Posts tagged cognitive function
Articles and news from the latest research reports.
Neuroscientists find Broca’s area is really two subunits, each with its own function
A century and a half ago, French physician Pierre Paul Broca found that patients with damage to part of the brain’s frontal lobe were unable to speak more than a few words. Later dubbed Broca’s area, this region is believed to be critical for speech production and some aspects of language comprehension.
However, in recent years neuroscientists have observed activity in Broca’s area when people perform cognitive tasks that have nothing to do with language, such as solving math problems or holding information in working memory. Those findings have stimulated debate over whether Broca’s area is specific to language or plays a more general role in cognition.
A new study from MIT may help resolve this longstanding question. The researchers, led by Nancy Kanwisher, the Walter A. Rosenblith Professor of Cognitive Neuroscience, found that Broca’s area actually consists of two distinct subunits. One of these focuses selectively on language processing, while the other is part of a brainwide network that appears to act as a central processing unit for general cognitive functions.
"I think we’ve shown pretty convincingly that there are two distinct bits that we should not be treating as a single region, and perhaps we shouldn’t even be talking about ‘Broca’s area’ because it’s not a functional unit," says Evelina Fedorenko, a research scientist in Kanwisher’s lab and lead author of the new study, which recently appeared in the journal Current Biology.
New study shows that even your fat cells need sleep
In a study that challenges the long-held notion that the primary function of sleep is to give rest to the brain, researchers have found that not getting enough shut-eye has a harmful impact on fat cells, reducing by 30 percent their ability to respond to insulin, a hormone that regulates energy.
Sleep deprivation has long been associated with impaired brain function, causing decreased alertness and reduced cognitive ability. The latest finding—published by University of Chicago Medicine researchers in the Oct. 16 issue of the Annals of Internal Medicine—is the first description of a molecular mechanism directly connecting sleep loss to the disruption of energy regulation in humans, a process that can lead over time to weight gain, diabetes and other health problems. The study suggests that sleep’s role in energy metabolism is at least as important as it is in brain function.
"We found that fat cells need sleep to function properly," said study author Matthew Brady, PhD, associate professor of medicine and vice-chair of the Committee on Molecular Metabolism and Nutrition at the University of Chicago.
Chronic Stress During Pregnancy Prevents Brain Benefits of Motherhood
(Credit: Oleg Zabielin / Shutterstock)
A new study in animals shows that chronic stress during pregnancy prevents brain benefits of motherhood, a finding that researchers suggest could increase understanding of postpartum depression.
Rat mothers showed an increase in brain cell connections in regions associated with learning, memory and mood. In contrast, the brains of mother rats that were stressed twice a day throughout pregnancy did not show this increase.
The researchers were specifically interested in dendritic spines – hair-like growths on brain cells that are used to exchange information with other neurons.
Previous animal studies conducted by lead author Benedetta Leuner of Ohio State University showed that an increase of dendritic spines in new mothers’ brains was associated with improved cognitive function on a task that requires behavioral flexibility – in essence, enabling more effective multitasking. The dendritic spines increased by about 20 percent in these brain regions in new mothers, according to her findings.
The stress in this new study negated those brain benefits of motherhood, causing the stressed rats’ brains to match brain characteristics of animals that had no reproductive or maternal experience.
The stressed rats also had less physical interaction with their babies than did unstressed rats, a behavior observed in human mothers who experience postpartum depression.
“Animal mothers in our research that are unstressed show an increase in the number of connections between neurons. Stressed mothers don’t,” said Leuner, assistant professor of psychology and neuroscience at Ohio State and lead author of the study. “We think that makes the stressed mothers more vulnerable. They don’t have the capacity for brain plasticity that the unstressed mothers do, and somehow that’s contributing to their susceptibility to depression.”
(Source: newswise.com)
Columbia University Medical Center (CUMC) researchers have identified a potential medical treatment for the cognitive effects of stress-related disorders, including post-traumatic stress disorder (PTSD). The study, conducted in a PTSD mouse model, shows that an experimental drug called S107, one of a new class of small-molecule compounds called Rycals, prevented learning and memory deficits associated with stress-related disorders. The findings were published in the online edition of Cell.
Based on his earlier work in heart and muscle disorders, Dr. Marks reasoned that chronic stress could lead to PTSD by destabilizing type 2 ryanodine receptors (RyR2) in the hippocampus, the brain region that plays a central role in learning and memory. RyR2 are channels that regulate the level of calcium in neurons, which is vital to cell survival and function.
“When we examined the hippocampal neurons of the stressed mice, we found that their RyR2 channels had become destabilized and leaky compared with channels from normal non-stressed mice which were not leaky. There was a remodeling of the channels that we had previously seen in heart and skeletal muscles from animal models of chronic diseases including heart failure and muscular dystrophy. We found these same leaky channels in samples from patients with these disorders but not in those from healthy humans,” said Dr. Marks.