Posts tagged psychology
Articles and news from the latest research reports.
Improving Memory for Specific Events Can Alleviate Symptoms of Depression
Hear the word “party” and memories of your 8th birthday sleepover or the big bash you attended last New Year’s may come rushing to mind. But it’s exactly these kinds of memories, embedded in a specific place and time, that people with depression have difficulty recalling.
Research has shown that people who suffer from, or are at risk of, depression have difficulty tapping into specific memories from their own past, an impairment that affects their ability to solve problems and leads them to focus on feelings of distress.
In a study forthcoming in Clinical Psychological Science, a new journal of the Association for Psychological Science, psychological scientists Hamid Neshat-Doost of the University of Isfahan, Iran, Laura Jobson of the University of East Anglia, Tim Dalgleish of the Cognition and Brain Sciences Unit, Medical Research Council, Cambridge and colleagues investigated whether a particular training program, Memory Specificity Training, might improve people’s memory for past events and ameliorate their symptoms of depression.
In Iran, the researchers recruited 23 adolescent Afghani refugees who had lost their fathers in the war in Afghanistan and who showed symptoms of depression. Twelve of the adolescents were randomly assigned to participate in the memory training program and 11 were randomly assigned to a control group that received no training.
All of the adolescents completed a memory test in which they saw 18 positive, neutral, and negative words in Persian and were asked to recall a specific memory related to each word. Their responses were categorized as either a specific or a non-specific type of memory. They also completed questionnaires design to measure symptoms of depression and anxiety symptoms.
For five weeks, the adolescents assigned to the training attended a weekly 80-minute group session, in which they learned about different types of memory and memory recall, and practiced recalling specific memories after being given positive, neutral, and negative keywords.
At the end of the five weeks, both the training group and the control group were given the same memory test that they were given at the beginning of the study. And they took the memory test again as part of a follow-up visit two months later.
The adolescents who participated in the training were able to provide more specific memories after the training than those who did not receive intervention. They also showed fewer symptoms of depression than the control group at the two month follow-up. The researchers found that the relationship between participant group (training or control) and their symptoms of depression at follow-up could be accounted for by changes in specific memory recall over time.
These findings are promising because they suggest that a standalone training program that focuses on specific memory recall can actually improve depression symptoms.
Based on the results of this study, Jobson, Dalgleish, and colleagues conclude that, for individuals suffering from depression, “including a brief training component that targets memory recall as an adjunct to cognitive behavioral therapy or prior therapy may have beneficial effects on memory recall and mood.”
Altruism connected to size of grey matter
What makes a person altruistic? Philosophers throughout the ages often pondered the question but failed to get concrete answers. New research from the University of Zurich in Switzerland shows that the answer may lie in our brains, or more accurately, that the volume of a small brain region can influences one’s predisposition for altruistic behaviour. The results, presented in the journal Neuron, indicate that individuals who behave more altruistically than others have more grey matter at the junction between the parietal and temporal lobe. This shows for the very first time that there is a connection between brain anatomy, brain activity and altruistic behaviour.
Contary to past studies that showed that social categories like gender, income or education cannot fully explain differences in altruistic behaviour, recent research in the area of neuroscience have demonstrated that differences in brain structure might be linked to differences in personality traits and abilities. Now, for the first time, a team of researchers from the University of Zurich, headed by Ernst Fehr, the director of the Department of Economics, demonstrates that there is a connection between brain anatomy and altruistic behaviour.
For their study, the researchers asked volunteers to divide money between themselves and someone else who was anonymous. The participants always had the option of sacrificing a certain portion of the money for the benefit of the other person. The monetary sacrifice was considered to be altruistic because it helped someone else at one’s own expense. The researchers found major differences in this respect: some participants were almost never willing to sacrifice money to benefit others while others behaved very altruistically.
Previous studies showed that the place where the parietal and temporal lobes meet is linked to the ability to put oneself in someone else’s shoes in order to understand their thoughts and feelings, an ability the researchers considered closely related to altruism.
So the team hypothesised that individual differences in this part of the brain might be linked to differences in altruistic behaviour. And, according to Yosuke Morishima, a postdoctoral researcher at the Department of Economics at the University of Zurich, they were right: ‘People who behaved more altruistically also had a higher proportion of grey matter at the junction between the parietal and temporal lobes.’
The researchers also discovered that the subjects displayed marked differences in brain activity while they were deciding how to split up the money. In the case of selfish people, the small brain region behind the ear is already active when the cost of altruistic behaviour is very low. In altruistic people, however, this brain region only becomes more active when the cost is very high. The brain region is activated especially strongly when people reach the limits of their willingness to behave altruistically. The reason, the researchers suspect, is that this is when there is the greatest need to overcome man’s natural self-centeredness by activating this brain region.
Said Dr Fehr: ‘These are exciting results for us. However, one should not jump to the conclusion that altruistic behaviour is determined by biological factors alone.’
It appears that the volume of grey matter can also be influenced by social processes. According to Dr Fehr, the findings therefore raise the question as to whether it is possible to promote the development of brain regions that are important for altruistic behaviour through training or social norms.
(Source: cordis.europa.eu)
Giving a voice to the voiceless has been a cause that many have championed throughout history, but it’s safe to say that none of those efforts involved packing a bunch of sensors into a glove. A team of Ukrainian students has done just that in order to translate sign language into vocalized speech via a smartphone.
The inspiration for the gloves came from observing fellow college students who were deaf have difficulty communicating with other students, which results in them being excluded from activities. Initially, the team looked at commercially available gloves that could be modified to interpret a range of signs, but in the end, they opted to develop their own.
In their glove, a total of 15 flex sensors in the fingers measure the degree of bending while a compass, accelerometer, and gyroscope determine the motion of the glove through space. The sensor data are processed by a microcontroller on the glove then sent via Bluetooth to a mobile device, which translates the positions of the hand and fingers into text when the pattern is recognized. Using Microsoft APIs for Speech and Bing, the text is spoken by the phone running Windows Phone 7. The glove can also plug into a PC for data syncing and charging of its battery.
A glance at a star-nosed mole (Condylura cristata) is enough to convince most people that something very strange has evolved in the bogs and wetlands of North America. There’s nothing else on the planet quite like this little palm-sized mammal. Its nose is ringed by 22 fleshy appendages, called rays, which are engorged with blood and in a constant flurry of motion when the animal searches for food.
What is this star? How did it evolve and what is it for? What advantage would be worth sporting such an ungainly structure? To a neuroscientist interested in sensory systems, this kind of biological anomaly represents an irresistible mystery. I first began studying star-nosed moles in the early ’90s in an attempt to answer some of these basic questions. But I soon discovered that this unusual animal, like many other specialized species, could reveal general principles about how brains process and represent sensory information. In fact, star-nosed moles have been a gold mine for discoveries about brains and behavior in general—and an unending source of surprises. The most obvious place to start the investigation was with that bizarre star.
(Source: the-scientist.com)
Learning faster with neurodegenerative disease
People who bear the genetic mutation for Huntington’s disease learn faster than healthy people. The more pronounced the mutation was, the more quickly they learned. This is reported by researchers from the Ruhr-Universität Bochum and from Dortmund in the journal Current Biology. The team has thus demonstrated for the first time that neurodegenerative diseases can go hand in hand with increased learning efficiency. “It is possible that the same mechanisms that lead to the degenerative changes in the central nervous system also cause the considerably better learning efficiency” says Dr. Christian Beste, head of the Emmy Noether Junior Research Group “Neuronal Mechanisms of Action Control” at the RUB.
Passive learning through repeated stimulus presentation
In a previous study, the Bochum psychologists reported that the human sense of vision can be changed in the long term by repeatedly exposing subjects to certain visual stimuli for short periods (we reported in May 2011). The task of the participants was to detect changes in the brightness of stimuli. They performed better if they had viewed the stimuli passively for a while first. In the current study, the researchers presented the same task to 29 subjects with the genetic mutation for Huntington’s disease, who, however, did not yet show any symptoms. They also tested 45 control subjects without such mutations in the genome. In both groups, the learning efficiency was better after passive stimulus presentation than without the passive training. Subjects with the Huntington’s mutation, however, increased their performance twice as fast as those without the mutation.
Glutamate may have paradoxical effect
Degenerative diseases of the nervous system are based on complex changes. A key mechanism is an increased release of the neurotransmitter glutamate. However, since glutamate is also important for learning, in some cases it could lead to the paradoxical effect: better learning efficiency despite degeneration of the nerve cells.
Detecting differences in brightness under aggravated conditions
In each experimental run, the subjects saw two consecutive small bars on a computer screen that either had the same or different brightness. Sometimes, however, not only the brightness changed from bar one to bar two, but also the orientation of the bar (vertical or horizontal). “Normally, the distraction stimulus, i.e. the change in orientation, draws all the attention” Christian Beste explains. “But after the passive training with the visual stimuli, the distraction stimulus has no effect at all.” The shift of attention from the non-relevant to the relevant properties of the stimulus was also visible in the electroencephalogram (EEG) in brain areas for early visual processing.
Better performance with stronger mutation
In Huntington’s disease, a short segment of a gene is repeated. The number of repetitions determines when the disease breaks out. In the present study, a greater number of repetitions was, however, also associated with higher learning efficiency. “This shows that neurodegenerative changes can cause paradoxical effects” says Christian Beste. “The everyday view that neurodegenerative changes fundamentally entail deterioration of various functions can no longer be maintained in this dogmatic form.”
(Source: aktuell.ruhr-uni-bochum.de)
A new study shows that newborns that have been exposed to nicotine from both active and passive smoking mothers show poor physiological, sensory, motor and attention responses.
"Newborns who have had intrauterine exposure to nicotine, whether in an active or passive way, show signs of being more affected in terms of their neurobehavioural development. This could be an indicator of pathologies, independently of sociodemographic, obstetric and paediatric factors," as explained to SINC by Josefa Canals and Carmen Hernández, the lead authors of the study.
During the 1980s, thousands of infants in Romanian orphanages spent up to 20 hours a day lying untouched in their cribs, deprived of human contact. As they grew up, neurological and psychological tests confirmed a haunting phenomenon observed in other species, such as mice and rhesus monkeys: Early isolation and neglect can produce lasting cognitive damage, ranging from severe emotional instability to mental retardation. Now, researchers say they have discovered a possible explanation for why early neglect wreaks such havoc—isolation may stunt the growth of the brain cells that insulate neurons, resulting in slower communication between different areas of the brain.
Scientists have known for 50 years that the strength and arrangement of connections between neurons changes as we learn and experience new things, says Gabriel Corfas, senior author of the paper published online today in Science and a neuroscientist at Harvard Medical School in Boston and Boston Children’s Hospital. But the role of the brain’s non-neuronal cells in creating, strengthening, and shaping these neural circuits is more mysterious. The brain’s “white matter”—as opposed to its gray matter, which is composed of neurons—consists mostly of glial cells, which produce the fat and protein myelin sheaths that insulate a neuron’s branching axons, the slender fibers that conduct electrical impulses to other cells. One purpose of myelin, scientists think, is to reduce “leakage” of electric current as electrochemical signals zip to and fro. When the myelin is thin or damaged, the signals can’t travel as fast; that slowdown can impair many different brain functions, including motor control, language, and memory.
Rewiring the Autistic Brain
Signs of autism—such as impaired social skills and repetitive, ritualistic movements—usually begin to appear when a child is about 18 months old. Autism is thought to result from miswired connections in the developing brain, and many experts believe that therapies must begin during a “critical window,” before the faulty circuits become fixed in place. But a new study online today in Science shows that at least one malfunctioning circuit can be repaired after that window closes, holding out hope that in some forms of autism, abnormal circuits in the brain can be corrected even after their development is complete.
Faulty wiring. Shutting off the Nlgn3 gene in mice (right panel) results in miswired synaptic connections, which may be fixable. Credit: S. J. Baudouin et al., Science
According to developmental neurobiologist Peter Scheiffele of the University of Basel in Switzerland, autism doesn’t result from a handful of “culprit” genes that point to a treatable flaw. Instead, patients appear to carry mutations in one out of dozens, even hundreds of risk genes. “This genetic complexity is a huge issue with respect to developing treatments [for autism],” Scheiffele says. To complicate the picture further, autism is not always an isolated disorder; it’s often a common feature in syndromes that otherwise differ drastically. For example, in fragile X syndrome, a form of mental retardation, about 25% of patients are also autistic.
Scheiffele and colleagues were studying a gene called neuroligin-3 (Nlgn3), involved in building the contact points, called synapses, between neurons. Many researchers believe that autism begins at the synapse, and mutations in Nlgn3 have appeared in some forms of the disorder. Sheiffele’s team was focusing on synapses in the cerebellum, a part of the brain that controls movement, but, according to recent research, may also be involved in social behavior. Abnormalities in this region may contribute to both the unusual movements and the social problems seen in autistic patients.
To get a better handle on the role of Nlgn3, the scientists studied mice whose Nlgn3 genes were engineered with an on-off switch, called a promoter region, that is controlled by the antibiotic doxycycline. The animals were raised with the drug in their drinking water, which kept the switch in the off position. With the Nlgn3 gene disabled in the mice, neurons in their cerebellum made the abnormal connections seen in the autistic brain.
Specifically, and much to the researchers’ surprise, the lack of Nlgn3 led to the overactivation of a receptor abbreviated as mGluR1α. This receptor is a component of a pathway that is also disrupted in fragile X syndrome, though it results from mutations in an entirely different gene. In the mice, the overabundance of these receptors led the neurons to make synaptic connections in the wrong places.
To see if turning Nlgn3 gene back on would correct these problems, the researchers withdrew the doxycycline. It worked: With Nlgn3 functioning once more, levels of the extraneous receptor receded back to normal, and the misplaced synapses began to disappear.
"Our finding demonstrates that there is still flexibility after the ‘critical window’ of brain development,” Scheiffele says. “It raises the question: To what extent can a miswired brain be corrected?” The next step, he says, is to see whether motor abnormalities, such as ladder-climbing difficulties, and social interactions can be corrected with similar treatment in the engineered mice. His team is also studying whether drugs that block the mGluR1α receptor can have the same effect as genetically controlling the Nlgn3 gene, which isn’t a treatment option for humans.
"This study holds out hope for children and even adults with developmental disorders. Maybe their conditions aren’t set in stone and can be treated," says neuroscientist Kimberly Huber of the University of Texas Southwestern Medical Center in Dallas. Huber adds that drugs that block a similar receptor, mGluR5, are in clinical trials to treat fragile X syndrome.
(Source: news.sciencemag.org)