Posts tagged psychology
Articles and news from the latest research reports.
Bipolar disorder and creativity found to be linked
Does some fine madness yield great artists, writers, and scientists? The evidence is growing for a significant link between bipolar disorder and creative temperament and achievement.
People with bipolar disorder swing repeatedly from depression to euphoria and hyperactivity, or intensely irritable mood states. Sometimes likened to being on an emotional rollercoaster, each swing up then down affects one’s behaviour, energy levels, thought patterns and sleep.
Also known as manic-depressive illness, bipolar disorder is strongly genetically linked, passing down through each generation of an affected family. It is fairly common and very treatable with modern medicines and psychotherapy.
(Source: machineslikeus.com)
Can’t sleep? You could have inherited the insomnia gene
21 August 2012 by Lois Rogers
Thousands of otherwise healthy people put up with a level of sleep deprivation that would drive the rest of us insane. But they are not the usual candidates for insomnia, such as shift workers or those with severe mental illness. Instead, they belong to a newly identified group of people born without the ‘comfort’ genes needed for easy sleep.
This means they are immune to the feeling of warmth and relaxation which sends an average person off to sleep within 15 minutes. Their genes are designed instead to maintain a state of mental alertness. This makes normal, prolonged sleep impossible so they sleep fitfully, in only short bursts. Even then, their lack of ‘comfort’ genes may mean they struggle to get comfortable, fussing about the bedding or finding their sleeping position.
There are other so-called insomnia genes — some cause repeated periods of wakefulness in the small hours of the night or at the slightest disturbance, or drive an affected person to leap out of bed raring to start the day at 4am, but leave them exhausted by 4pm. Until recently, insomnia was considered a purely psychological complaint triggered by stress, grief, or sleep disruption as a result of shift work or jet lag.
But doctors are now unravelling the genetic explanation of why at least one-third of us have intermittent or constant sleep problems. Even so, it’s already thought there could be six or more different types of insomnia linked to genes. This means it will be possible to develop drugs to block the effect of the chemical signals they produce.
(Source: Daily Mail)
Looking One Cell at a Time in the Brain to Better Understand Pain, Learning, Memory
ScienceDaily (Aug. 21, 2012) — Working with units of material so small that it would take 50,000 to make up one drop, scientists are developing the profiles of the contents of individual brain cells in a search for the root causes of chronic pain, memory loss and other maladies that affect millions of people.
They described the latest results of this one-by-one exploration of cells or “neurons” from among the millions present in an animal brain at the 244th National Meeting & Exposition of the American Chemical Society (ACS), the world’s largest scientific society. The meeting, expected to attract almost 14,000 scientists and others from around the world, continues in Philadelphia through Thursday, with 8,600 presentations on new discoveries in science and other topics.
Jonathan Sweedler, Ph.D., a pioneer in the field, explained in a talk at the meeting that knowledge of the chemistry occurring in individual brain cells would provide the deepest possible insights into the causes of certain diseases and could point toward new ways of diagnosis and treatment. Until recently, however, scientists have not had the technology to perform such neuron-by-neuron research.
"Most of our current knowledge about the brain comes from studies in which scientists have been forced to analyze the contents of multiple nerve cells, and, in effect, average the results," Sweedler said. He is with the University of Illinois at Urbana-Champaign and also serves as editor-in-chief of Analytical Chemistry, which is among ACS’ more than 40 peer-reviewed scientific journals. “That approach masks the sometimes-dramatic differences that can exist even between nerve cells that are shoulder-to-shoulder together. Suppose that only a few cells in that population are changing, perhaps as a disease begins to take root or starts to progress or a memory forms and solidifies. Then we would miss those critical changes by averaging the data.”
However, scientists have found it difficult to analyze the minute amounts of material inside single brain cells. Those amounts are in the so-called “nanoliter” range, units so small that it would take 355 billion nanoliters to fill a 12-ounce soft-drink can. Sweedler’s group spent much of the past decade developing the technology to analyze the chemicals found in individual cells — a huge feat with a potentially big pay-off. “We are using our new approaches to understand what happens in learning and memory in the healthy brain, and we want to better understand how long-lasting, chronic pain develops,” he said.
The 85 billion neurons in the brain are highly interconnected, forming an intricate communications network that makes the complexity of the Internet pale in comparison. The neural net’s chemical signaling agents and electrical currents orchestrate a person’s personality, thoughts, consciousness and memories. These connections are different from person to person and change over the course of a lifetime, depending on one’s experiences. Even now, no one fully understands how these processes happen.
To get a handle on these complex workings, Sweedler’s team and others have zeroed in on small sections of the central nervous system ― the brain and spinal cord ― using stand-ins for humans such as sea slugs and laboratory rats. Sweedler’s new methods enable scientists to actually select areas of the nervous system, spread out the individual neurons onto a glass surface, and one-by-one analyze the proteins and other substances inside each cell.
One major goal is to see how the chemical make-up of nerve cells changes during pain and other disorders. Pain from disease or injuries, for instance, is a huge global challenge, responsible for 40 million medical appointments annually in the United States alone.
Sweedler reported that some of the results are surprising, including tests on cells in an area of the nervous system involved in the sensation of pain. Analysis of the minute amounts of material inside the cells showed that the vast majority of cells undergo no detectable change after a painful event. The chemical imprint of pain occurs in only a few cells. Finding out why could point scientists toward ways of blocking those changes and in doing so, could lead to better ways of treating pain.
Source: Science Daily
Bonobo genius makes stone tools like early humans did
Kanzi the bonobo continues to impress. Not content with learning sign language or making up “words” for things like banana or juice, he now seems capable of making stone tools on a par with the efforts of early humans.
Learning to play a musical instrument could help to improve children’s reading and their ability to listen in noisy classrooms, according to new research.
Neuroscientists have found that musicians benefit from heightened brain activity that allows them to process information from their eyes and ears more efficiently than non-musicians.
They found that the part of the brain that interprets sound, known as the auditory cortex, responds faster in people with musical training and is better primed to pick out subtle patterns from the huge volumes of information that flood into the brain from our senses.
Professor Nina Kraus, a neuroscientist and amateur musician at Northwestern University in Evanston, Illinois, has also found that this part of the brain plays a crucial role in reading.
Low oxygen boosts stem cell survival in muscular dystrophy therapy
Controlling the amount of oxygen that stem cells are exposed to can significantly increase the effectiveness of a procedure meant to combat an often fatal form of muscular dystrophy, according to Purdue University research.
A genetic mutation in patients with Duchenne muscular dystrophy causes the constant breakdown of muscles and gradual depletion of stem cells that are responsible for repairing the damage and progressive muscle wasting. A healthy stem cell tends to duplicate in a regular pattern that creates one copy of itself that continues to function as a stem cell, and a differentiated cell, which performs a specific function. In a healthy person, a torn or damaged muscle would be repaired through this process.
Stem cell therapy - implanting healthy stem cells to combat tissue wasting - has shown promise against muscular dystrophy and other neurodegenerative diseases, but few of the implanted stem cells survive the procedure. Shihuan Kuang, a Purdue assistant professor of animal sciences, and Weiyi Liu, a postdoctoral research associate, showed that survival of implanted muscle stem cells could be increased by as much as fivefold in a mouse model if the cells are cultured under oxygen levels similar to those found in human muscles.
"Stem cells survive in a microenvironment in the body that has a low oxygen level," Kuang said. "But when we culture cells, there is a lot of oxygen around the petri dish. We wanted to see if less oxygen could mimic that microenvironment. When we did that, we saw that more stem cells survived the transplant."
Liu thinks that’s because the stem cells grown in higher oxygen levels acclimate to their surroundings. When they’re injected into muscles with lower oxygen levels, they essentially suffocate.
"By contrast, in our study the cells become used to the host environment when they are conditioned under low oxygen levels prior to transplantation," Liu said.
In the mouse model, Kuang and Liu saw more stem cells survive the transplants, and those stem cells retained their ability to duplicate themselves.
"When we lower the oxygen level, we can also maintain the self-renewal process," Kuang said. "If these stem cells self-renew, they should never be used up and should continue to repair damaged muscle."
The findings, reported in the journal Development, shows promise for increasing the effectiveness of stem cell therapy for patients with Duchenne muscular dystrophy, which affects about one in 3,500 boys starting at about 3-5 years old. The disease, which confines almost all patients to wheelchairs by their 20s, is often fatal as muscles that control the abilities to breathe and eat deteriorate.
Source: Purdue University
Alzheimer Protein Seems to Slow Down Neurotransmitter Production
ScienceDaily (Aug. 21, 2012) — How abnormal protein deposits in the brains of Alzheimer’s patients disrupt the signalling between nerve cells has now been reported by researchers in Bochum and Munich, led by Dr. Thorsten Müller from the Medizinisches Proteom-Center of the Ruhr-Universität, in the journal Molecular and Cellular Proteomics. They varied the amount of APP protein and related proteins associated with Alzheimer’s disease in cell cultures, and then analysed how this manipulation affected other proteins in the cell. The result: the amount of APP present was related to the amount of an enzyme that is essential for the production of neurotransmitters and therefore for communication amongst nerve cells.
Mass spectrometer: The proteins are injected into the apparatus via a very thin needle. (Credit: © RUB-Pressestelle, Marion Nelle)
Proteomics: analysing all the proteins of the cells at once
Amyloid plaques are a characteristic feature of Alzheimer’s disease. They consist largely of cleavage products of the so-called amyloid precursor protein APP, which occur in excess in the brains of Alzheimer’s patients. What role APP plays in healthy people and why the abnormal accumulation of amyloid disrupts the regular functioning of the brain is still largely unclear. To understand the function of APP, the RUB researchers established a new cell model. The new cells produced only a very small amount of APP. What impact this had on all the other proteins of these cells was examined by the researchers through the use of mass spectrometry, among other things. With this method they identified over 2000 proteins and determined their concentrations. They were looking specifically for molecules whose concentrations in the newly established low-APP cells were different than in the reference cells that contained normal amounts of APP.
Abnormal protein able to curb neurotransmitter production
"One candidate has particularly caught our attention, this being the enzyme methionine adenosyltransferase II, alpha, MAT2A for short," Thorsten Müller said. Among other things, the enzyme is crucially involved in the production of neurotransmitters. Low-APP cells contained less MAT2A than the reference cells. To confirm the connection between the "Alzheimer’s protein" APP and the neurotransmitter-producing MAT2A, the team studied tissue samples from the brains of deceased Alzheimer’s patients and from healthy individuals. In the tissue of the Alzheimer’s patients there was less MAT2A than in the healthy samples. These results suggest that APP and MAT2A concentrations are related and are linked to the synthesis of neurotransmitters. "Our results point to a new mechanism by which the defective cleavage of the APP protein in Alzheimer’s disease could be directly related to altered neurotransmitter production," Müller said. "As a result, the signal transduction of nerve cells could be disrupted, which, over an extended period, could possibly also cause the death of cells."
Source: Science Daily
Though the seconds may tick by on the clock at a regular pace, our experience of the ‘fourth dimension’ is anything but uniform. When we’re waiting in line or sitting in a boring meeting, time seems to slow down to a trickle. And when we get caught up in something completely engrossing – a gripping thriller, for example – we may lose sense of time altogether.
But what about the idea that time flies when we’re having fun? New research from psychological science suggests that the familiar adage may really be true, with a caveat: time flies when we’re have goal-motivated fun.
Sleep improves memory in people with Parkinson’s disease
Aug. 20, 2012 by Quinn Eastman
People with Parkinson’s disease performed markedly better on a test of working memory after a night’s sleep, and sleep disorders can interfere with that benefit, researchers have shown.
The ability of sleep to improve scores on a test of working memory specifically depends on how much slow wave sleep Parkinson’s patients obtain, researchers have found.
While the classic symptoms of Parkinson’s disease include tremors and slow movements, Parkinson’s can also affect someone’s memory, including “working memory.” Working memory is defined as the ability to temporarily store and manipulate information, rather than simply repeat it. The use of working memory is important in planning, problem solving and independent living.
The findings underline the importance of addressing sleep disorders in the care of patients with Parkinson’s, and indicate that working memory capacity in patients with Parkinson’s potentially can be improved with training. The results also have implications for the biology of sleep and memory.
The results were published this week in the journal Brain.
"It was known already that sleep is beneficial for memory, but here, we’ve been able to analyze what aspects of sleep are required for the improvements in working memory performance," says postdoctoral fellow Michael Scullin, who is the first author of the paper. The senior author is Donald Bliwise, professor of neurology at Emory University School of Medicine.
The performance boost from sleep was linked with the amount of slow wave sleep, or the deepest stage of sleep. Several research groups have reported that slow wave sleep is important for synaptic plasticity, the ability of brain cells to reorganize and make new connections.
Sleep apnea, the disruption of sleep caused by obstruction of the airway, interfered with sleep’s effects on memory. Study participants who showed signs of sleep apnea, if it was severe enough to lower their blood oxygen levels for more than five minutes, did not see a working memory test boost.
In this study, participants took a “digit span test,” in which they had to repeat a list of numbers forward and backward. The test was conducted in an escalating fashion: the list grows incrementally until someone makes a mistake. Participants took the digit span test eight times during a 48-hour period, four during the first day and four during the second. In between, they slept.
Repeating numbers in the original order is a test of short-term memory, while repeating the numbers in reverse order is a test of working memory.
"Repeating the list in reverse order requires some effort to manipulate the numbers, not just spit them back out again," Scullin says. "It’s also a purely verbal test, which is important when working with a population that may have motor impairments."
54 study participants had Parkinson’s disease, and 10 had dementia with Lewy bodies: a more advanced condition, where patients may have hallucinations or fluctuating cognition as well as motor symptoms. Those who had dementia with Lewy bodies saw no working memory boost from the night’s rest. As expected, their baseline level of performance was lower than the Parkinson’s group.
Participants with Parkinson’s who were taking dopamine-enhancing medications saw their performance on the digit span test jump up between the fourth and fifth test. On average, they could remember one more number backwards. The ability to repeat numbers backward improved, even though the ability to repeat numbers forward did not.
Patients needed to be taking dopamine-enhancing medications to see the most performance benefit from sleep. Patients not taking dopamine medications, even though they had generally had Parkinson’s for less time, did not experience as much of a performance benefit. This may reflect a role for dopamine, an important neurotransmitter, in memory.
Scullin and Bliwise are planning an expanded study of sleep and working memory, in healthy elderly people as well as patients with neurodegenerative diseases.
"Many elderly people go through a decline in how much slow wave sleep they experience, and this may be a significant contributor to working memory difficulties," Scullin says.
Source: Emory
The frontal lobes are the largest part of the human brain, and thought to be the part that expanded most during human evolution. Damage to the frontal lobes—which are located just behind and above the eyes—can result in profound impairments in higher-level reasoning and decision making. To find out more about what different parts of the frontal lobes do, neuroscientists at the California Institute of Technology (Caltech) recently teamed up with researchers at the world’s largest registry of brain-lesion patients. By mapping the brain lesions of these patients, the team was able to show that reasoning and behavioral control are dependent on different regions of the frontal lobes than the areas called upon when making a decision.