Posts tagged neuroscience
Articles and news from the latest research reports.
Can your body sense future events without any external clue?
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."
(Source: eurekalert.org)
Early Intervention Improves Social Skills and Brain Activity in Preschoolers with Autism
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.
Mayo Clinic Researchers Develop New Tools to Better Treat ADHD Patients in Early Stages
Mayo Clinic researchers are presenting new findings on the early treatment of child and adolescent attention deficit hyperactivity disorder this week at the American Academy of Childhood and Adolescent Psychiatry annual meeting in San Francisco. They include a method to get better input from parents and teachers of children who are being diagnosed with ADHD for the first time — allowing for more effective treatment upon the first consultation. Researchers also showed how a tool can help clinicians better diagnose and treat children who have both ADHD and oppositional defiance disorder.
(Image credit: Psyc3330 w11, Wikimedia Commons)
University of Toronto study demonstrates impact of adversity on early life development
It is time to put the nature versus nurture debate to rest and embrace growing evidence that it is the interaction between biology and environment in early life that influences human development, according to a series of studies recently published in a special edition of the Proceedings of the National Academy of Sciences (PNAS).
"Biologists used to think that our differences are pre-programmed in our genes, while psychologists argued that babies are born with a blank slate and their experience writes on it to shape them into the adults they become. Instead, the important question to be asking is, ‘How is our experience in early life getting embedded in our biology?’" says University of Toronto behavioural geneticist Marla Sokolowski. She is co-editor of the PNAS special edition titled "Biological Embedding of Early Social Adversity: From Fruit Flies to Kindergarteners" along with professors Tom Boyce (University of British Columbia) and Gene Robinson (University of Illinois).
Sokolowski, who is a University Professor in the Department of Ecology & Evolutionary Biology (EEB), the inaugural academic director of Uof T’s Fraser Mustard Institute for Human Development and co-director of the Experience-based Brain and Biological Development Program (EBBD) at the Canadian Institute for Advanced Research (CIFAR) says that relatively little is known about the gene-environment interplay that underlies the impact of early life adversity on adult health and behaviour.
In one of the studies in the series, Sokolowski and her colleagues found that chronic food deprivation and lack of adequate nutrition in the early life of the fruit fly Drosophila melanogaster had significant impact on adult behaviour and quality of life. Fruit flies are especially useful for genetic studies because they share a surprising number of qualities with humans, are inexpensive to care for and reproduce rapidly, allowing for several generations to be studied in just a few months.
Stimulating brain cells with light
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.
(Source: lunduniversity.lu.se)
Drug shows promise in animal model of Alzheimer’s and Parkinson’s with dementia
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.
(Source: eurekalert.org)
Diabetes Raises Levels of Proteins Linked to Alzheimer’s Features
Growing evidence suggests that there may be a link between diabetes and Alzheimer’s disease, but the physiological mechanisms by which diabetes impacts brain function and cognition are not fully understood. In a new study published in Aging Cell, researchers at the Salk Institute for Biological Studies show, for the first time, that diabetes enhances the development of aging features that may underlie early pathological events in Alzheimer’s.
Specifically, the Salk team found increases in two hallmarks of Alzheimer’s-accumulations of amyloid beta (Abeta) and tau protein-in the brains of diabetic mice, especially in cells surrounding blood vessels. Abeta, the misfolded peptide that is thought in part to cause Alzheimer’s disease, aggregated inside astrocytes, star-shaped brain cells that, upon interaction with Abeta, release inflammatory molecules that can destroy neurons. Previously, this had not been shown in mouse models of type 1 diabetes (T1D).
"Our study supports and extends the links between diabetes, aging and Alzheimer’s," says senior author Pamela Maher, a senior staff scientist in Salk’s Laboratory of Cellular Neurobiology. "We show that type 1 diabetes increases vascular-associated amyloid beta buildup in the brain and causes accelerated brain aging."
The findings suggest that the neurovascular system may be a good candidate for new therapeutic targets to treat Alzheimer’s in the early stages of the disease.
Magnetic brain stimulation treats depression independent of sleep effect
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.”
(Source: news.georgiahealth.edu)
New clues to how the brain and body communicate to regulate weight
Maintaining a healthy body weight may be difficult for many people, but it’s reassuring to know that our brains and bodies are wired to work together to do just that—in essence, to achieve a phenomenon known as energy balance, a tight matching between the number of calories consumed versus those expended. This careful balance results from a complex interchange of neurobiological crosstalk within regions of the brain’s hypothalamus, and when this “conversation” goes awry, obesity or anorexia can result.
Given the seriousness of these conditions, it’s unfortunate that little is known about the details of this complex interchange. Now research led by investigators at Beth Israel Deaconess Medical Center (BIDMC) provides new insights that help bring order to this complexity. Described in the October 26 issue of the journal Cell, the findings demonstrate how the GABA neurotransmitter selectively drives energy expenditure, and importantly, also help explain the neurocircuitry underlying the fat-burning properties of brown fat.
"Our group has built up a research program with the overall goal of unraveling the ‘wiring diagram’ by which the brain controls appetite and the burning of calories," says senior author Bradford Lowell, MD, PhD, a Professor of Medicine in BIDMC’s Division of Endocrinology and Harvard Medical School. "To advance our understanding to this level, we need to know the function of specific subsets of neurons, and in addition, the upstream neurons providing input to, and the downstream neurons receiving output from, these functionally defined neurons. Until recently, such knowledge in the hypothalamus has been largely unobtainable."
Omega-3 Intake Heightens Working Memory in Healthy Young Adults
While Omega-3 essential fatty acids—found in foods like wild fish and grass-fed livestock—are necessary for human body functioning, their effects on the working memory of healthy young adults have not been studied until now.
In the first study of its kind, researchers at the University of Pittsburgh have determined that healthy young adults ages 18-25 can improve their working memory even further by increasing their Omega-3 fatty acid intake. Their findings have been published online in PLOS One.
“Before seeing this data, I would have said it was impossible to move young healthy individuals above their cognitive best,” said Bita Moghaddam, project investigator and professor of neuroscience. “We found that members of this population can enhance their working memory performance even further, despite their already being at the top of their cognitive game.”
(Image credit: Matt Allworth/Courtesy Flickr)