Neuroscience

Articles and news from the latest research reports.

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Older adults have morning brains! Study shows noticeable differences in brain function across the day

Older adults who are tested at their optimal time of day (the morning), not only perform better on demanding cognitive tasks but also activate the same brain networks responsible for paying attention and suppressing distraction as younger adults, according to Canadian researchers.

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The study, published online July 7th in the journal Psychology and Aging (ahead of print publication), has yielded some of the strongest evidence yet that there are noticeable differences in brain function across the day for older adults.

Time of day really does matter when testing older adults. This age group is more focused and better able to ignore distraction in the morning than in the afternoon,” said lead author John Anderson, a PhD candidate with the Rotman Research Institute at Baycrest Health Sciences and University of Toronto, Department of Psychology.

“Their improved cognitive performance in the morning correlated with greater activation of the brain’s attentional control regions – the rostral prefrontal and superior parietal cortex – similar to that of younger adults.” 

Asked how his team’s findings may be useful to older adults in their daily activities, Anderson recommended that older adults try to schedule their most mentally-challenging tasks for the morning time. Those tasks could include doing taxes, taking a test (such as a driver’s license renewal), seeing a doctor about a new condition, or cooking an unfamiliar recipe.

In the study, 16 younger adults (aged 19 – 30) and 16 older adults (aged 60-82) participated in a series of memory tests during the afternoon from 1 – 5 p.m. The tests involved studying and recalling a series of picture and word combinations flashed on a computer screen. Irrelevant words linked to certain pictures and irrelevant pictures linked to certain words also flashed on the screen as a distraction. During the testing, participants’ brains were scanned with fMRI which allows researchers to detect with great precision which areas of the brain are activated. Older adults were 10 percent more likely to pay attention to the distracting information than younger adults who were able to successfully focus and block this information. The fMRI data confirmed that older adults showed substantially less engagement of the attentional control areas of the brain compared to younger adults. Indeed, older adults tested in the afternoon were “idling” – showing activations in the default mode (a set of regions that come online primarily when a person is resting or thinking about nothing in particular) indicating that perhaps they were having great difficulty focusing. When a person is fully engaged with focusing, resting state activations are suppressed.

When 18 older adults were morning tested (8:30 a.m. – 10:30 a.m.) they performed noticeably better, according to two separate behavioural measures of inhibitory control. They attended to fewer distracting items than their peers tested at off-peak times of day, closing the age difference gap in performance with younger adults. Importantly, older adults tested in the morning activated the same brain areas young adults did to successfully ignore the distracting information. This suggests that when older adults are tested is important for both how they perform and what brain activity one should expert to see.

“Our research is consistent with previous science reports showing that at a time of day that matches circadian arousal patterns, older adults are able to resist distraction,” said Dr. Lynn Hasher, senior author on the paper and a leading authority in attention and inhibitory functioning in younger and older adults.

The Baycrest findings offer a cautionary flag to those who study cognitive function in older adults. “Since older adults tend to be morning-type people, ignoring time of day when testing them on some tasks may create an inaccurate picture of age differences in brain function,” said Dr. Hasher, senior scientist at Baycrest’s Rotman Research Institute and Professor of Psychology at University of Toronto.

(Source: baycrest.org)

Filed under aging cognitive performance prefrontal cortex parietal cortex brain activity brain function psychology neuroscience science

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(Image caption: In mice whose brain tumor cells (in green) couldn’t make galectin-1, the body’s immune system was able to recognize and attack the cells, causing them to die. In this microscope image, the orange areas show where tumor cells had died in just the first three days after the tumor was implanted in the brain. Six days later, the tumor had been eradicated. Credit: University of Michigan Medical School)
Brain tumors fly under the body’s radar like stealth jets
Brain tumors fly under the radar of the body’s defense forces by coating their cells with extra amounts of a specific protein, new research shows.
Like a stealth fighter jet, the coating means the cells evade detection by the early-warning immune system that should detect and kill them. The stealth approach lets the tumors hide until it’s too late for the body to defeat them.
The findings, made in mice and rats, show the key role of a protein called galectin-1 in some of the most dangerous brain tumors, called high grade malignant gliomas. A research team from the University of Michigan Medical School made the discovery and has published it online in the journal Cancer Research.
In a stunning example of scientific serendipity, the team uncovered galectin-1’s role by pursuing a chance finding. They had actually been trying to study how the extra production of galectin-1 by tumor cells affects cancer’s ability to grow and spread in the brain.
Instead, they found that when they blocked cancer cells from making galectin-1, the tumors were eradicated; they did not grow at all. That’s because the “first responders” of the body’s immune system – called natural killer or NK cells – spotted the tumor cells almost immediately and killed them.
But when the tumor cells made their usual amounts of galectin-1, the immune cells couldn’t recognize the cancerous cells as dangerous. That meant that the immune system couldn’t trigger the body’s “second line of defense”, called T cells – until the tumors had grown too large for the body to beat.
Team leader Pedro Lowenstein, M.D., Ph.D, of the U-M Department of Neurosurgery, says the findings open the door to research on the effect of blocking galectin-1 in patients with gliomas.
"This is an incredibly novel and exciting development, and shows that in science we must always be open-minded and go where the science takes us; no matter where we thought we wanted to go," says Lowenstein, whose graduate student Gregory J. Baker is the first author of the paper.
"In this case, we found that over-expression of galectin-1 inhibits the innate immune system, and this allows the tumor to grow enough to evade any possible effective T cell response," he explains. "By the time it’s detected, the battle is already lost."
The NK-evading “stealth” function of the extra-thick coating of galectin-1 came as a surprise, because glioma researchers everywhere had assumed the extra protein had more to do with the insidious ability of gliomas to invade the brain, and to evade the attacks of T cells.
Gliomas, which make up about 80 percent of all malignant brain tumors, include anaplastic oligodendrogliomas, anaplastic astrocytomas, and glioblastoma multiforme. More than 24,000 people in the U.S. are diagnosed with a primary malignant brain tumor each year.
The tiny tendrils of tumor that extend into brain tissue from a glioma are what make them so dangerous. Even when a neurosurgeon removes the bulk of the tumor, small invasive areas escape detection and keep growing, unchecked by the body.
Helping the innate immune system to recognize early stages of cancer growth, and sound the alarm for the body’s defense system to act while the remaining cancer is still small enough for them to kill, could potentially help patients.
While the new discovery opens the door to that kind of approach, much work needs to be done before the mouse-based research could help human patients, says Lowenstein, who is the Richard Schneider Collegiate Professor in Neurosurgery and also holds an appointment in the U-M Department of Cell and Developmental Biology. Galectin-1 may help other types of tumor evade the innate NK cells, too
The new research suggests that in the brain’s unique environment, galectin-1 creates an immunosuppressive effect immediately around tumor cells. The brain cancer cells seem to have evolved the ability to express their galectin-1 genes far more than normal, to allow the tumor to keep growing.
Lowenstein and co-team leader Maria Castro, Ph.D., have long studied the immune system’s interactions with brain cancer, using funding from the National Institutes of Health, and are co-leading a new clinical trial for malignant glioma (NCT01811992), that aims to translate prior research achievements into new trials for patients with brain tumors.
Most brain tumor immune research has focused on triggering the action of the adaptive immune system – whose cells control the process that allows the body to kill invaders from outside or within.
But that system take days or even weeks to reach full force – enough time for incipient tumors to grow too large for immune cells to eliminate solid tumor growth. The new research suggests the importance of enhancing the ability of the innate immune system’s “early warning” sentinels to spot glioma cells as early as possible.

(Image caption: In mice whose brain tumor cells (in green) couldn’t make galectin-1, the body’s immune system was able to recognize and attack the cells, causing them to die. In this microscope image, the orange areas show where tumor cells had died in just the first three days after the tumor was implanted in the brain. Six days later, the tumor had been eradicated. Credit: University of Michigan Medical School)

Brain tumors fly under the body’s radar like stealth jets

Brain tumors fly under the radar of the body’s defense forces by coating their cells with extra amounts of a specific protein, new research shows.

Like a stealth fighter jet, the coating means the cells evade detection by the early-warning immune system that should detect and kill them. The stealth approach lets the tumors hide until it’s too late for the body to defeat them.

The findings, made in mice and rats, show the key role of a protein called galectin-1 in some of the most dangerous brain tumors, called high grade malignant gliomas. A research team from the University of Michigan Medical School made the discovery and has published it online in the journal Cancer Research.

In a stunning example of scientific serendipity, the team uncovered galectin-1’s role by pursuing a chance finding. They had actually been trying to study how the extra production of galectin-1 by tumor cells affects cancer’s ability to grow and spread in the brain.

Instead, they found that when they blocked cancer cells from making galectin-1, the tumors were eradicated; they did not grow at all. That’s because the “first responders” of the body’s immune system – called natural killer or NK cells – spotted the tumor cells almost immediately and killed them.

But when the tumor cells made their usual amounts of galectin-1, the immune cells couldn’t recognize the cancerous cells as dangerous. That meant that the immune system couldn’t trigger the body’s “second line of defense”, called T cells – until the tumors had grown too large for the body to beat.

Team leader Pedro Lowenstein, M.D., Ph.D, of the U-M Department of Neurosurgery, says the findings open the door to research on the effect of blocking galectin-1 in patients with gliomas.

"This is an incredibly novel and exciting development, and shows that in science we must always be open-minded and go where the science takes us; no matter where we thought we wanted to go," says Lowenstein, whose graduate student Gregory J. Baker is the first author of the paper.

"In this case, we found that over-expression of galectin-1 inhibits the innate immune system, and this allows the tumor to grow enough to evade any possible effective T cell response," he explains. "By the time it’s detected, the battle is already lost."

The NK-evading “stealth” function of the extra-thick coating of galectin-1 came as a surprise, because glioma researchers everywhere had assumed the extra protein had more to do with the insidious ability of gliomas to invade the brain, and to evade the attacks of T cells.

Gliomas, which make up about 80 percent of all malignant brain tumors, include anaplastic oligodendrogliomas, anaplastic astrocytomas, and glioblastoma multiforme. More than 24,000 people in the U.S. are diagnosed with a primary malignant brain tumor each year.

The tiny tendrils of tumor that extend into brain tissue from a glioma are what make them so dangerous. Even when a neurosurgeon removes the bulk of the tumor, small invasive areas escape detection and keep growing, unchecked by the body.

Helping the innate immune system to recognize early stages of cancer growth, and sound the alarm for the body’s defense system to act while the remaining cancer is still small enough for them to kill, could potentially help patients.

While the new discovery opens the door to that kind of approach, much work needs to be done before the mouse-based research could help human patients, says Lowenstein, who is the Richard Schneider Collegiate Professor in Neurosurgery and also holds an appointment in the U-M Department of Cell and Developmental Biology. Galectin-1 may help other types of tumor evade the innate NK cells, too

The new research suggests that in the brain’s unique environment, galectin-1 creates an immunosuppressive effect immediately around tumor cells. The brain cancer cells seem to have evolved the ability to express their galectin-1 genes far more than normal, to allow the tumor to keep growing.

Lowenstein and co-team leader Maria Castro, Ph.D., have long studied the immune system’s interactions with brain cancer, using funding from the National Institutes of Health, and are co-leading a new clinical trial for malignant glioma (NCT01811992), that aims to translate prior research achievements into new trials for patients with brain tumors.

Most brain tumor immune research has focused on triggering the action of the adaptive immune system – whose cells control the process that allows the body to kill invaders from outside or within.

But that system take days or even weeks to reach full force – enough time for incipient tumors to grow too large for immune cells to eliminate solid tumor growth. The new research suggests the importance of enhancing the ability of the innate immune system’s “early warning” sentinels to spot glioma cells as early as possible.

Filed under galectin-1 brain tumours glioma cancer cells t cells immune system neuroscience science

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Could your brain be reprogrammed to work better?

Researchers from The University of Western Australia have shown that electromagnetic stimulation can alter brain organisation which may make your brain work better.

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In results from a study published today in the prestigious Journal of Neuroscience, researchers from The University of Western Australia and the Université Pierre et Marie Curie in France demonstrated that weak sequential electromagnetic pulses (repetitive transcranial magnetic stimulation - or rTMS) on mice can shift abnormal neural connections to more normal locations.

The discovery has important implications for treatment of many nervous system disorders related to abnormal brain organisation such as depression, epilepsy and tinnitus.

To better understand what magnetic stimulation does to the brain Research Associate Professor Jennifer Rodger from UWA’s School of Animal Biology and her colleagues tested a low-intensity version of the therapy - known as low-intensity repetitive transcranial magnetic stimulation (LI-rTMS) - on mice born with abnormal brain organisation.

Lead author, PhD candidate Kalina Makowiecki, said the research demonstrated that even at low intensities, pulsed magnetic stimulation could reduce abnormally located neural connections, shifting them towards their correct locations in the brain.

"This reorganisation is associated with changes in a specific brain chemical, and occurred in several brain regions, across a whole network. Importantly, this structural reorganisation was not seen in the healthy brain or the appropriate connections in the abnormal mice, suggesting that the therapy could have minimal side effects in humans.

"Our findings greatly increase our understanding of the specific cellular and molecular events that occur in the brain during this therapy and have implications for how best to use it in humans to treat disease and improve brain function," Ms Makowiecki said.

(Source: news.uwa.edu.au)

Filed under brain function transcranial magnetic stimulation depression epilepsy brain stimulation neuroscience science

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Dementia Risk Quadrupled in People with Mild Cognitive Impairment

In a long-term, large-scale population-based study of individuals aged 55 years or older in the general population researchers found that those diagnosed with mild cognitive impairment (MCI) had a four-fold increased risk of developing dementia or Alzheimer’s disease (AD) compared to cognitively healthy individuals. Several risk factors including older age, positive APOE-ɛ4 status, low total cholesterol levels, and stroke, as well as specific MRI findings were associated with an increased risk of developing MCI. The results are published in a supplement to the Journal of Alzheimer’s Disease.

“Mild cognitive impairment has been identified as the transitional stage between normal aging and dementia,” comments M. Arfan Ikram, MD, PhD, a neuroepidemiologist at Erasmus MC University Medical Center (Rotterdam). “Identifying persons at a higher risk of dementia could postpone or even prevent dementia by timely targeting modifiable risk factors.”

Unlike a clinical trial, the Rotterdam study is an observational cohort study focusing on the general population, instead of persons referred to a memory clinic. The Rotterdam study began in 1990, when almost 8,000 inhabitants of Rotterdam aged 55 years or older agreed to participate in the study. Ten years later, another 3,000 individuals were added. Participants undergo home interviews and examinations every four years.

“This important prospective study adds to the accumulating evidence that strokes, presumably related to so called ‘vascular’ risk factors, also contribute to the appearance of dementia in Alzheimer’s disease. This leads to the conclusion that starting at midlife people should minimize those risk factors. The recent results of the Finish FINGER study corroborate this idea. It should be remembered that delaying the onset of dementia by five years will reduce the prevalence of the disease by half. And of course, since there is no cure for AD, prevention is the best approach at present,” explains Professor Emeritus Amos D Korczyn, Tel Aviv University, Ramat Aviv, Israel, and Guest Editor of the Supplement.

To be diagnosed with MCI in the study, individuals were required to meet three criteria: a self-reported awareness of having problems with memory or everyday functioning; deficits detected on a battery of cognitive tests; and no evidence of dementia. They were categorized into those with memory problems (amnestic MCI) and those with normal memory (non-amnestic MCI).

Of 4,198 persons found to be eligible for the study, almost 10% were diagnosed with MCI. Of these, 163 had amnestic MCI and 254 had non-amnestic MCI.

The risk of dementia was especially high for people with amnestic MCI. Similar results were observed regarding the risk for Alzheimer’s disease. Those with MCI also faced a somewhat higher risk of death. 

The research team investigated possible determinants of MCI, considering factors such as age, APOE-ɛ status, waist circumference, hypertension, diabetes mellitus, total and HDL-cholesterol levels, smoking, and stroke. Only older age, being an APOE-ɛ4 carrier, low total cholesterol levels, and stroke at baseline were associated with developing MCI. Having the APOE-ɛ4 genotype and smoking were related only to amnestic MCI.

When the investigators analysed MRI studies of the brain, they found that participants with MCI, particularly those with non-amnestic MCI, had larger white matter lesion volumes and worse microstructural integrity of normal-appearing white matter compared to controls. They were also three-times more likely than controls to have lacunes (3 to 15 mm cerebrospinal fluid (CSF)-filled cavities in the basal ganglia or white matter, frequently observed when imaging older people). MCI was not associated with total brain volume, hippocampal volume, or cerebral microbleeds.

“Our results suggest that accumulating vascular damage plays a role in both amnestic and non-amnestic MCI,” says Dr. Ikram. “We propose that timely targeting of modifiable vascular risk factors might contribute to the prevention of MCI and dementia.”

Reference:

Determinants, MRI Correlates, and Prognosis of Mild Cognitive Impairment: The Rotterdam Study. Renée F.A.G. de Bruijn, Saloua Akoudad, Lotte G.M. Cremers, Albert Hofman, Wiro J. Niessen, Aad van der Lugt, Peter J. Koudstaal, Meike W. Vernooij, M. Arfan Ikram. Journal of Alzheimer’s Disease, Volume 42/Supplement 3 (August 2014): 2013 International Congress on Vascular Dementia (Guest Editor: Amos D. Korczyn)

(Source: iospress.nl)

Filed under cognitive impairment dementia alzheimer's disease memory brain structure neuroscience science

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Link between vitamin D and dementia risk confirmed

Vitamin D deficiency is associated with a substantially increased risk of dementia and Alzheimer’s disease in older people, according to the most robust study of its kind ever conducted.

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An international team, led by Dr David Llewellyn at the University of Exeter Medical School, found that study participants who were severely Vitamin D deficient were more than twice as likely to develop dementia and Alzheimer’s disease.

The team studied elderly Americans who took part in the Cardiovascular Health Study. They discovered that adults in the study who were moderately deficient in vitamin D had a 53 per cent increased risk of developing dementia of any kind, and the risk increased to 125 per cent in those who were severely deficient.

Similar results were recorded for Alzheimer’s disease, with the moderately deficient group 69 per cent more likely to develop this type of dementia, jumping to a 122 per cent increased risk for those severely deficient.

The study was part-funded by the Alzheimer’s Association, and is published in August 6 2014 online issue of Neurology, the medical journal of the American Academy of Neurology. It looked at 1,658 adults aged 65 and over, who were able to walk unaided and were free from dementia, cardiovascular disease and stroke at the start of the study. The participants were then followed for six years to investigate who went on to develop Alzheimer’s disease and other forms of dementia.

Dr Llewellyn said: “We expected to find an association between low Vitamin D levels and the risk of dementia and Alzheimer’s disease, but the results were surprising – we actually found that the association was twice as strong as we anticipated.

“Clinical trials are now needed to establish whether eating foods such as oily fish or taking vitamin D supplements can delay or even prevent the onset of Alzheimer’s disease and dementia. We need to be cautious at this early stage and our latest results do not demonstrate that low vitamin D levels cause dementia. That said, our findings are very encouraging, and even if a small number of people could benefit, this would have enormous public health implications given the devastating and costly nature of dementia.”

Research collaborators included experts from Angers University Hospital, Florida International University, Columbia University, the University of Washington, the University of Pittsburgh and the University of Michigan. The study was supported by the Alzheimer’s Association, the Mary Kinross Charitable Trust, the James Tudor Foundation, the Halpin Trust, the Age Related Diseases and Health Trust, the Norman Family Charitable Trust, and the National Institute for Health Research Collaboration for Leadership in Applied Research and Care South West Peninsula (NIHR PenCLAHRC).

Dementia is one of the greatest challenges of our time, with 44 million cases worldwide – a number expected to triple by 2050 as a result of rapid population ageing. A billion people worldwide are thought to have low vitamin D levels and many older adults may experience poorer health as a result.

The research is the first large study to investigate the relationship between vitamin D and dementia risk where the diagnosis was made by an expert multidisciplinary team, using a wide range of information including neuroimaging. Previous research established that people with low vitamin D levels are more likely to go on to experience cognitive problems, but this study confirms that this translates into a substantial increase in the risk of Alzheimer’s disease and dementia.

Vitamin D comes from three main sources – exposure of skin to sunlight, foods such as oily fish, and supplements. Older people’s skin can be less efficient at converting sunlight into Vitamin D, making them more likely to be deficient and reliant on other sources. In many countries the amount of UVB radiation in winter is too low to allow vitamin D production.

The study also found evidence that there is a threshold level of Vitamin D circulating in the bloodstream below which the risk of developing dementia and Alzheimer’s disease increases.  The team had previously hypothesized that this might lie in the region of 25-50 nmol/L, and their new findings confirm that vitamin D levels above 50 nmol/L are most strongly associated with good brain health.

Commenting on the study, Dr Doug Brown, Director of Research and Development at Alzheimer’s Society said: “Shedding light on risk factors for dementia is one of the most important tasks facing today’s health researchers. While earlier studies have suggested that a lack of the sunshine vitamin is linked to an increased risk of Alzheimer’s disease, this study found that people with very low vitamin D levels were more than twice as likely to develop any kind of dementia.

“During this hottest of summers, hitting the beach for just 15 minutes of sunshine is enough to boost your vitamin D levels. However, we’re not quite ready to say that sunlight or vitamin D supplements will reduce your risk of dementia. Large scale clinical trials are needed to determine whether increasing vitamin D levels in those with deficiencies can help prevent the dementia from developing.”

(Source: exeter.ac.uk)

Filed under alzheimer's disease dementia vitamin deficiency vitamin d neuroscience science

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Patients with autism spectrum disorder are not sensitive to ‘being imitated’

A Japanese research group led by Prof Norihiro Sadato, a professor of the National Institute for Physiological Sciences (NIPS), National Institutes of Natural Sciences (NINS), has found that people with autism spectrum disorders (ASD) have decreased activity in an area in the brain critical for understanding if his/her movement was imitated by others. These results will be published in Neuroscience Research.

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The research group of Norihiro Sadato, a professor of NIPS, Hirotaka Kosaka, a specially-assigned associate professor of the University of Fukui, and Toshio Munesue, a professor of Kanazawa University measured brain activity by functional magnetic resonance imaging (fMRI) when one’s movement was imitated by others. The group studied brain activity when a subject saw his/her finger movement imitated or not imitated by others. Normal subjects have increased activity in the extrastriate body area (EBA) when they are imitated compared to when they are not being imitated. The EBA is a region in the visual cortex for visual processing that responds powerfully during the perception of human body parts. On the other hand, because this kind of activity in the EBA of subjects with ASD was not observed, it shows that the EBA of subjects with ASD is not working properly when imitated.

Persons with ASD are known to have difficulty in interpersonal communication and have trouble noticing that their movement was imitated. Behavioral intervention research to alleviate ASD is proceeding and indicates that training utilizing imitation is useful. The result of the above research not only provided clues to ASD, but also can be used in the evaluation of behavioral intervention to alleviate the disorder.

(Source: eurekalert.org)

Filed under autism extrastriate body area brain activity neuroimaging visual processing neuroscience science

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Blood-oxytocin levels in normal range in children with autism

Autism does not appear to be solely caused by a deficiency of oxytocin, but the hormone’s universal ability to boost social function may prove useful in treating a subset of children with the developmental disorder, according to new findings from the Stanford University School of Medicine and Lucile Packard Children’s Hospital Stanford.

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Low levels of oxytocin, a hormone involved in social functioning, have for years been suspected of causing autism. Prior research seeking a link has produced mixed results. Now, in the largest-ever study to test the purported connection, the range of blood oxytocin levels has been shown to be the same in children with autism as that observed in two comparison groups: children with autistic siblings and children without autistic siblings. In other words, similar numbers of children with low, medium and high oxytocin levels were found in all three groups.

A paper describing the new findings was published online Aug. 4 in Proceedings of the National Academy of Sciences.

Although autism was not directly linked to oxytocin deficiency, the Stanford team found that higher oxytocin levels were linked to better social functioning in all groups. All children with autism have social deficits, but in the study these deficits were worst in those with the lowest blood oxytocin and mildest in those with the highest oxytocin. In the comparison groups, children’s social skills also fell across a range that correlated to their oxytocin levels.

Regulator of social functioning

“Oxytocin appears to be a universal regulator of social functioning in humans,” said Karen Parker, PhD, assistant professor of psychiatry and behavioral sciences and the lead author of the study. “That encompasses both typically developing children as well as those with the severe social deficits we see in children with autism.”

Autism is a developmental disorder that affects 1 of every 68 children in the United States. It is characterized by social and communication deficits, repetitive behaviors and sensory problems. The new study included 79 children with autism, 52 of their unaffected siblings and 62 unrelated children without autism. All of the children were between the ages of 3 and 12.

“It didn’t matter if you were a typically developing child, a sibling or an individual with autism: Your social ability was related to a certain extent to your oxytocin levels, which is very different from what people have speculated,” said Antonio Hardan, MD, professor of psychiatry and behavioral sciences and the study’s senior author. Hardan is a child and adolescent psychiatrist who treats children with autism at the hospital.

“The previous hypotheses saying that low oxytocin was linked to autism were maybe a little bit simplistic,” he said. “It’s much more complex: Oxytocin is a vulnerability factor that has to be accounted for, but it’s not the only thing leading to the development of autism.”

The researchers caution, however, that blood oxytocin measurements may be different than oxytocin levels in the cerebrospinal fluid bathing the brain, which they did not measure.

In addition to examining blood oxytocin levels, the researchers examined the importance of small variations in the gene coding for the oxytocin receptor. Certain receptor variants were correlated to higher scores on standard tests of social ability, the study found.

Inheriting social abilities

The team also discovered that blood levels of oxytocin are highly heritable: The levels are influenced by inheritance to about the same degree as adult height, which is often described as being strongly influenced by genetics.

"What our study hints at is that social function may be heritable in families," Parker said.

The study will help to guide future research to determine whether oxytocin is a useful autism treatment. The study’s findings suggest that some children with autism — such as the subset of kids with autism who have naturally low oxytocin levels, or those with oxytocin receptor gene variants associated with worse social functioning — might benefit most from oxytocin-like drugs.

 “Autism is so heterogeneous,” Parker said. “If we can identify biomarkers that help us identify the patients most likely to benefit from a specific therapy, we expect that will be very useful.”

(Source: med.stanford.edu)

Filed under autism oxytocin social interaction social function genetics neuroscience science

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Common chemical in mothers may negatively affect the IQ of their unborn children

In some women abnormally high levels of a common and pervasive chemical may lead to adverse effects in their offspring. The study, published recently in the Journal of Clinical Endocrinology & Metabolism, is the first of its kind to shed light on the possible harmful side effects of perchlorate in mothers and their children.

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Using data from the Controlled Antenatal Thyroid Study (CATS) cohort, researchers at Boston University School of Medicine (BUSM) and Cardiff University studied the effect of perchlorate, an environmental contaminant found in many foods and in some drinking water supplies, and its effects on children born to mothers with above average levels of this substance in their system. They studied 487 mother-child pairs from women with underactive thyroid glands and in the 50 women with the highest levels of perchlorate in their body, their offspring had below average IQ levels when compared to other children.

"The reason people really care about perchlorate is because it is ubiquitous. It’s everywhere," said Elizabeth Pearce, MD, MSc, associate professor of medicine at BUSM. "Prior studies have already shown perchlorate, at low levels, can be found in each and every one of us."

Perchlorate is a compound known to affect the thyroid gland, an organ needed to help regulate hormone levels in humans. According to Pearce previous studies have attempted to implicate this anti-thyroid activity in pregnant mothers as a possible cause of hypothyroidism, or an underactive thyroid gland. Hypothyroidism in newborns and children can lead to an array of unwelcome side effects, including below average intelligence.

(Source: eurekalert.org)

Filed under perchlorate intelligence pregnancy thyroid gland cognitive development neuroscience science

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New brain mechanism study could advance artificial intelligence

Research at the University of Reading has provided a new understanding of how our brain processes information to change how we see the world.

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Using a simple computer game, akin to a 3D version of the 80s game Pong, the researchers examined how the brain recalibrates its perception of slant in order to bounce a moving ball through a target hoop.

They found that the brain uses an internal simulation of the laws of physics to change its perception of slant in order to ‘score’ consistently.

The findings provide a unique insight into why humans are such an adaptable and skillful species. With the development of effective autonomous robots, engineers are starting to look at how humans’ sensory systems effortlessly achieve what is currently impossible for robotic systems.

The study, funded by the Engineering and Physical Sciences Research Council and the Wellcome Trust, saw participants play a 3D game where they had to adjust the slant of a surface so that a moving ball bounced off it and through a target hoop.

Part way through the game, without telling the participants, researchers altered the bounce of the ball so that the surface behaved differently to the slant signalled by visual cues. 

When faced with the altered bounce, participants changed their behaviour to continue scoring points. At the same time, their brain recalibrated their perception of slant - simulating the laws of physics to actually change how the slant looked. In a separate group, making the ball spin eliminated this recalibration.

Dr. Peter Scarfe from the School of Psychology and Clinical Language Sciences, who conducted the study with colleague Prof. Andrew Glennerster, said: “We take for granted our amazing ‘adaptability’ which allows us to enjoy such past-times as DIY or playing ball sports. However, little is known about the brain mechanisms that enable us to do these activities. Our research shows how our brains appear to have an intimate understanding of the laws of physics. In addition to aiding skillful action, this can change how we perceive the world around us.”

The researchers say understanding the basic mechanisms that allow the brain to calibrate sensory information will prove vital in the design of future autonomous robots.

Dr. Scarfe continued: “The human brain exhibits expert skill in making predictions about how the world behaves. For example, a child can bounce a ball off a wall and understand how spinning the ball alters its bounce. However, many of the fine motor skills of a young child are currently way beyond the capability of modern robots. Understanding how sensory systems adapt to feedback about the consequences of actions is likely to be key in solving this problem.”

Humans Use Predictive Kinematic Models to Calibrate Visual Cues to Three-Dimensional Surface Slant is published in the Journal of Neuroscience

(Source: reading.ac.uk)

Filed under AI somatosensory system kinematics perception psychology neuroscience science

122 notes

In search for Alzheimer’s drug, a major STEP forward

Researchers at Yale School of Medicine have discovered a new drug compound that reverses the brain deficits of Alzheimer’s disease in an animal model. Their findings are published in the Aug. 5 issue of the journal PLoS Biology.

The compound, TC-2153, inhibits the negative effects of a protein called STtriatal-Enriched tyrosine Phosphatase (STEP), which is key to regulating learning and memory. These cognitive functions are impaired in Alzheimer’s.

"Decreasing STEP levels reversed the effects of Alzheimer’s disease in mice," said lead author Paul Lombroso, M.D., professor in the Yale Child Study Center and in the Departments of Neurobiology and Psychiatry at Yale School of Medicine.

Lombroso and co-authors studied thousands of small molecules, searching for those that would inhibit STEP activity. Once identified, those STEP-inhibiting compounds were tested in brain cells to examine how effectively they could halt the effects of STEP. They examined the most promising compound in a mouse model of Alzheimer’s disease, and found a reversal of deficits in several cognitive exercises that gauged the animals’ ability to remember previously seen objects.

High levels of STEP proteins keep synapses in the brain from strengthening. Synaptic strengthening is a process that is required for people to turn short-term memories into long-term memories. When STEP is elevated in the brain, it depletes receptors from synaptic sites, and inactivates other proteins that are necessary for proper cognitive function. This disruption can result in Alzheimer’s disease or a number of neuropsychiatric and neurodegenerative disorders, all marked by cognitive deficits.

"The small molecule inhibitor is the result of a five-year collaborative effort to search for STEP inhibitors," said Lombroso. "A single dose of the drug results in improved cognitive function in mice. Animals treated with TC compound were indistinguishable from a control group in several cognitive tasks."

The team is currently testing the TC compound in other animals with cognitive defects, including rats and non-human primates. “These studies will determine whether the compound can improve cognitive deficits in other animal models,” said Lombroso. “Successful results will bring us a step closer to testing a drug that improves cognition in humans.”

(Source: eurekalert.org)

Filed under alzheimer's disease STEP TC-2153 cognitive function animal model neuroscience science

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