Don’t Underestimate Your Mind’s Eye
Take a look around, and what do you see? Much more than you think you do, thanks to your finely tuned mind’s eye, which processes images without your even knowing.
A University of Arizona study has found that objects in our visual field of which we are not consciously aware still may influence our decisions. The findings refute traditional ideas about visual perception and cognition, and they could shed light on why we sometimes make decisions — stepping into a street, choosing not to merge into a traffic lane — without really knowing why.
Laura Cacciamani, who recently earned her doctorate in psychology with a minor in neuroscience, has found supporting evidence. Cacciamani’s is the lead author on a co-authored study, published online in the journal Attention, Perception and Psychophysics, shows that the brain’s subconscious processing has an impact on behavior and decision-making.
This seems to make evolutionary sense, Cacciamani said. Early humans would have required keen awareness of their surroundings on a subliminal level in order to survive.
"Your brain is always monitoring for meaning in the world, to be aware of your general surroundings and potential predators," Cacciamani said. "You can be focused on a task, but your brain is assessing the meaning of everything around you – even objects that you’re not consciously perceiving."
The study builds on the findings of earlier research by Jay Sanguinetti, who also was a doctoral candidate in the UA Department of Psychology. Both studies go against conventional wisdom among vision scientists.
"According to the traditional view, the brain accesses the meaning – or the memory – of an object after you perceive it," Cacciamani said. "Against this view, we have now shown that the meaning of an object can be accessed before conscious perception.
"We’re showing that there’s more interplay between memory and perception than previously has been assumed," she said.
Cacciamani asked participants in her study to classify nouns that appeared on a computer screen as naming a natural object or artificial object by pressing one of two buttons labeled “natural” or “artificial.” For example, the word “leaf” indicates an object found in nature, while “anchor” indicates a man-made or artificial object.
But before each word appeared on the screen, the computer flashed a black silhouette that – unknown to participants – had portions of natural or artificial objects suggested along the white outside regions (called the “ground” regions) of the image. Participants were not told to look for anything in the silhouettes, and they were flashed so quickly – 50 milliseconds – that it would have been difficult to notice the objects in the ground regions even if someone knew what to look for. Participants never were aware that the silhouette’s grounds suggested recognizable objects.
Cacciamani measured how well study participants performed at categorizing the words as natural or artificial by recording speed and accuracy.
"We found that participants performed better on the natural/artificial word task when that word followed a silhouette whose ground contained an object of the same rather than a different category," Cacciamani said.
This indicates that the brain accessed the meaning of the objects in the silhouette’s grounds even though study participants didn’t know the objects were there, she said.
"Every day our visual systems are bombarded with more information than we can consciously be aware of," Cacciamani said. "We’re showing that your brain might still be accessing information without your conscious awareness, and that could influence your behavior."
Filed under visual perception decision making visual awareness object perception psychology neuroscience science
A type of lipid that naturally declines in the aging brain impacts – within laboratory models used to study Parkinson’s disease – a protein associated with the disease, according to a study co-authored by University of Alabama researchers.
The study, which published today in the Proceedings of the National Academy of Sciences, focuses on lipids, fat-like molecules that naturally occur in organisms, and their potential roles in a complex process that leads to the death of neurons that produce dopamine. When dopamine-producing neurons malfunction or die, this leads to the symptoms associated with Parkinson’s disease.
“This gets right to the heart of understanding, possibly, the mechanism by which one form of lipid is impacting the process of neuron degeneration,” said Dr. Guy Caldwell, UA professor of biological sciences and one of the study’s co-authors.
The study, led by researchers at the Louisiana State University Health Sciences Center, focused on phosphatidylethanolamine, a lipid known as PE. Today’s scholarly article details how low levels of PE lead to high-levels of alpha-synuclein, a protein previously linked to Parkinson’s. It also show the promise a second lipid, ethanolamine, or ETA, has in boosting PE levels.
To function correctly, proteins must fold properly within cells. One misfolding, as can occur when extra copies of the protein alpha-synuclein are present, can lead to others and, subsequently, to aggregation, or clumping, of proteins. Aggregation of proteins can lead to neuron malfunction or cell death.
Previous research had shown that excess alpha-synuclein can serve as an intra-cellular “roadblock,” preventing proteins, dopamine and other things cells need from being delivered to their necessary locations. This delivery disruption can lead to serious disorders.
“That situation is being applied here, but in a different way,” Caldwell said. “We’re gaining a better understanding of the importance these lipids, which are components of cellular membranes, have in maintaining proper trafficking.”
A proper link with alpha-synuclein helps “lipid rafts” in their transport of proteins.
“As the name implies, lipid rafts are like rafts of fat,” Caldwell said. “If alpha-synuclein can’t associate with those rafts, it could be a toxic situation for these cells.”
Using yeast and the tiny nematode C. elegans as laboratory models, the researchers showed they could reverse the delivery problem by adding ETA to the mix.
“This supplementation of ETA basically tells us that if we can restore the amount of PE that is being made, we can create a healthier situation in neurons, and this might help them to survive longer.”
UA’s lead author on the study is Siyuan “Alice” Zhang, a third-year UA doctoral student who works in the Caldwell lab. Dr. Kim Caldwell, UA professor of biological sciences, is also a co-author. LSU’s senior researcher on the project is Dr. Stephan Witt.
Additional study is needed in rodents and patient-derived stem cells before knowing how beneficial the discovery could eventually prove, Caldwell said.
Perhaps one day, Caldwell said, a supplement could be developed to prevent the decline of PE or possibly a drug could be developed to activate an enzyme that converts ETA to PE.
“I think it has promise as a new way of looking at alleviating toxicity,” Caldwell said. “It’s a different angle.”
(Source: uanews.ua.edu)
Filed under parkinson's disease lipids dopamine ethanolamine neuroscience science
Xenon gas protects the brain after head injury
Head injury is the leading cause of death and disability in people aged under 45 in developed countries, mostly resulting from falls and road accidents. The primary injury caused by the initial mechanical force is followed by a secondary injury which develops in the hours and days afterwards. This secondary injury is largely responsible for patients’ mental and physical disabilities, but there are currently no drug treatments that can be given after the accident to stop it from occurring.
Scientists at Imperial College London found that xenon, given within hours of the initial injury, limits brain damage and improves neurological outcomes in mice, both in the short term and long term. The findings, published in the journal Critical Care Medicine, could lead to clinical trials of xenon as a treatment for head injury in humans.
Although xenon is chemically inert, this does not mean it is biologically inactive. Xenon has been known to have general anaesthetic properties since the 1950s. Previous studies at Imperial have found that xenon can protect brain cells from mechanical injury in the lab, but this new study is the first time such an effect has been shown in live animals, a vital step before any new treatments can be tested in humans.
Mice were anaesthetised before having a controlled mechanical force applied to the brain. Some were then treated with xenon at different concentrations and at different times after injury.
Mice treated with xenon performed better in tests assessing their neurological deficits, such as movement and balance problems, in the days after injury and after one month. They also had less brain damage, even if treatment was delayed up to three hours after the injury.
Dr Robert Dickinson from the Department of Surgery and Cancer at Imperial College London, who led the study, said: “After a blow to the head, most of the damage to the brain doesn’t occur immediately but in the hours and days afterwards. At present we have no specific drugs to limit the spread of the secondary injury, but we think that is the key to successful treatment.
“This study shows that xenon can prevent brain damage and disability in mice, and crucially it’s effective when given up to at least three hours after the injury. It’s feasible that someone who hits their head in an accident could be treated in the hospital or in an ambulance in this timeframe.
“These findings provide crucial evidence to support doing clinical trials in humans.”
Filed under TBI xenon brain injury brain damage neuroscience science
Brain injuries no match for sPIF treatment
Researchers at Yale School of Medicine and their colleagues have uncovered a new pathway to help treat perinatal brain injuries. This research could also lead to treatments for traumatic brain injuries and neurodegenerative disorders such as Alzheimer’s and Parkinson’s.
The findings are published in the Sept. 8 issue of Proceedings of the National Academy of Sciences.
The MicroRNA molecule let-7 is known to cause the death of neurons in the central nervous system. The research team found that a synthetic molecule derived from the embryo called PreImplantation Factor (sPIF) protects against neuronal death and brain injury by targeting let-7.
“We would never have connected the dots between PIF and let-7 without prior knowledge and experience on let-7 and H19, a developmentally regulated gene that is highly expressed in the developing embryo,” said senior author Dr. Yingqun Huang, associate professor in the Department of Obstetrics, Gynecology & Reproductive Sciences at Yale School of Medicine.
Using a rat perinatal brain injury model, Huang and the team found that sPIF rescued damaged neurons and reduced inflammation. The team performed a series of in vivo and in vitro experiments and found that sPIF helped to stop the production of let-7. “We showed that sPIF works by destabilizing the key microRNA processing protein called KH-type splicing regulatory protein,” said Huang.
Lead author Martin Mueller, who helped develop the rat perinatal brain injury model, was surprised at the consistency of the results from both the in vivo and in vitro studies. “Collectively, our findings suggest that sPIF mitigates brain damage through a novel pathway,” said Mueller. “We saw more cortical brain volume and more neurons restored in brain damaged animals receiving sPIF.”
“For the first time, we have clear indication to pursue a new line of investigation in the treatment of perinatal brain injury, and possibly traumatic brain injury,” said co-author Dr. Michael Paidas, professor in the Department of Obstetrics, Gynecology & Reproductive Sciences at Yale School of Medicine.
Paidas, who is also vice chair of obstetrics at Yale, has helped to identify PIF’s effects with co-author Eytan R. Barnea, founder of the Society for the Investigation of Early Pregnancy (SIEP) and chief scientific officer of BioIncept, LLC. Barnea discovered and characterized PIF and described key elements of its mode of action.
Based on this promising data, the FDA has awarded sPIF fast-track designation and allowed a phase 1 sPIF clinical trial to treat patients with autoimmune liver disease at the University of Miami.
Filed under brain injury perinatal brain injury TBI neurodegenerative diseases neuroscience science
People can become addicted to eating for its own sake but not to consuming specific foods such as those high in sugar or fat, research suggests.
An international team of scientists has found no strong evidence for people being addicted to the chemical substances in certain foods.
The brain does not respond to nutrients in the same way as it does to addictive drugs such as heroin or cocaine, the researchers say.
Instead, people can develop a psychological compulsion to eat, driven by the positive feelings that the brain associates with eating.
"This is a behavioural disorder and could be categorised alongside conditions such as gambling addiction", say scientists at Edinburgh.
They add that the focus on tackling the problem of obesity should be moved from food itself towards the individual’s relationship with eating.
The study, which examined the scientific evidence for food addiction as a substance-based addiction, is published in Neuroscience & Biobehavioral Reviews.
The researchers also say that the current classification of mental disorders, which does not permit a formal diagnosis of eating addiction, could be redrawn.
However, more research would be needed to define a diagnosis, the scientists add.
They add that the focus on tackling the problem of obesity should be moved from food itself towards the individual’s relationship with eating.
(Source: ed.ac.uk)
Filed under eating behavior food addiction obesity reward system addictive disorders neuroscience science
Eating habits, body fat related to differences in brain chemistry
People who are obese may be more susceptible to environmental food cues than their lean counterparts due to differences in brain chemistry that make eating more habitual and less rewarding, according to a National Institutes of Health study published in Molecular Psychiatry.
Researchers at the NIH Clinical Center found that, when examining 43 men and women with varying amounts of body fat, obese participants tended to have greater dopamine activity in the habit-forming region of the brain than lean counterparts, and less activity in the region controlling reward. Those differences could potentially make the obese people more drawn to overeat in response to food triggers and simultaneously making food less rewarding to them. A chemical messenger in the brain, dopamine influences reward, motivation and habit formation.
"While we cannot say whether obesity is a cause or an effect of these patterns of dopamine activity, eating based on unconscious habits rather than conscious choices could make it harder to achieve and maintain a healthy weight, especially when appetizing food cues are practically everywhere," said Kevin D. Hall, Ph.D., lead author and a senior investigator at National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of NIH. "This means that triggers such as the smell of popcorn at a movie theater or a commercial for a favorite food may have a stronger pull for an obese person – and a stronger reaction from their brain chemistry – than for a lean person exposed to the same trigger."
Study participants followed the same eating, sleeping and activity schedule. Tendency to overeat in response to triggers in the environment was determined from a detailed questionnaire. Positron emission tomography (PET) scans evaluated the sites in the brain where dopamine was able to act.
According to the Centers for Disease Control and Prevention, more than one-third of U.S. adults are obese. Obesity-related conditions include heart disease, type 2 diabetes and certain types of cancer, some of the leading causes of preventable death.
"These findings point to the complexity of obesity and contribute to our understanding of how people with varying amounts of body fat process information about food," said NIDDK Director Griffin P. Rodgers, M.D. "Accounting for differences in brain activity and related behaviors has the potential to inform the design of effective weight-loss programs."
The study did not demonstrate cause and effect among habit formation, reward, dopamine activity, eating behavior and obesity. Future research will examine dopamine activity and eating behavior in people over time as they change their diets, physical activity, and their weight.
Filed under obesity eating behavior dopamine brain chemistry striatum neuroscience science
Feeling socially disconnected may lead us to lower our threshold for determining that another being is animate or alive, according to new research published in Psychological Science, a journal of the Association for Psychological Science.
“This increased sensitivity to animacy suggests that people are casting a wide net when looking for people they can possibly relate to — which may ultimately help them maximize opportunities to renew social connections,” explains psychological scientist and lead researcher Katherine Powers of Dartmouth College.
These findings enhance our understanding of the factors that contribute to face perception, mind perception, and social relationships, but they could also shed light on newer types of relationships that have emerged in the modern age, Powers argues, including our relationships with pets, online avatars, and even pieces of technology, such as computers, robots, and cell phones.
Feeling socially connected is a critical part of human life that impacts both mental and physical health; when we feel disconnected from others, we try to replenish our social connections.
“As social beings, we have an intrinsic motivation to pay attention to and connect with other people,” says Powers. “We wanted to examine the influence of this social motive on one of the most basic, low-level aspects of social perception: deciding whether or not a face is alive.”
Powers and colleagues had 30 college students view images of faces, which were actually morphs created by combining inanimate faces (such as a doll’s face) with human faces. The morphs ranged from 0% human to 100% human and showed both male and female faces.
The morphs were presented in random order and the students had to decide whether each face was animate or inanimate. Afterwards, they completed a survey that gauged their desire for social connections, in which they rated their agreement with statements such as “I want other people to accept me.”
The data revealed that desire for social connections was associated with a lower threshold for animacy. In other words, participants who had high scores on the social connections measure didn’t need to see as many human-like features in a face order to decide that it was alive.
To see if there might be a causal link, Powers and colleagues conducted another study in which they experimentally manipulated feelings of social connection.
A separate group of college students completed a personality questionnaire and were provided feedback ostensibly based on the questionnaire. In reality, the feedback was determined by random assignment. Some students were told that their future lives would be isolated and lonely, while others were told their lives would contain long-lasting, stable relationships. The feedback also included personality descriptions and statements tailored to each participant to ensure believability.
The students then viewed the face morphs.
As expected, students who had been told they would be isolated and lonely showed lower thresholds for animacy than those who were told they would have long-lasting relationships.
These findings are particularly interesting, the researchers argue, because previous research has shown that people are typically cautious in determining whether a face is alive:
“What’s really interesting here is the degree of variability in this perception,” says Powers. “Even though two people may be looking at the same face, the point at which they see life and decide that person is worthy of meaningful social interaction may not be the same — our findings show that it depends on an individual’s social relationship status and motivations for future social interactions.”
“I think the fact that we can observe such a bias in the perception of basic social cues really underscores the fundamental nature of the human need for social connection,” Powers adds.
Filed under face perception social perception social interaction psychology neuroscience science
Brain damage caused by severe sleep apnea is reversible
A neuroimaging study is the first to show that white matter damage caused by severe obstructive sleep apnea can be reversed by continuous positive airway pressure therapy. The results underscore the importance of the “Stop the Snore” campaign of the National Healthy Sleep Awareness Project, a collaboration between the Centers for Disease Control and Prevention, American Academy of Sleep Medicine, Sleep Research Society and other partners.
Results show that participants with severe, untreated sleep apnea had a significant reduction in white matter fiber integrity in multiple brain areas. This brain damage was accompanied by impairments to cognition, mood and daytime alertness. Although three months of CPAP therapy produced only limited improvements to damaged brain structures, 12 months of CPAP therapy led to an almost complete reversal of white matter abnormalities. Treatment also produced significant improvements in nearly all cognitive tests, mood, alertness and quality of life.
“Structural neural injury of the brain of obstructive sleep apnea patients is reversible with effective treatment,” said principal investigator and lead author Vincenza Castronovo, PhD, clinical psychologist at the Sleep Disorders Center at San Raffaele Hospital and Vita-Salute San Raffaele University in Milano, Italy. “Treatment with CPAP, if patients are adherent to therapy, is effective for normalizing the brain structure.”
The study results are published in the September issue of the journal Sleep.
“Obstructive sleep apnea is a destructive disease that can ruin your health and increase your risk of death,” said American Academy of Sleep Medicine President Dr. Timothy Morgenthaler, a national spokesperson for the Healthy Sleep Project. “Treatment of sleep apnea can be life-changing and potentially life-saving.”
The “Stop the Snore” campaign was launched recently to encourage people to talk to a doctor about the warning signs for sleep apnea, which afflicts at least 25 million adults in the U.S. Sleep apnea warning signs include snoring and choking, gasping or silent breathing pauses during sleep. Pledge to stop the snore at www.stopsnoringpledge.org.
The study involved 17 men with severe, untreated obstructive sleep apnea who had an average age of 43 years. They were evaluated at baseline and after both three months and 12 months of treatment with CPAP therapy. At each time point they underwent a neuropsychological evaluation and a diffusion tensor imaging examination. DTI is a form of magnetic resonance imaging that measures the flow of water through brain tissue. Participants were compared with 15 age-matched, healthy controls who were evaluated only at baseline.
A previous study by Castronovo’s research team found similar damage to gray matter volume in multiple brain regions of people with severe sleep apnea. Improvements in gray matter volume appeared after three months of CPAP therapy. According to the authors, the two studies suggest that the white matter of the brain takes longer to respond to treatment than the gray matter.
“We are seeing a consistent message that the brain can improve with treatment,” said co-principal investigator Mark Aloia, PhD, Associate Professor of Medicine at National Jewish Health in Denver, Colorado, and Senior Director of Global Clinical Research for Philips Respironics, Inc. “We know that PAP therapy keeps people breathing at night; but demonstrating effects on secondary outcomes is critical, and brain function and structure are strong secondary outcomes.”
Filed under sleep apnea white matter cognitive impairment brain function diffusion tensor imaging neuroscience science
Broken signals lead to neurodegeneration
Researchers from the RIKEN Brain Science Institute in Japan, in collaboration with Juntendo University and the Japan Science and Technology Agency, have discovered that a cell receptor widely involved in intracellular calcium signaling—the IP3R receptor—can be locked into a closed state by enzyme action, and that this locking may potentially play a role in the reduction of neuron signaling seen in neurodegenerative diseases such as Huntington’s and Alzheimer’s disease.
In the research published today in the Proceedings of the National Academy of Sciences, the scientists reported experiments in human cells and a mouse model of Huntington’s disease revealing that transglutaminase type 2—a protein cross-linking enzyme elevated in the cells of patients with neurodegenerative diseases—interacts with the IP3R receptor to lock it in a closed non-functional conformation preventing it from fulfilling its essential calcium-releasing role. They identified a specific amino acid site on the receptor, Gln2746, where the modification takes place, deepening our understanding of how receptors are locked and potentially opening the door to studies on other functional proteins that are also regulated by conformational changes.
The IP3R channel, which is located in the endoplasmic reticulum, a protein assembly and transport compartment, plays a crucial role in intracellular calcium signaling, and is involved in a wide range of cell functions including mitochondrial energy production and the regulation of autophagy, the process through which cells consume and degrade unused components to maintain a healthy balance of functional proteins. Although autophagy is normally a mechanism that sustains cell maintenance, it can also trigger a loss of cell function and has been associated with prominent diseases including Huntington’s disease, Alzheimer’s disease, and Parkinson’s disease.
In this work, the scientists propose a general model under which abnormal IP3R-mediated calcium signaling caused by the action of transglutaminase type 2 leads to cellular dysfunction and subsequently to the emergence of progressive brain dysfunction. Transglutaminase 2 activation is commonly associated with inflammation and stress, and its action on the IP3R channel might provide an explanation for the initiation and progression steps common to different neurodegenerative diseases.
According to Katsuhiko Mikoshiba, who led the study, “We think that the mechanism we identified in this study could provide us with a more general model of other diseases both of the brain and other parts of the body, where transglutaminase type 2 is upregulated. We hope that this insight could eventually lead to the development of new drug therapies for a number of neurodegenerative diseases that place a high burden on patients and society.”
Filed under neurodegenerative diseases neurodegeneration transglutaminase type 2 transamidation neuroscience science
An international team of researchers has identified a new inherited neuromuscular disorder. The rare condition is the result of a genetic mutation that interferes with the communication between nerves and muscles, resulting in impaired muscle control.
The new disease was diagnosed in two families – one in the U.S. and the other in Great Britain – and afflicts multiple generations. The discovery was published in the American Journal of Human Genetics.
“This discovery gives us new insight into the mechanisms of diseases that are caused by a breakdown in neuromuscular signal transmission,” said David Herrmann, M.B.B.Ch., a professor in the Department of Neurology at the University of Rochester School of Medicine and Dentistry and co-lead author of the study. “It is our hope that these findings will help identify new targets for therapies that can eventually be used to treat these diseases.”
The focus of the research is the neuromuscular junction, the point at which the axon fibers that extend from peripheral nerves meet the muscle cells. The chemical signals that pass across the junction are essential for motor function.
There are a number of disorders – both acquired and inherited – that interfere with the communication that occurs at the neuromuscular junction. For example, in Lambert-Eaton myasthenic syndrome, which is most commonly triggered by certain cancers, the body’s own immune system attacks the neuromuscular junction, interrupting signal transmission. These diseases, which are rare, result in muscle weakness and fatigue, primarily in the limbs.
While the families in the study had at one point been diagnosed with other neuromuscular conditions, the researchers identified them as unique, due to their particular motor abnormalities, including problems resembling Lambert-Eaton, and because the disease was passed from one generation to the next.
The researchers compiled a genetic profile of the family members. Specifically, they analyzed the section of DNA code responsible for creating proteins using a technique called whole exome sequencing.
They discovered that the two different families had mutations in the code that creates the protein synaptotagmin 2 (SYT2). Scientists have long understood the function of this protein, but it had never before been associated with a disease in humans.
SYT2 is present at the pre-synaptic terminal, the end of the nerve cell that sits at the neuromuscular junction and helps the cells sense fluctuations in calcium levels. Calcium plays an important role in the electrical function of cells and, in the case of the neuromuscular junction, helps dictate the release of acetylcholine, a chemical responsible for passing communication between the nerve and muscle cells.
In the two families, the mutation disrupted the ability of the nerve cells to sense the changes in calcium levels that would normally trigger the release of acetylcholine. As a result, communication was disrupted and muscle control was impaired.
The authors have used the mutation in SYT2 to create a fruit fly (drosophila) model of the disease. Fruit flies are an important research tool and the study of their neurobiology has contributed greatly to our understanding of neurological development and diseases and the researchers see this as a first step to the development of potential new therapies to treat the condition.
(Source: urmc.rochester.edu)
Filed under neuromuscular junction muscle cells neuromuscular diseases synaptotagmin 2 gene mutation neuroscience science
