Neuroscience
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A short burst of moderate exercise enhances the consolidation of memories in both healthy older adults and those with mild cognitive impairment, scientists with UC Irvine’s Center for the Neurobiology of Learning & Memory have discovered.
Most research has focused on the benefits of a long-term exercise program on overall health and cognitive function with age. But the UCI work is the first to examine the immediate effects of a brief bout of exercise on memory.
In their study, post-doctoral researcher Sabrina Segal and neurobiologists Carl Cotman and Lawrence Cahill had people 50 to 85 years old with and without memory deficits view pleasant images – such as photos of nature and animals – and then exercise on a stationary bicycle for six minutes at 70 percent of their maximum capacity immediately afterward.
One hour later, the participants were given a surprise recall test on the previously viewed images. Results showed a striking enhancement of memory by exercise in both the healthy and cognitively impaired adults, compared with subjects who did not ride the bike.
“We found that a single, short instance of moderately intense exercise particularly improved memory in individuals with memory deficits,” Segal said. “Because of its implications and the need to better understand the mechanism by which exercise may enhance memory, we’re following up this study with an investigation of potential underlying biological factors.”
She believes the improved memory may be related to the exercise-induced release of norepinephrine, a chemical messenger in the brain known to play a strong role in memory modulation. This hypothesis is based on previous work demonstrating that increasing norepinephrine through pharmacological manipulation sharpens memory and that blocking norepinephrine impairs memory.
In the more recent research, Segal and her colleagues discovered that levels of salivary alpha amylase, a biomarker that reflects norepinephrine activity in the brain, significantly increased in participants after exercise. This correlation was especially strong in people with memory impairment.
“The current findings offer a natural and relatively safe alternative to pharmacological interventions for memory enhancement in healthy older individuals as well as those who suffer from cognitive deficits,” Segal noted. “With a growing population of the aged, the need for improvement of quality of life and prevention of mental decline is more important than ever before.”
Study results appear in the November issue (Volume 32, Number 4) of the Journal of Alzheimer’s Disease.
By using a model, researchers at the University of Montreal have identified and “switched off” a chemical chain that causes neurodegenerative diseases such as Huntington’s disease, amyotrophic lateral sclerosis and dementia. The findings could one day be of particular therapeutic benefit to Huntington’s disease patients. “We’ve identified a new way to protect neurons that express mutant huntingtin proteins,” explained Dr. Alex Parker of the University of Montreal’s Department of Pathology and Cell Biology and its affiliated CRCHUM Research Centre. A cardinal feature of Huntington’s disease – a fatal genetic disease that typically affects patients in midlife and causes progressive death of specific areas of the brain – is the aggregation of mutant huntingtin protein in cells. “Our model revealed that increasing another cell chemical called progranulin reduced the death of neurons by combating the accumulation of the mutant proteins. Furthermore, this approach may protect against neurodegenerative diseases other than Huntington’s disease.”
There is no cure for Huntingdon’s disease and current strategies show only modest benefits, and a component of the protein aggregates involved are also present in other degenerative diseases. “My team and I wondered if the proteins in question, TDP-43 and FUS, were just innocent bystanders or if they affected the toxicity caused by mutant huntingtin,” Dr. Parker said. To answer this question, Dr. Parker and University of Montreal doctoral student Arnaud Tauffenberger turned to a simple genetic model based on the expression of mutant huntingtin in the nervous system of the transparent roundworm C. elegans. A large number of human disease genes are conserved in worms, and C. elegans in particular enables researchers to rapidly conduct genetic analyses that would not be possible in mammals.
Dr. Parker’s team found that deleting the TDP-43 and FUS genes, which produce the proteins of the same name, reduced neurodegeneration caused by mutant huntingtin. They then confirmed their findings in the cell of a mammal cell, again by using models. The next step was then to determining how neuroprotection works. TDP-43 targets a chemical called progranulin, a protein linked to dementia. “We demonstrated that removing progranulin from either worms or cells enhanced huntingtin toxicity, but increasing progranulin reduced cell death in mammalian neurons. This points towards progranulin as a potent neuroprotective agent against mutant huntingtin neurodegeneration,” Dr. Parker said. The researchers will need to do further testing this in more complex biological models to determine if the same chemical switches work in all mammals. If they do, then progranulin treatment may slow disease onset or progression in Huntington’s disease patients.
Some people live their lives by the motto “no risk - no fun!” and avoid hardly any risks. Others are clearly more cautious and focus primarily on safety when investing and for other business activities. Scientists from the University of Bonn in cooperation with colleagues from the University of Zurich studied the attitudes towards risk in a group of 56 subjects. They found that in people who preferred safety, certain regions of the brain show a higher level of activation when they are confronted with quite unforeseeable situations. In addition, they do not distinguish as clearly as risk takers whether a situation is more or less risky than expected. The results have just been published in the renowned “Journal of Neuroscience.”
"We were especially interested in the link between risk preferences and the brain regions processing this information," says Prof. Dr. Bernd Weber from the Center for Economics and Neuroscience (CENs) at the University of Bonn. First, the researchers tested a total of 56 subjects for their willingness to take risks. "In an economic game, the test subjects had a choice between a secured payout and a lottery," reports Sarah Rudorf from CENs, the study’s principal author. Those who showed a strong preference for the lottery in this test were categorized as risk takers. Others preferred the secured payout even if the lottery’s odds of winning were clearly better. They were put in the risk-averse group.
In risk-averse individuals, certain regions of the brain are activated more strongly
Then the test subjects played a card game in a brain scanner to study their risk perception. Cards carrying numbers from one to ten were shown on the video glasses in front of their eyes. Each time, two cards were randomly drawn. Before the subjects were shown the cards, they were asked to place bets on whether the second card would have a higher or a lower number than the first one. “The statistical probability for either case to occur is always the same: fifty-fifty,” says Prof. Weber. “This is important so that all subjects, whether they are risk takers or not, experience risky situations inside the scanner.” They were not able to assess their probability of winning their bet until they saw the first card. Here, the researchers found that in the subjects who tended to avoid risks, two specific regions of the brain were activated more strongly than in those who were willing to take risks. These areas are the ventral striatum and the insular cortex. The ventral striatum reacts both to the probability of winning, as well as to how well an individual can predict the outcome of the bet. The insular cortex is particularly sensitive to the risk a situation carries, and for whether it is higher or lower than anticipated.
Risk seekers adjust their strategy after lucky streaks
Sarah Rudorf summarized the results, “Individuals in whom these regions of the brain are activated at a higher level seem to perceive risks more clearly and assess them as more negative than those who are willing to take risks.” Risk-averse individuals seem to overestimate the con¬sequences of risk, and they did not distinguish as clearly between situations that turned out to be more or less risky than expected. In contrast, the test subjects who tended to take greater risks also focused their behavior more towards the wins and losses, and more clearly changed their strategy after negative situations.
Study is first to show the neurobiological mechanisms
"This study is the first to show the neurobiological mechanisms of how individual risk preferences determine risk perception," says Prof. Weber. "This also has effects on behavior in the areas of finance and health."
In a next step, the researchers want to study the consequences these results have on economic decisions such as in the stock market. “This might even allow improving the advising process for investors with regard to their individual risk behavior,” says Prof. Weber. And he considers health another important area. Smokers know that what they do is very dangerous, and yet they smoke. “If we learned more about smokers’ attitudes towards risk, we might be able to provide information for developing better anti-smoking campaigns.”
Drinking during pregnancy can have a severe, adverse effect on the central nervous systems of children after birth, researchers from Poland have discovered.
The study, which was presented Sunday at the annual meeting of the Radiological Society of North America (RSNA), looked at 200 children who were exposed to alcohol during their fetal stage, as well as 30 other kids whose mothers did not drink while pregnant or during lactation.
The researchers used a trio of different MRI techniques in order to study the brain development of both groups of subjects. First, they used standard MRI scans to observe the size and shape of the corpus callosum, which is a group of nerve fibers that oversees communication between the two halves of the brain.
Fetal alcohol exposure is believed to be one of the primary causes of impaired development of the corpus callosum, and sure enough, the MRI scans revealed those who had been exposed to alcohol had “statistically significant thinning of the corpus callosum… compared with the other group,” the RSNA said in a statement.
They also used diffusion weighted imaging (DWI) to study six areas of the central nervous system in both groups. The DWI technique maps the diffusion of water in the brain and can be more successful in detecting tissue abnormalities than regular MRI scans, the researchers explained.
Again, children who had been exposed to alcohol “exhibited statistically significant increases in diffusion on DWI” than their counterparts — an indication there had been damage to the brain tissue, or the presence of neurological disorders, according to Dr Andrzej Urbanik, chair of the Department of Radiology at Jagiellonian University.
Finally, they used proton (hydrogen) magnetic resonance spectroscopy (HMRS) to study the metabolism in the youngsters’ brains. The results uncovered “a high degree of metabolic changes that were specific for particular locations within the brain,” according to Dr. Urbanik.
The RSNA, citing US Centers for Disease Control and Prevention (CDC) statistics, reports as many as 1.5 out of every 1,000 children born alive suffer from fetal alcohol syndrome, and the costs of treating those victims tops $4 billion annually in America alone.