Posts tagged brain
Articles and news from the latest research reports.
Decreased Gene Activity Is Likely Involved in Childhood Risk for Anxiety and Depression
Decreased activity of a group of genes may explain why in young children the “fear center” of the anxious brain can’t learn to distinguish real threats from the imaginary, according to a new University of Wisconsin study.
The study, published this week in the Proceedings of the National Academy of Sciences (PNAS), lays out evidence that young primates with highly anxious temperaments have decreased activity of specific genes within the amygdala, the brain’s fear center.
The authors hypothesize that this may result in over activity of the brain circuit that leads to higher risk for developing disabling anxiety and depression.
This may be particularly important since the genes involved play a major role in forming the brain connections needed for learning about fears. While all children have fears and anxieties, the authors suggest that children with low levels of activity of these genes develop anxious dispositions because they fail to learn to cope by overcoming their early childhood fears.
“Working with my close collaborator and graduate student, Drew Fox, we focused on understanding the function of genes that promote learning and plasticity in the amygdala,” says Dr. Ned H. Kalin, chair of psychiatry at the University of Wisconsin School of Medicine and Public Health, who led the research. “We found reduced activity in key genes that could impair the ability to sculpt the brain, resulting in a failure to develop the capacity to discriminate between real and imaginary fears.”
Kalin says the study helps support the need for early intervention in children identified as excessively shy and anxious. It may also point a way to better treatments aimed at decreasing the likelihood of children developing more severe psychiatric problems. Anxiety in children is quite common and can lead to anxiety and depression in adolescence and often precedes anxiety disorders, depression and substance abuse in adults.
Most small children go through a phase when they’re frightened of many things, including monsters or new social situations, Kalin says, but their maturing brains soon learn to distinguish real threats from the imaginary. But some children do not adapt, generalize their fears to numerous situations, and may later develop serious anxiety and mood disorders. These children tend to be more sensitive to stress, produce more stress hormones and have heightened nervous-system activity.
Kalin, Fox and co-authors wondered whether some differences in the developing amygdala prevent it from learning how to regulate and adapt to anxiety. Kalin’s earlier work identified a subset of young monkeys, similar to extremely shy children, with an inherited anxious disposition. Using brain imaging, the authors showed that high levels of amygdala activity predicted trait-like anxiety in anxious young primates. Like their stable and enduring anxious dispositions, these individuals also had chronically elevated levels of amygdala activity.
“We believe that this pinpoints a critical region in the brain that determines an individual’s level of trait anxiety,’’ Kalin explains.
In examining a specific part of the amygdala, the central nucleus, the researchers analyzed gene expression, which reflects both environmental and inherited influences. Within the central nucleus of the amygdala the authors found that anxious individuals tended to have decreased expression of a gene called neurotrophic tyrosine kinase, receptor, type 3 (NTRK3). Low levels of this gene that encodes for a brain cell surface receptor may be why the amygdala of an anxious monkey or child is chronically overactive and unable to overcome anxiety and fears.
“This is the first demonstration that the early risk to develop anxiety and depression may be related to the underactivity of particular genes in the developing primate amygdala,’’ Kalin says. “These findings have provided the basis for our hypothesis that can explain the early childhood risk to develop anxiety and depression. It also suggests some creative ways to help children with extreme anxiety by developing new treatments focused on increasing the activity of specific genes involved in facilitating the brain development that underlies fear learning and coping.”
(Source: newswise.com)
Fear really resides in a different area of the brain than its inhibitory mechanisms
Do you suffer from a phobia? Maybe arachnophobia? Then you know very well that even if you do not feel uneasy when imagining a huge and hairy tarantula in the therapist’s office, you still jump out of the shower screaming upon seeing a tiny spider. Why is it so hard to get rid of a phobia?
Extinguishing the fear response does not consist of erasing the memory of the fear provoking stimuli, but creating new, competitive memory traces. It has been suspected for some time that neuronal brain circuits responsible for extinguishing fear differ from circuits involved in reoccurrence of the fear response. This assumption has finally been experimentally confirmed. Novel experiments, described in PNAS, a prestigious journal of the American National Academy of Sciences, have been conducted by scientists from the Nencki Institute of Experimental Biology of the Polish Academy of Sciences and the International Institute of Molecular and Cell Biology in Warsaw. This research team was headed by Dr Ewelina Knapska, Dr Jacek Jaworski and Prof. Leszek Kaczmarek.
“Research has been carried out using a special, genetically modified strain of rats developed in the Nencki Institute. As a result we were able to observe the connections between neurons activated in the brains of animals experiencing fear”, explains Dr Ewelina Knapska, head of the Laboratory of Emotions Neurobiology in the Nencki Institute.
Cutis Verticis Gyrata
A 21-year-old man presented with scalp changes that had begun 2 years earlier. Physical examination revealed excessive growth of the scalp, with the formation of convoluted folds and furrows in a cerebriform pattern. The patient had intellectual impairment, although he had no symptoms of neurologic or psychiatric disorders. A 4-mm punch-biopsy specimen from the scalp revealed no inflammatory or neoplastic changes. This clinical presentation was consistent with a diagnosis of cutis verticis gyrata, which is an unusual morphologic condition of the scalp characterized by ridges and furrows resembling the brain’s surface. No intervention was attempted because the patient had no associated disorders and the condition did not bother him cosmetically. At the 1-year follow-up, there were no changes in the patient’s presentation.
A glance at the brain’s circuit diagram
The human brain accomplishes its remarkable feats through the interplay of an unimaginable number of neurons that are interconnected in complex networks. A team of scientists from the Max Planck Institute for Dynamics and Self-Organization, the University of Göttingen and the Bernstein Center for Computational Neuroscience Göttingen has now developed a method for decoding neural circuit diagrams. Using measurements of total neuronal activity, they can determine the probability that two neurons are connected with each other.
From the twitching whiskers of babes: Naptime behavior shapes the brain
The whiskers of newborn rats twitch as they sleep, and that could open the door to new understandings about the intimate connections between brain and body. The discovery reinforces the notion that such involuntary movements are a vital contributor to the development of sensorimotor systems, say researchers who report their findings along with video of those whisker twitches on October 18 in Current Biology, a Cell Press publication.
"We found that even whiskers twitch during sleep—and they do so in infant rats long before they move their whiskers in the coordinated fashion known as whisking," said Mark Blumberg of The University of Iowa. "This discovery opens up new avenues for investigating how we develop critical connections between the sensors in our body and the parts of the brain that interpret and organize sensory information."
BUSM Study Identifies Pathology of Huntington’s Disease
A study led by researchers at Boston University School of Medicine (BUSM) provides novel insight into the impact that Huntington’s disease has on the brain. The findings, published online in Neurology, pinpoint areas of the brain most affected by the disease and opens the door to examine why some people experience milder forms of the disease than others.
Richard Myers, PhD, professor of neurology at BUSM, is the study’s lead/corresponding author. This study, which is the largest to date of brains specific to Huntington’s disease, is the product of nearly 30 years of collaboration between the lead investigators at BUSM and their colleagues at the McLean Brain Tissue Resource Center, Massachusetts General Hospital and Columbia University.
Huntington’s disease (HD) is an inherited and fatal neurological disorder that typically is diagnosed when a person is approximately 40 years old. The gene responsible for the disease was identified in 1993, but the reason why certain neurons or brain cells die remains unknown.
The investigators examined 664 autopsy brain samples with HD that were donated to the McLean Brain Bank. They evaluated and scored more than 50 areas of the brain for the effects of HD on neurons and other brain cell types. This information was combined with a genetic study to characterize variations in the Huntington gene. They also gathered the clinical neurological information on the patients’ age when HD symptoms presented and how long the patient survived with the disease.
Based on this analysis, the investigators discovered that HD primarily damages the brain in two areas. The striatum, which is located deep within the brain and is involved in motor control and involuntary movement, was the area most severely impacted by HD. The outer cortical regions, which are involved in cognitive function and thought processing, also showed damage from HD, but it was less severe than in the striatum.
The investigators identified extraordinary variation in the extent of cell death in different brain regions. For example, some individuals had extremely severe outer cortical degeneration while others appeared virtually normal. Also, the extent of involvement for these two regions was remarkably unrelated, where some people demonstrated heavy involvement in the striatum but very little involvement in the cortex, and vice versa.
“There are tremendous differences in how people with Huntington’s disease are affected,” Myers said. “Some people with the disease have more difficulty with motor control than with their cognitive function while others suffer more from cognitive disability than motor control issues.”
When studying these differences, the investigators noted that the cell death in the striatum is heavily driven by the effects of variations in the Huntington gene itself, while effects on the cortex were minimally affected by the HD gene and are thus likely to be a consequence of other unidentified causes. Importantly, the study showed that some people with HD experienced remarkably less neuronal cell death than others.
“While there is just one genetic defect that causes Huntington’s disease, the disease affects different parts of the brain in very different ways in different people,” said Myers. “For the first time, we can measure these differences with a very fine level of detail and hopefully identify what is preventing brain cell death in some individuals with HD.”
The investigators have initiated extensive studies into what genes and other factors are associated with the protection of neurons in HD, and they hope these protective factors will point to possible novel treatments.
(Source: bumc.bu.edu)
Might lefties and righties benefit differently from a power nap?
At ‘rest,’ right hemisphere of the brain ‘talks’ more than the left hemisphere does
People who like to nap say it helps them focus their minds post a little shut eye. Now, a study from Georgetown University Medical Center may have found evidence to support that notion.
The research, presented at Neuroscience 2012, the annual meeting of the Society for Neuroscience, found that when participants in a study rested, the right hemisphere of their brains talked more to itself and to the left hemisphere than the left hemisphere communicated within itself and to the right hemisphere – no matter which of the participants’ hands was dominant. (Neuroscientists say right-handed people use their left hemisphere to a greater degree, and vice versa.)
Results of this study, the first known to look at activity in the two different hemispheres during rest, suggests that the right hemisphere “is doing important things in the resting state that we don’t yet understand,” says Andrei Medvedev, Ph.D., an assistant professor in the Center for Functional and Molecular Imaging at Georgetown. The activities being processed by the right hemisphere, which is known to be involved in creative tasks, could be daydreaming or processing and storing previously acquired information. “The brain could be doing some helpful housecleaning, classifying data, consolidating memories,” Medvedev says. “That could explain the power of napping. But we just don’t know yet the relative roles of both hemispheres in those processes and whether the power nap might benefit righties more then lefties.”
To find out what happens in the resting state, the research team connected 15 study participants to near-infrared spectroscopy (NIRS) equipment. This technology, which is low cost and portable, uses light to measure changes in oxygenated hemoglobin inside the body.
The study participants wore a cap adorned with optical fibers that delivers infrared light to the outermost layers of the brain and then measures the light that bounces back. In this way, the device can “see” which parts of the brain are most active and communicating at a higher level based on increased use of oxygen in the blood and heightened synchronicity of their activities.
"The device can help delineate global networks inside the brain — how the components all work together," Medvedev says. "The better integrated they are, the better cognitive tasks are performed."
To their surprise, the researchers found that left and right hemispheres behaved differently during the resting state. “That was true no matter which hand a participant used. The right hemisphere was more integrated in right-handed participants, and even stronger in the left-handed,” he says.
Medvedev is exploring the findings for an explanation. And he suggests that brain scientists should start focusing more of their attention on the right hemisphere. “Most brain theories emphasize the dominance of the left hemisphere especially in right handed individuals, and that describes the population of participants in these studies,” Medvedev says. “Our study suggests that looking at only the left hemisphere prevents us from a truer understanding of brain function.”
(Source: eurekalert.org)
Study finds association between rare neuromuscular disorder and loss of smell
Changes in the ability to smell and taste can be caused by a simple cold or upper respiratory tract infection, but they may also be among the first signs of neurodegenerative disorders such as Alzheimer’s disease and Parkinson’s disease. Now, new research from the Perelman School of Medicine at the University of Pennsylvania has revealed an association between an impaired sense of smell and myasthenia gravis (MG), a chronic autoimmune neuromuscular disease characterized by fluctuating fatigue and muscle weakness. The findings are published in the latest edition of PLOS ONE.
Most humans experience five types of tastes: sweet, salty, sour, bitter, and savory. The sense of taste is mediated by taste receptor cells which are bundled in our taste buds. “Sour” and “bitter” taste sensations alert the body to harmful foods that have spoiled or are toxic. But based on genetics, up to 25 percent of the population cannot detect certain bitter flavors (non-tasters), 25 percent can detect exceedingly small quantities (super-tasters), and the rest of us fall somewhere between these two extremes.
So what exactly does drinking a cup of bitter coffee have to do with chronic sinus infections, which account for approximately 18-22 million physician visits in the U.S. each year? Recent investigations have shown that these taste receptors (T2Rs) are also found in both upper and lower human respiratory tissue, likely signaling a connection between activation of bitter tastes and the need to launch an immune response in these areas when they are exposed to potentially harmful bacteria and viruses.
“With this information in mind, we wanted to better understand the exact role that bitter taste receptors play in the upper airway, especially between these super and non-tasters,” says Noam Cohen, MD, PhD, assistant professor of Otorhinolaryngology: Head and Neck Surgery, staff physician at the Philadelphia VAMC, and senior author of the new study.
(Source: medicalxpress.com)
Research discovers two opposite ways our brain voluntarily forgets unwanted memories
If only there were a way to forget that humiliating faux pas at last night’s dinner party. It turns out there’s not one, but two opposite ways in which the brain allows us to voluntarily forget unwanted memories, according to a study published by Cell Press October 17 in the journal Neuron. The findings may explain how individuals can cope with undesirable experiences and could lead to the development of treatments to improve disorders of memory control.
"This study is the first demonstration of two distinct mechanisms that cause such forgetting: one by shutting down the remembering system, and the other by facilitating the remembering system to occupy awareness with a substitute memory," says lead study author Roland Benoit of the MRC Cognition and Brain Sciences Unit at the University of Cambridge.
Previous studies have shown that individuals can voluntarily block memories from awareness. Although several neuroimaging studies have examined the brain systems involved in intentional forgetting, they have not revealed the cognitive tactics that people use or the precise neural underpinnings. Two possible ways to forget unwanted memories are to suppress them or to substitute them with more desirable memories, and these tactics could engage distinct neural pathways.
(Source: medicalxpress.com)
Understanding Alzheimer’s: Study gives insights into how disease kills brain cells
Exactly how Alzheimer’s disease kills brain cells is still somewhat of a mystery, but University of Michigan researchers have uncovered a clue that supports the idea that small proteins prick holes into neurons.
The team also found that a certain size range of clumps of these proteins are particularly toxic to cells, while smaller and larger aggregates of the protein appear to be benign.
The findings, which appear in the journal PLOS ONE, add important detail to the knowledge base regarding this disease that affects 5.4 million Americans in 2012 but remains incurable and largely untreatable. The results could potentially help pharmaceutical researchers target drugs to the right disease mechanisms.
Small proteins called amyloid-beta peptides are the prime suspect for causing cell death in Alzheimer’s. They make up most of the senile plaque fibers found in the brains of autopsied patients. Researchers offer several hypotheses for how the peptides might cause the disease. They blame inflammation, oxidative stress or an imbalance of calcium ions possibly caused by holes in the cell membranes.
The U-M findings strongly support the idea that amyloid peptides damage the membrane around nerve cells and lead to uncontrolled movement of calcium ions into them. Calcium signaling is an important way that cells communicate and healthy cells regulate its flow precisely. The toxic mechanism implicated in the new study could act on its own or together with the other proposed courses and ultimately lead to a loss of brain cells in patients, the researchers say.