Posts tagged neuroscience
Articles and news from the latest research reports.
Spinal Stimulation Helps Four Patients with Paraplegia Regain Voluntary Movement
Four people with paraplegia are able to voluntarily move previously paralyzed muscles as a result of a novel therapy that involves electrical stimulation of the spinal cord, according to a study funded in part by the National Institutes of Health and the Christopher & Dana Reeve Foundation. The participants, each of whom had been paralyzed for more than two years, were able to voluntarily flex their toes, ankles, and knees while the stimulator was active, and the movements were enhanced over time when combined with physical rehabilitation. Researchers involved in the study say the therapy has the potential to change the prognosis of people with paralysis even years after injury.
“When we first learned that a patient had regained voluntary control as a result of spinal stimulation, we were cautiously optimistic,” said Roderic Pettigrew, Ph.D., M.D., director of the National Institute of Biomedical Imaging and Bioengineering (NIBIB) at NIH, which provided support for the study. “Now that spinal stimulation has been successful in 4 out of 4 patients, there is evidence to suggest that a large cohort of individuals, previously with little realistic hope of any meaningful recovery from spinal cord injury, may benefit from this intervention.”
One of the most impressive and unexpected findings of the study is that two of the patients who benefited from the spinal stimulation had complete motor and sensory paralysis. In these patients, the pathway that sends information about sensation from the legs to the brain is disrupted, in addition to the pathway that sends information from the brain to the legs in order to control movement. The researchers were surprised by the outcome; they had assumed that at least some of the sensory pathway needed to be intact for the therapy to be effective.
Don’t beat yourself up, you’ll live longer
Brandeis researchers explore the relationship between self-compassion and health
We all have stress in our lives, whether it’s a daily commute, workplace pressures or relationship troubles. But how we deal with that stress could impact our health and longevity.
In a recently published paper in Brain, Behavior and Immunity, Brandeis University researchers report they found a connection between a self-compassionate attitude and lower levels of stress-induced inflammation. The discovery could lead to new techniques to lower stress and improve health.
The paper was authored by psychology professor Nicolas Rohleder, with postdoctoral fellows Juliana Breines and Myriam Thoma, and graduate students Danielle Gianferante, Luke Hanlin and Xuejie Chen.
It’s long known that psychological stress can trigger biological responses similar to the effects of illness or injury, including inflammation. While regulated inflammation can help stave off infection or promote healing, unregulated inflammation can lead to cardiovascular disease, cancer and Alzheimer’s.
Self-compassion describes behaviors such as self-forgiveness or, more colloquially, cutting yourself some slack. A person with high levels of self-compassion may not blame themselves for stress beyond their control or may be more willing to move on from an argument, rather than dwelling on it for days.
To understand the connection between self-compassion and inflammatory responses to stress, Rohleder and his team asked 41 participants to rank their levels of self-compassion. The participants ranked their agreement to statements such as, “I try to be understanding and patient toward aspects of my personality I do not like” and “I’m disapproving and judgmental about my own flaws and inadequacies.”
Then, the participants took one stress test a day for two days and their levels of interleukin-6 (IL-6), an inflammatory agent linked to stress, were recorded before and after each test. After the first stress test, participants with higher self-compassion had significantly lower levels of IL-6.
On the second day, Rohleder and his team found something unexpected. Those with low self-compassion had higher base levels of IL-6 before the test, suggesting that they may have been carrying the stress they experienced the day before.
“The high responses of IL-6 on the first day and the higher baseline levels on the second day suggest that people with low self-compassion are especially vulnerable to the adverse effects of this kind of stress,” Rohleder says.
The research illustrates how easy it is for stress to build over time and how a seemingly small daily stressor, such as traffic, can impact a person’s health if they don’t have the right strategies to deal with it.
“Hopefully, this research can provide more effective ways to cope with stress and reduce disease, not only by relieving negative emotions but by fostering positive ideas of self compassion,” Rohleder says.
Genes increase the stress of social disadvantage for some children
Genes amplify the stress of harsh environments for some children, and magnify the advantage of supportive environments for other children, according to a study that’s one of the first to document how genes interacting with social environments affect biomarkers of stress.
"Our findings suggest that an individual’s genetic architecture moderates the magnitude of the response to external stimuli—but it is the environment that determines the direction" says Colter Mitchell, lead author of the paper and a researcher at the University of Michigan Institute for Social Research (ISR).
The study, published today in the Proceedings of the National Academy of Sciences, uses telomere length as a marker of stress. Found at the ends of chromosomes, telomeres generally shorten with age, and when individuals are exposed to disease and chronic stress, including the stress of living in a disadvantaged environment.
For the study, Mitchell and colleagues used telomere samples from a group of 40 nine-year-old boys from two very different environments – one nurturing and the other harsh. Those in the nurturing environment came from stable families, with nurturing parenting, good maternal mental health, and positive socioeconomic conditions, while those in the harsh environment experienced high levels of poverty, harsh parenting, poor maternal mental health, and high family instability.
For those children with heightened sensitivity in the serotonergic and dopaminergic genetic pathways compared to other children, telomere length was shortest in a disadvantaged environment, and longest in a supportive environment.
New research suggests connection between white matter and cognitive health
A multidisciplinary group of scientists from the Sanders-Brown Center on Aging at the University of Kentucky have identified an interesting connection between the health of the brain tissue that supports cognitive functioning and the presence of dementia in adults with Down syndrome.
Published in the Neurobiology of Aging, the study, which focused on detecting changes in the white matter connections of the brain, offers tantalizing potential for the identification of biomarkers connected to the development of dementia, including Alzheimer’s disease.
"We used magnetic resonance imaging to compare the health of the brain’s white matter and how strongly it connects different parts of the brain," explains Elizabeth Head, Ph.D., the study’s senior author. "The results indicate a compelling progression of deterioration in the integrity of white matter in the brains of our study participants commensurate with their cognitive health."
Research team member David Powell, PhD, compared the brain scans of three groups of volunteers: persons with Down syndrome but no dementia, persons with Down syndrome and dementia, and a healthy control group.
Using MRI technologies, brain scans of subjects with Down syndrome showed some compromise in the tissues of brain’s frontal lobe compared to those from the control group. When people with Down syndrome and dementia were compared to people with Down syndrome without dementia, those same white matter connections were even less healthy.
Perhaps the most intriguing aspect of the study was the correlation between the cognitive abilities of participants with Down Syndrome and the integrity of their white matter– those who had higher motor skill coordination and better learning and memory ability had healthier frontal white matter connections.
Persons with Down syndrome are at an extremely high risk for developing Alzheimer’s disease after the age of 40. The team hopes their work might eventually lead to the identification of biomarkers for the development of Alzheimer’s disease in people with Down syndrome and, potentially, extend that to the general population as well.
Head cautions that these results are to some extent exploratory due to the small cohort of 30 participants. But, she says, “If we are able to identify people who, based on biomarkers, have a higher risk of developing Alzheimer’s disease, we might be able to intervene at an earlier point to retard the progression of the disease.”
Caffeine against Alzheimer’s disease
A team of researchers working with Prof. Dr. Christa E. Müller from the University of Bonn demonstrates a positive effect on tau deposits
As part of a German-French research project, a team led by Dr. Christa E. Müller from the University of Bonn and Dr. David Blum from the University of Lille was able to demonstrate for the first time that caffeine has a positive effect on tau deposits in Alzheimer’s disease. The two-years project was supported with 30,000 Euro from the non-profit Alzheimer Forschung Initiative e.V. (AFI) and with 50,000 Euro from the French Partner organization LECMA. The initial results were published in the online edition of the journal “Neurobiology of Aging”
Tau deposits, along with beta-amyloid plaques, are among the characteristic features of Alzheimer’s disease. These protein deposits disrupt the communication of the nerve cells in the brain and contribute to their degeneration. Despite intensive research there is no drug available to date which can prevent this detrimental process. Based on the results of Prof. Dr. Christa Müller from the University of Bonn, Dr. David Blum and their team, a new class of drugs may now be developed for the treatment of Alzheimer’s disease.
Caffeine, an adenosine receptor antagonist, blocks various receptors in the brain which are activated by adenosine. Initial results of the team of researchers had already indicated that the blockade of the adenosine receptor subtype A2A in particular could play an important role. Initially, Prof. Müller and her colleagues developed an A2A antagonist in ultrapure and water-soluble form (designated MSX-3). This compound had fewer adverse effects than caffeine since it only blocks only the A2A adenosine receptor subtype, and at the same time it is significantly more effective. Over several weeks, the researchers then treated genetically altered mice with the A2A antagonist. The mice had an altered tau protein which, without therapy, leads to the early development of Alzheimer’s symptoms.
In comparison to a control group which only received a placebo, the treated animals achieved significantly better results on memory tests. The A2A antagonist displayed positive effects in particular on spatial memory. Also, an amelioration of the pathogenic processes was demonstrated in the hippocampus, which is the site of memory in rodents.
"We have taken a good step forward," says Prof. Müller. "The results of the study are truly promising, since we were able to show for the first time that A2A adenosine receptor antagonists actually have very positive effects in an animal model simulating hallmark characteristics and progression of the disease. And the adverse effects are minor."
The researchers now want to test the A2A antagonist in additional animal models. If the results are positive, a clinical study may follow. “Patience is required until A2A adenosine receptor antagonists are approved as new therapeutic agents for Alzheimer’s disease. But I am optimistic that clinical studies will be performed,” says Prof. Müller.
(Image: Shutterstock)
Green tea is said to have many putative positive effects on health. Now, researchers at the University of Basel are reporting first evidence that green tea extract enhances the cognitive functions, in particular the working memory. The Swiss findings suggest promising clinical implications for the treatment of cognitive impairments in psychiatric disorders such as dementia. The academic journal Psychopharmacology has published their results.
In the past the main ingredients of green tea have been thoroughly studied in cancer research. Recently, scientists have also been inquiring into the beverage’s positive impact on the human brain. Different studies were able to link green tea to beneficial effects on the cognitive performance. However, the neural mechanisms underlying this cognitive enhancing effect of green tea remained unknown.
Better memory
In a new study, the researcher teams of Prof. Christoph Beglinger from the University Hospital of Basel and Prof. Stefan Borgwardt from the Psychiatric University Clinics found that green tea extract increases the brain’s effective connectivity, meaning the causal influence that one brain area exerts over another. This effect on connectivity also led to improvement in actual cognitive performance: Subjects tested significantly better for working memory tasks after the admission of green tea extract.
For the study healthy male volunteers received a soft drink containing several grams of green tea extract before they solved working memory tasks. The scientists then analyzed how this affected the brain activity of the men using magnetic resonance imaging (MRI). The MRI showed increased connectivity between the parietal and the frontal cortex of the brain. These neuronal findings correlated positively with improvement in task performance of the participants. «Our findings suggest that green tea might increase the short-term synaptic plasticity of the brain», says Borgwardt.
Clinical implications
The research results suggest promising clinical implications: Modeling effective connectivity among frontal and parietal brain regions during working memory processing might help to assess the efficacy of green tea for the treatment of cognitive impairments in neuropsychiatric disorders such as dementia.
Switching off anxiety with light
G protein coupled receptors play an important role in medicine and health
One receptor, which is important for the regulation of serotonin levels in the brain, is the 5-HT1A receptor. It belongs to a protein family called G protein coupled receptors (GPCRs). These receptors can activate different signalling pathways in cells to support or suppress various signalling events. “About 30 per cent of the current drugs target specifically GPCRs”, says Prof Dr Stefan Herlitze from the Department of General Zoology and Neurobiology at the RUB. Due to the lack of tools to control intracellular signalling pathways with high temporal and spatial accuracy, it was so far difficult to analyse these pathways precisely.
Coupling of visual pigments to serotonin receptors
Applying optogenetic methods the scientists in Bochum used cone opsins from the mouse and human eye to control specifically serotonin signalling pathways either with blue or red light. Prof Dr Stefan Herlitze has been working with optogenetic techniques since 2005 and is one of the pioneers in the field. The light-activated serotonin receptors can be switched on within milliseconds, are extremely light sensitive in comparison to other optogenetic tools and can be repetitively activated. “We hope that with the help of these optogenetic tools, we will be able to gain a better understanding about how anxiety and depression originate”, states RUB neuroscientist Dr Olivia Masseck.
Successful behavioural tests
The scientists also demonstrated that they were able to modulate mouse emotional behaviour using the light-activated receptors. When they switched on the serotonergic signals by light in a certain brain area, the mice became less anxious.
Exploring the Genetics of “I’ll Do It Tomorrow”
Procrastination and impulsivity are genetically linked, suggesting that the two traits stem from similar evolutionary origins, according to research published in Psychological Science, a journal of the Association for Psychological Science. The research indicates that the traits are related to our ability to successfully pursue and juggle goals.
“Everyone procrastinates at least sometimes, but we wanted to explore why some people procrastinate more than others and why procrastinators seem more likely to make rash actions and act without thinking,” explains psychological scientist and study author Daniel Gustavson of the University of Colorado Boulder. “Answering why that’s the case would give us some interesting insights into what procrastination is, why it occurs, and how to minimize it.”
From an evolutionary standpoint, impulsivity makes sense: Our ancestors should have been inclined to seek immediate rewards when the next day was uncertain.
Procrastination, on the other hand, may have emerged more recently in human history. In the modern world, we have many distinct goals far in the future that we need to prepare for – when we’re impulsive and easily distracted from those long-term goals, we often procrastinate.
Thinking about the two traits in that context, it seems logical that people who are perpetual procrastinators would also be highly impulsive. Many studies have observed this positive relationship, but it is unclear what cognitive, biological, and environmental influences are responsible for it.
The most effective way to understand why these traits are correlated is to study human twins. Identical twins — who share 100% of their genes — tend to show greater similarities in behavior than fraternal twins, who only share 50% of their genes (just like any other siblings). Researchers take advantage of this genetic discrepancy to figure out the relative importance of genetic and environmental influences on particular behaviors, like procrastination and impulsivity.
Gustavson and colleagues had 181 identical-twin pairs and 166 fraternal-twin pairs complete several surveys intended to probe their tendencies toward impulsivity and procrastination, as well as their ability to set and maintain goals.
They found that procrastination is indeed heritable, just like impulsivity. Not only that, there seems to be a complete genetic overlap between procrastination and impulsivity — that is, there are no genetic influences that are unique to either trait alone.
That finding suggests that, genetically speaking, procrastination is an evolutionary byproduct of impulsivity — one that likely manifests itself more in the modern world than in the world of our ancestors.
In addition, the link between procrastination and impulsivity also overlapped genetically with the ability to manage goals, lending support to the idea that delaying, making rash decisions, and failing to achieve goals all stem from a shared genetic foundation.
Gustavson and colleagues are now investigating how procrastination and impulsivity are related to higher-level cognitive abilities, such as executive functions, and whether these same genetic influences are related to other aspects of self-regulation in our day-to-day lives.
“Learning more about the underpinnings of procrastination may help develop interventions to prevent it, and help us overcome our ingrained tendencies to get distracted and lose track of work,” Gustavson concludes.
The Social Circuits that Track How We Like People and Ideas
Whether at the office, dorm, PTA meeting, or any other social setting, we all know intuitively who the popular people are – who is most liked – even if we can’t always put our finger on why. That information is often critical to professional or social success as you navigate your social networks. Yet until now, scientists have not understood how our brains recognize these popular people. In new work, researchers say that we track people’s popularity largely through the brain region involved in anticipating rewards.
“Being able to track other people’s status in your group is incredibly important in survival terms,” says Kevin Ochsner of Columbia University. “Knowing who is popular or likeable is critically important in times of need or distress, when you seek an alliance, or need help – whether physical or political – etc.” While sociologists, psychologists, and anthropologists have long studied these group dynamics, neuroscientists have only begun to scratch the surface of how we think about people’s social status.
That is all changing, though, Ochsner says with many areas of work bringing together social psychology and sociology with cognitive neuroscience to better understand how individual brain processes connect to group membership. As will be presented today at the annual meeting of the Cognitive Neuroscience Society (CNS) in Boston, researchers are now studying at the neural level everything from social popularity to how ideas successfully spread in groups.
(Source: cogneurosociety.org)
Loneliness impacts DNA repair: The long and the short of telomeres
Telomeres are DNA-protein complexes that function as protective caps at the ends of chromosomes. Biologists and veterinarians at the Vetmeduni Vienna recently examined the telomere length of captive African grey parrots. They found that the telomere lengths of single parrots were shorter than those housed with a companion parrot, which supports the hypothesis that social stress can interfere with cellular aging and a particular type of DNA repair. It suggests that telomeres may provide a biomarker for assessing exposure to social stress. The findings have been published in the open access journal PLOS ONE.
In captivity, grey parrots are often kept in social isolation, which can have detrimental effects on their health and wellbeing. So far there have not been any studies on the effects of long term social isolation from conspecifics on cellular aging. Telomeres shorten with each cell division, and once a critical length is reached, cells are unable to divide further (a stage known as ‘replicative senescence’). Although cellular senescence is a useful mechanism to eliminate worn-out cells, it appears to contribute to aging and mortality. Several studies suggest that telomere shortening is accelerated by stress, but until now, no studies have examined the effects of social isolation on telomere shortening.
Using molecular genetics to assess exposure to stress
To test whether social isolation accelerates telomere shortening, Denise Aydinonat, a doctorate student at the Vetmeduni Vienna, conducted a study using DNA samples that she collected from African grey parrots during routine check-ups. African greys are highly social birds, but they are often reared and kept in isolation from other parrots (even though such conditions are illegal in Austria). She and her collaborators compared the telomere lengths of single birds versus pair-housed individuals with a broad range of ages (from 1 to 45 years). Not surprisingly, the telomere lengths of older birds were shorter compared to younger birds, regardless of their housing. However, the important finding of the study was that single-housed birds had shorter telomeres than pair-housed individuals of the same age group.
Reading signs of stress by erosion of DNA
“Studies on humans suggest that people who have experienced high levels of social stress and deprivation have shorter telomeres,” says Dustin Penn from the Konrad Lorenz Institute of Ethology at the Vetmeduni Vienna. “But this study is the first to examine the effects of social isolation on telomere length in any species.” Penn and his team previously conducted experiments on mice, which were the first to show that exposure to crowding stress causes telomere shortening. He points out that this new finding suggests that both extremes of social conditions affect telomere attrition. However, he also cautions “further ‘longitudinal’ studies, in which changes in telomeres of the same individuals over time, are needed to investigate the consequences of stress on telomere shortening and the subsequent effects on health and longevity.”