Neuroscience

There is a long history of research on impaired eye movements associated with schizophrenia. Using a series of simple viewing tests, researchers of a new paper in Biological Psychiatry explored the ability of these eye movement tests to distinguish people with and without the diagnosis of schizophrenia.

Using their complete dataset, they were able to develop a model that could discriminate all schizophrenia cases from healthy control subjects with an impressive 98.3% accuracy.

Drs. Philip Benson and David St. Clair, lead authors on the paper, agreed that their findings were remarkable: “It has been known for over a hundred years that individuals with psychotic illnesses have a variety of eye movement abnormalities, but until our study, using a novel battery of tests, no one thought the abnormalities were sensitive enough to be used as potential clinical diagnostic biomarkers.”

Their battery of tests included smooth pursuit, free-viewing, and gaze fixation tasks. In smooth pursuit, people with schizophrenia have well-documented deficits in the ability to track slow-moving objects smoothly with their eyes. Their eye movements tend to fall behind the moving object and then catch-up with the moving object using a rapid eye movement, called a saccade.. A picture is displayed in the free-viewing test, and where most individuals follow a typical pattern with their gaze as they scan the picture, those with schizophrenia follow an abnormal pattern. In a fixation task, the instruction is to keep a steady gaze on a single unmoving target, which tends to be difficult for individuals with schizophrenia.

As expected, the researchers found that the performance of individuals with schizophrenia was abnormal compared to the healthy volunteer group on each of the eye tests. At right is an example of the differences, with the eye tracking of a schizophrenia case in red and a healthy control in blue.

The researchers then used several methods to model the data. The accuracy of each of the created algorithms was then tested by using eye test data from another group of cases and controls. Combining all the data, one of the models achieved 98.3% accuracy.

"It is encouraging to see the high sensitivity of this model for the diagnosis of schizophrenia. It will be interesting to see the extent to which this approach enables clinical investigators to distinguish people with schizophrenia from individuals with other psychiatric disorders," commented Dr. John Krystal, Editor of Biological Psychiatry.

Benson and St Clair have already started that work, stating, “We now have exciting unpublished data showing that patterns of eye movement abnormalities are specific to different psychiatric subgroups, another key requirement for diagnostic biomarkers. The next thing we want to know is when the abnormalities are first detectable and can they be used as disease markers for early intervention studies in major mental illness?”

"We are also keen to explore how best our findings can be developed for use in routine clinical practice," they added. Typical neuropsychological assessments are time-consuming, expensive, and require highly trained individuals to administer. In comparison, these eye tests are simple, cheap, and take only minutes to conduct. This means that a predictive model with such precision could potentially be incorporated in clinics and hospitals to aid physicians by augmenting traditional symptom-based diagnostic criteria.

Scientists at Freie Universität, Universität Hohenheim, and Katholieke Universiteit Leuven Breed Fruit Flies for First Time without the Neurobeachin Protein and Facilitate Study of Nervous Diseases in Humans

In experiments on the brain of the fruit fly Drosophila, scientists at Freie Universität Berlin have advanced the research on brain function and diseases in humans. Neuroscientists in the Emmy Noether Junior Research Group “Biological Memory Systems” headed by Dr. Martin Schwärzel and based at Freie Universität succeeded in breeding fruit flies without the neurobeachin protein. Among other things, BEACH proteins affect the development and function of the brain in animals and humans. The results were published in the most recent issue of The Journal of Neuroscience. In the future such animal models could be of particular importance for the understanding of certain diseases in humans, such as autism. Scientists from the University of Hohenheim and the Belgian Katholieke Universiteit Leuven were also involved.

Up to now there were no animal models suitable for understanding the significance of neurobeachin proteins in the functioning of the nervous system, for example in memory formation. Mice that are lacking the neurobeachin protein die shortly after birth. Fruit flies, on the other hand, can be alive and well without neurobeachin. The scientists also found in experiments on the flies that neurobeachin has a function in learning as the flies exhibit characteristic learning disabilities due to the absence of the protein.

The flies were also found to have a number of other abnormalities with regard to the development and function of the nervous system. Through a “genetic rescue experiment,” the researchers were able to localize the distribution of these defects in the brain. The function of the lacking neurobeachin gene was reintroduced in certain areas of the nervous system. With this procedure, the researchers were able to show, among other things, that certain features of the neurobeachin protein in flies and mice are identical.

Amyotrophic lateral sclerosis, also called Lou Gehrig’s disease, is a devastatingly cruel neurodegenerative disorder that robs sufferers of the ability to move, speak and, finally, breathe. Now researchers at the Stanford University School of Medicine and San Francisco’s Gladstone Institutes have used baker’s yeast — a tiny, one-celled organism — to identify a chink in the armor of the currently incurable disease that may eventually lead to new therapies for human patients.

“Even though yeast and humans are separated by a billion years of evolution, we were able to use the power of yeast genetics to identify an unexpected potential drug target for ALS,” said Aaron Gitler, PhD, an associate professor of genetics at Stanford. “Many neurodegenerative disorders such as ALS, Parkinson’s and Alzheimer’s exhibit protein clumping or misfolding within the neurons that is thought to either cause or contribute to the conditions. We are trying to figure out why these proteins aggregate in neurons in the brain and spinal cord, and what happens when they do.”

In 2008, Gitler received a New Innovator award from the National Institutes of Health to use yeast as a model for understanding human neurodegenerative diseases and as a way to identify new targets for drug development.

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Vulnerability to major depression is linked with how satisfied we are with our lives. This association is largely due to genes.

This is the main finding of a new twin study from the Norwegian Institute of Public Health in collaboration with the University of Oslo. The researchers compared longitudinal information from identical and fraternal twins to determine how vulnerability to major depression is associated with dispositional (overall) lifetime satisfaction.

Previous studies have systematically shown that life satisfaction is considerably stable over time. People who are satisfied at any one point in life are often also satisfied at other times in their lives. This stability—the dispositional life satisfaction—is often said to reflect an underlying positive mood or a positive disposition. Previous studies have also shown that people with such a positive disposition are less depressed, but very few studies have examined the mechanisms behind this relationship.

Results

• Both men and women who met the criteria for lifetime major depression (15.8% and 11.1% respectively) reported lower life satisfaction.

• 74% of the relationship between major depression and life satisfaction could be explained by genes.

• The remaining association (26%) could be explained by unique environmental factors.

• The researchers also calculated the heritability of dispositional life satisfaction and major depression separately. The heritability of dispositional life satisfaction, which has not previously been reported, was estimated to be 72%. In other words, it is largely genes that explain why we differ in our tendency to be satisfied and content with our lives.

• Major depression had a heritability of 34%, which is highly consistent with previous studies.

“The stable tendency to see the bright side of life is associated with lower risk of major depression because some genetic factors influence both conditions”, says researcher Ragnhild Bang Nes from the Division of Mental Health. Genes involved in satisfaction and positivity thus give protection against major depression. Nes is the main author of the study that was recently published in the Journal of Affective Disorders.

Susceptibility to both depression and overall life satisfaction is partly influenced by the same set of genes, but is also influenced by genes that are unique to each.

“The heritability figures mean that 72% of the individual differences in overall satisfaction, and 34% of the differences in depression, are caused by genes. These figures do not provide information on the importance of specific genes for an individual’s life satisfaction or risk of major depression. Traits and propensities like dispositional life satisfaction and vulnerability to major depression are not heritable in themselves. Heritability refers to the importance of genes for explaining the differences between people and the estimates may vary across time and place”, explains Nes.

Although the heritability of major depression was lower than that of life satisfaction, this does not necessarily mean that life satisfaction is far more heritable than depression. The researchers used questionnaire data from two time points to measure dispositional life satisfaction, and a single clinical interview to measure the prevalence of lifetime major depression. The use of only a single assessment to measure depression may partly explain why the heritability of depression is so much lower than life satisfaction.

Can we prevent depression by promoting life satisfaction?

“We found that depression and life satisfaction did not share as many environmental factors as genetic factors. This means that environmental factors of importance to life satisfaction (for example, activities and interventions that make you happy and content) only to a small extent protect against depression”, says Nes.

“Although our underlying disposition to life satisfaction and positivity appears to be relatively stable, small actions in our daily lives may provide temporary pleasures, and these are also important. How we spend our time is tremendously important for our happiness and well-being. It is therefore important to encourage and follow up on activities that make us happy”.

Nes adds:

“To some extent, positive experiences may also accumulate over time and create favorable conditions for our quality of life”.

I suddenly noticed I could move my pinkie. I was cruising towards the highway when this old guy tried to cross the 4-lane road really fast. He hit me and I ejected over to the opposite lane. Luckily someone found me before the traffic got to me.

Paralysis may no longer mean life in a wheelchair. A man who is paralysed from the trunk down has recovered the ability to stand and move his legs unaided thanks to training with an electrical implant.

Andrew Meas of Louisville, Kentucky, says it has changed his life. The stimulus provided by the implant is thought to have either strengthened persistent “silent” connections across his damaged spinal cord or even created new ones, allowing him to move even when the implant is switched off.

The results are potentially revolutionary, as they indicate that the spinal cord is able to recover its function years after becoming damaged.

Previous studies in animals with lower limb paralysis have shown that continuous electrical stimulation of the spinal cord below the area of damage allows an animal to stand and perform locomotion-like movements. That’s because the stimulation allows information about proprioception – the perception of body position and muscle effort – to be received from the lower limbs by the spinal cord. The spinal cord, in turn, allows lower limb muscles to react and support the body without any information being received from the brain (Journal of Neuroscience, doi.org/czq67d).

Last year, Susan Harkema and Claudia Angeli at the Frazier Rehab Institute and University of Louisville in Kentucky and colleagues tested what had been learned on animals in a man who was paralysed after being hit by a car in 2006. He was diagnosed with a “motor complete” spinal lesion in his neck, which means that no motor activity can be recorded below the lesion.

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Wouldn’t it be amazing if our bodies prepared us for future events that could be very important to us, even if there’s no clue about what those events will be?

Presentiment without any external clues may, in fact, exist, according to new Northwestern University research that analyzes the results of 26 studies published between 1978 and 2010.

Researchers already know that our subconscious minds sometimes know more than our conscious minds. Physiological measures of subconscious arousal, for instance, tend to show up before conscious awareness that a deck of cards is stacked against us.

"What hasn’t been clear is whether humans have the ability to predict future important events even without any clues as to what might happen," said Julia Mossbridge, lead author of the study and research associate in the Visual Perception, Cognition and Neuroscience Laboratory at Northwestern.

A person playing a video game at work while wearing headphones, for example, can’t hear when his or her boss is coming around the corner.

"But our analysis suggests that if you were tuned into your body, you might be able to detect these anticipatory changes between two and 10 seconds beforehand and close your video game," Mossbridge said. "You might even have a chance to open that spreadsheet you were supposed to be working on. And if you were lucky, you could do all this before your boss entered the room."

This phenomenon is sometimes called “presentiment,” as in “sensing the future,” but Mossbridge said she and other researchers are not sure whether people are really sensing the future.

"I like to call the phenomenon ‘anomalous anticipatory activity,’" she said. "The phenomenon is anomalous, some scientists argue, because we can’t explain it using present-day understanding about how biology works; though explanations related to recent quantum biological findings could potentially make sense. It’s anticipatory because it seems to predict future physiological changes in response to an important event without any known clues, and it’s an activity because it consists of changes in the cardiopulmonary, skin and nervous systems."

The Early Start Denver Model (ESDM), a comprehensive behavioral early intervention program that is appropriate for children with autism spectrum disorder (ASD) as young as 12 months, has been found to be effective in improving social skills and brain responses to social cues in a randomized controlled study published online today in the Journal of the American Academy of Child & Adolescent Psychiatry. 

“So much of a toddler’s learning involves social interaction, and early intervention that promotes attention to people and social cues may pay dividends in promoting the normal development of the brain and behavior,” said Geraldine Dawson, Ph.D., Autism Speaks chief science officer and the study’s lead author. This is the first controlled study of an intensive early intervention that demonstrates both improvement of social skills and brain responses to social stimuli resulting from intensive early intervention. Given that the American Academy of Pediatrics recommends that all 18- and 24-month-old children be screened for autism, “it is vital that we have effective therapies available for young children as soon as they are diagnosed,” continued Dr. Dawson. 

“This may be the first demonstration that a behavioral intervention for autism is associated with changes in brain function as well as positive changes in behavior,” said Thomas R. Insel, M.D., director of the National Institute of Mental Health. “By studying changes in the neural response to faces, Dawson and her colleagues have identified a new target and a potential biomarker that can guide treatment development.”

ESDM, which combines applied behavioral analysis (ABA) teaching methods with developmental ‘relationship-based’ approaches, was previously demonstrated to achieve significant gains in cognitive, language and daily living skills compared to children with ASD who received commonly available community interventions. On average, the preschoolers receiving ESDM for two years improved 17.5 standard score points compared to 7.0 points in the community intervention comparison group.

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Introducing a light-sensitive protein in transgenic nerve cells… transplanting nerve cells into the brains of laboratory animals… inserting an optic fibre in the brain and using it to light up the nerve cells and stimulate them into releasing more dopamine to combat Parkinson’s disease… These events may sound like science fiction but they are soon to become a reality in a research laboratory at Lund University in Sweden.

For the time being, this is basic research but the long term objective is to find new ways of treating Parkinson’s disease. This increasingly common disease is caused by degeneration of the brain cells producing signal substance dopamine.

Many experiments have been conducted on both animals and humans, transplanting healthy nerve cells to make up for the lack of dopamine, but it is difficult to study what happens to the transplant.

“We don’t know how the new nerve cells behave once they have been transplanted into the brain. Do they connect to the surrounding cells as they should, and can they function normally and produce dopamine as they should? Can we use light to reinforce dopamine production? These are the issues we want to investigate with optogenetics”, says Professor Merab Kokaia.

Optogenetics allows scientists to control certain cells in the brain using light, leaving other cells unaffected. In order to do this, the relevant cells are equipped with genes for a special light-sensitive protein. The protein makes the cells react when they are illuminated with light from a thin optic fibre which is also implanted in the brain. The cells can then be “switched on” when they are illuminated.

“If we get signals as a response to light from the host brain, we know that they come from the transplanted cells since they are the only ones to carry the light-sensitive protein. This gives us a much more specific way of studying the brain’s reactions than inserting an electrode, which is the current method. With an electrode, we do not know whether the electric signals that are detected come from “new” or “old” brain cells”, explains Merab Kokaia.

The work will be conducted on laboratory rats modelling Parkinson’s disease. The transplanted cells will be derived from skin from an adult human and will have been “reprogrammed” as nerve cells. Merab Kokaia will be collaborating with neuro-researchers Malin Parmar and Olle Lindvall on the project.

The three Lund researchers have received a grant of USD 75 000 from the Michael J. Fox Foundation, started by actor Michael J. Fox and dedicated to Parkinson’s research.

The light-sensitive protein is obtained from a bacterium, which uses light to gain energy. Since it is not a human protein, the safety checks will be extra strict if the method is to be used on humans.

”We know that this is long term research. But the methodology is interesting and it will be exciting to see what we can come up with,” says Merab Kokaia.

New research presented in October at the 6th Neurodegenerative Conditions Research and Development Conference in San Francisco demonstrates the role of the investigational compound IRX4204 in alleviating cognitive decline in animal models of Alzheimer’s disease (AD). The presentation entitled “Investigation of the RXR-specific agonist IRX4204 as a Disease Modifying Agent of Alzheimer’s Disease Neuropathology and Cognitive Impairment” was made by lead researcher Giulio Maria Pasinetti, MD, PhD, of the Mount Sinai School of Medicine in New York City.

IRX4204 is a retinoid X receptor (RXR) agonist, meaning it stimulates the retinoid receptor in the brain.The data demonstrates attenuation of AD including prevention of plaque deposits associated with cognitive deterioration in an IRX4204-treated mouse model genetically determined to develop AD. IRX4204 also prevents neuropathological features associated with abnormal tau processing, another form of abnormal protein also found in a form of Parkinson’s disease associated with dementia.

"The treatment of AD remains a serious unmet medical need which IRX4204 may be able to address," Dr. Pasinetti said "Our research show that IRX4204 and other RXR agonists have potential for slowing, and possibly reversing pathology and cognitive deficits in Alzheimer’s disease patients."

Ongoing translational studies in subjects with Alzheimer’s disease and Parkinson’s disease with dementia are currently being developed.

Alzheimer’s disease currently afflicts more than 5 million Americans and may triple in prevalence to more than 16 million Americans by 2050, according to data from The Alzheimer’s Association.

While powerful magnetic stimulation of the frontal lobe of the brain can alleviate symptoms of depression, those receiving the treatment did not report effects on sleep or arousal commonly seen with antidepressant medications, researchers say.

“People’s sleep gets better as their depression improves, but the treatment doesn’t itself cause sedation or insomnia.” said Dr. Peter B. Rosenquist, Vice Chair of the Department of Psychiatry and Health Behavior at the Medical College of Georgia at Georgia Health Sciences University.

The finding resulted from a secondary analysis of a study of 301 patients at 23 sites comparing the anti-depressive effects of the Neuronetics Transcranial Magnetic Stimulation Therapy System to sham (placebo) treatment in patients resistant to antidepressant medications. TMS sessions were given for 40 minutes, five days a week for six weeks. Initial findings, published in the journal Biological Psychiatry in 2007, were the primary evidence in the Food and Drug Administration’s approval of TMS for depression.  The secondary review reaffirmed TMS’s effectiveness in depression but revealed no differences in rates of insomnia or sleepiness among those who got actual and sham (placebo) therapy. Patients in the treatment group were also no more likely to request medication for insomnia or anxiety.

“It’s important for us to understand the full range of the effects of any treatment we give,” said Rosenquist, corresponding author of the study in the journal Psychiatric Research. The new findings will assuage worries of sleep-related side effects and remind physicians to remain alert to residual insomnia in depressed patients they are treating with TMS, the researchers report.

Sleep problems are a common side effect of major antidepressants: some drugs sedate patients while others stimulate them and increase insomnia. Insomnia occurs in 50-90 percent of patients with major depressive disorder. Other depressed patients complain they sleep too much. The good news is that TMS does not contribute to insomnia or oversleeping.

“One of the many bad things about depression is that often patients cannot sleep. We think it’s a significant symptom,” Rosenquist said. “If patients can’t sleep, it really adds to their distress, and even increases the likelihood of suicide.  We need antidepressant treatments that patients can tolerate so that they will stay with the treatment, which takes weeks to fully achieve.  Our study adds to the evidence showing that TMS has remarkably few side effects.” Patients often seek TMS as an option or adjunct to medication to avoid medication side effects.

“Mood disorders are associated with widespread structural and functional changes in the human brain, which can be reversed with successful treatment,” Rosenquist said.  “Clinical researchers are working to find the optimal way to restore normal brain function.”

TMS targets the prefrontal cortex of the brain, involved in mood regulation as well as other higher-order functions like planning, evaluating and decision-making. In this procedure, patients sit in a recliner and receive brief pulses of a MRI strength magnet held against the front of the head. The magnetic energy of TMS causes the brain cells closest to the surface of the brain to increase their activity which in turn influences the activity of the brain as a whole.

Major Depressive Disorder affects approximately 14.8 million, or about 6.7 percent of American adults in a given year, according to the National Institute of Mental Health. It’s the leading cause of disability in ages 15 to 44. Despite the numbers, Rosenquist concedes that it’s not clear what causes depression or exactly how antidepressants and other therapies, such as TMS, work.  “It’s an important puzzle and the work continues.  We are excited to be a part of this effort at Georgia Health Sciences University.”

Genetics researchers at the University of Adelaide have solved a 40-year mystery for a family beset by a rare intellectual disability - and they’ve discovered something new about the causes of intellectual disability in the process.

While many intellectual disabilities are caused directly by a genetic mutation in the so-called “protein coding” part of our genes, the researchers found that in their case the answer laid outside the gene and in the regulation of proteins.

Protein regulation involves the switching on or off of a protein by specific genes. As a consequence in this case, either too much or too little of this protein can trigger the disability.

The team has studied a large (anonymous) Australian family of 100 people, who for generations have not known the source of their genetically inherited condition.

The disability - which results in a lower IQ, behavioural problems such as aggression, and memory loss, and is linked with developmental delays, epilepsy, schizophrenia and other problems - affects only the male family members and can be passed on by the female family members to their children.

Genetic samples taken from the family and laboratory testing involving mice have confirmed that the protein produced by the HCFC1 (host cell factor C1) gene is the cause of this disability.

"The causes of intellectual disability generally are highly variable and the genetic causes in particular are numerous. The vast majority of intellectual disabilities are due to genetic mutations in proteins, so it was rather unexpected that we found this particular disability to be due to a regulatory mutation," says the leader of the study, Professor Jozef Gecz from the University of Adelaide’s School of Paediatrics and Reproductive Health.

"We’ve been researching this specific disability for 10 years and it’s taken us the last three years to convince ourselves that the protein regulation is the key," he says.

"For the family, this means we now have a genetic test that will determine whether or not a female member of the family is a carrier, which brings various benefits for the family.

"From a scientific point of view, this widens our viewpoint on the causes of these disabilities and tells us where we should also look for answers for those families and individuals without answers.

"This is just the tip of the iceberg in understanding the impact of altered gene regulation on intellectual disability - the gene regulatory landscape is much bigger than the protein coding landscape. We have already found, and I would expect to continue finding, a number of other intellectual disabilities linked with protein regulation over the next 20 years or so."

Professor Gecz and his team have published their findings in this month’s issue of the American Journal of Human Genetics.

Everyone feels refreshed after a good night’s sleep, but sleep does more than just rejuvenate, it can also consolidate memories. ‘The rapid eye movement form of sleep and slow wave sleep are involved in cognitive forms of memory such as learning motor skills and consciously accessible memory’, explains Randolf Mezel from the Freie Universtät Berlin, Germany. According to Menzel, the concept that something during sleep reactivates a memory for consolidation is a basic theory in sleep research. However, the human brain is far too complex to begin dissecting the intricate neurocircuits that underpin our memories, which is why Menzel has spent the last four decades working with honey bees: they are easy to train, well motivated and it is possible to identify the miniaturised circuits that control specific behaviours in their tiny brains. Intrigued by the role of sleep in memory consolidation and knowing that a bee is sleeping well when its antennae are relaxed and collapsed down, Menzel decided to focus on the role of sleep in one key memory characteristic: relearning (p. 3981). The challenge that Menzel set the bees was to learn a new route home after being displaced from a familiar path.

Menzel and his colleague Lisa Beyaert provided a hive with a well-stocked feeder and trained the bees to visit the feeder and return home fully laden. Then, when the duo were convinced that the bees had memorized the routine, they cunningly intercepted the bees at the feeder and transported them to a new location before releasing the insects to find their way home. According to Menzel, foragers learn the general lay of the land as novices before specialising in a few well-travelled routes later in their careers. He explains that the displaced bees had to rely on their earlier experiences to learn their new way home. How would loss of sleep affect the bee’s ability to learn the new route? To determine this, Menzel and Beyeart first had to check that the bees could learn the new route and that sleep deprivation hadn’t made them too tired or altered their motivation to forage.

Teaming up with electrical engineer Uwe Greggers, Menzel kitted the bees out with tiny RADAR transponders; the RADAR technology was particularly demanding to operate. Tracking the insects’ progress as they tried to learn the alternative route home, Menzel and his colleagues saw that by the second run home, the displaced bees had learned the new route. And when the trio disturbed the insects’ sleep during the night before the initial displacement by shaking them awake every 5 min, they found that the bees were unfazed. In fact they didn’t seem to need sleep to maintain their foraging energy levels and the foragers that were deprived of sleep before the first displacement run had no problems learning the new route home.

However, when the team disrupted the bees’ sleep after they had allowed the bees a single run along the new displaced route, the lack of sleep played havoc with their memories on the following day. Fewer than half of the sleep-deprived foragers made it home successfully, and those that did took more than twice as long as bees that had enjoyed an uninterrupted night’s sleep.

Sleep deprivation had dramatically affected the bees’ ability to alter a well-established memory and the team is now keen to see whether they can identify characteristic activity patterns in the slumbering insects’ brains that could represent memory formation.

When the era of regenerative medicine dawned more than three decades ago, the potential to replenish populations of cells destroyed by disease was seen by many as the next medical revolution. However, what followed turned out not to be a sprint to the clinic, but rather a long tedious slog carried out in labs across the globe required to master the complexity of stem cells and then pair their capabilities and attributes with specific diseases.

In a review article appearing today in the journal Science, University of Rochester Medical Center scientists Steve Goldman, M.D., Ph.D., Maiken Nedergaard, Ph.D., and Martha Windrem, Ph.D., contend that researchers are now on the threshold of human application of stem cell therapies for a class of neurological diseases known as myelin disorders – a long list of diseases that include conditions such as multiple sclerosis, white matter stroke, cerebral palsy, certain dementias, and rare but fatal childhood disorders called pediatric leukodystrophies.

"Stem cell biology has progressed in many ways over the last decade, and many potential opportunities for clinical translation have arisen," said Goldman. "In particular, for diseases of the central nervous system, which have proven difficult to treat because of the brain’s great cellular complexity, we postulated that the simplest cell types might provide us the best opportunities for cell therapy."

The common factor in myelin disorders is a cell called the oligodendrocyte. These cells arise, or are created, by another cell found in the central nervous system called the glial progenitor cell. Both oligodendrocytes and their “sister cells” – called astrocytes – share this same parent and serve critical support functions in the central nervous systems.

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Five scientists, including two from Simon Fraser University, have discovered that 30 per cent of our likelihood of developing Multiple Sclerosis (MS) can be explained by 475,806 genetic variants in our genome. Genome-wide Association Studies (GWAS) commonly screen these variants, looking for genetic links to diseases.

Corey Watson, a recent SFU doctoral graduate in biology, his thesis supervisor SFU biologist Felix Breden and three scientists in the United Kingdom have just had their findings published online in Scientific Reports. It’s a sub-publication of the journal Nature.

An inflammatory disease of the central nervous system, MS is the most common neurological disorder among young adults. Canada has one of the highest MS rates in the world.

Watson and his colleagues recently helped quantify MS genetic susceptibility by taking a closer look at GWAS-identified variants in the major histocompatibility complex (MHC) region in 1,854 MS patients. The region has long been associated with MS susceptibility.

The MS patients’ variants were compared to those of 5,164 controls, people without MS.

They noted that eight percent of our 30-per-cent genetic susceptibility to MS is linked to small DNA variations on chromosome 6, which have also long been associated with MS susceptibility.

The MHC encodes proteins that facilitate communication between certain cells in the immune system. Outside of the MHC, a good majority of genetic susceptibility can’t be nailed down because current studies don’t allow for all variants in our genome to be captured.

 “Much of the liability is unaccounted for because current research methods don’t enable us to fully interrogate our genome in the context of risk for MS or other diseases,” says Watson.

The researchers believe that one place to look for additional genetic causes of MS may be in genes that have variants that are rare in the population. “The importance of rare gene variants in MS has been illustrated in two recent studies,” notes Watson, now a postdoctoral researcher at the Mount Sinai School of Medicine in New York.

“But these variants, too, are generally poorly represented by genetic markers captured in GWAS, like the one our study was based on.”

Researchers from UCL have found that lonely people have less grey matter in a part of the brain associated with decoding eye gaze and other social cues.

Published in the journal of Current Biology, the study also suggests that through training people might be able to improve their social perception and become less lonely.

“What we’ve found is the neurobiological basis for loneliness,” said lead author Dr Ryota Kanai (UCL Institute of Cognitive Neuroscience). “Before conducting the research we might have expected to find a link between lonely people and the part of the brain related to emotions and anxiety, but instead we found a link between loneliness and the amount of grey matter in the part of the brain involved in basic social perception.” 

To see how differences in loneliness might be reflected in the structure of the brain regions associated with social processes, the team scanned the brains of 108 healthy adults and gave them a number of different tests. Loneliness was self-reported and measured using a UCLA loneliness scale questionnaire.

When looking at full brain scans they saw that lonely individuals have less greymatter in the left posterior superior temporal sulcus (pSTS)—an area implicated in basic social perception, confirming that loneliness was associated with difficulty in processing social cues.

“The pSTS plays a really important role in social perception, as it’s the initial step of understanding other people,” said Dr Kanai. “Therefore the fact that lonely people have less grey matter in their pSTS is likely to be the reason why they have poorer perception skills.”

In order to gauge social perception, participants were presented with three different faces on a screen and asked to judge which face had misaligned eyes and whether they were looking either right or left. Lonely people found it much harder to identify which way the eyes were looking, confirming the link between loneliness, the size of the pSTS and the perception of eye gaze. 

“From the study we can’t tell if loneliness is something hardwired or environmental,” said co-author Dr Bahador Bahrami (UCL Institute of Cognitive Neuroscience). “But one possibility is that people who are poor at reading social cues may experience difficulty in developing social relationships, leading to social isolation and loneliness.” 

One way to counter this loneliness could be through social perception training with a smartphone app.

“The idea of training is one way to address this issue, as by maybe using a smartphone app to improve people’s basic social perception such as eye gaze, hopefully we can help them to lead less lonely lives,” said Dr Kanai.