Neuroscience

Articles and news from the latest research reports.

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Researchers discover new treatment possibilities for Lou Gehrig’s disease

A team led by Dr. Alex Parker, a professor of pathology and cellular biology and a researcher at the University of Montreal Hospital Research Centre (CRCHUM), has identified an important therapeutic target for alleviating the symptoms of Lou Gehrig’s disease, also known as amyotrophic lateral sclerosis (ALS), and other related neurodegenerative disorders such as Alzheimer’s disease, Parkinson’s disease and Huntington’s disease.

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In a study published in the online version of Neurobiology of Disease, the team both confirmed the importance of this new target as well as a series of compounds that can be used to attenuate the dysregulation of one of the important cellular processes that lead to neuronal dysfunction and ultimately to brain cell death.

Although scientists are unclear about causes of ALS, they have made headway in identifying the cellular process potentially implicated in disease onset and progression. One such process which has attracted researcher interest involves the endoplasmic reticulum (ER), a component of cells that plays an important role in maintaining cell health. In collaboration with Dr. Pierre Drapeau at the University of Montreal and using worm and zebrafish models of ALS, Parker’s team not only confirmed that incapacitated ER leads to the motor neuron death typical of ALS, but also identified a series of compounds that alleviate the fatal consequences of defective ER.

“Since Riluzole, the one approved treatment compound for treating ALS, only has a modest effect on slowing disease progression, we set out to test a number of other compounds, and in so doing we discovered that they work by compensating for defective ER” explains Dr Parker. The compounds in question, Methylene blue, Salubrinal, Guanabenz and Phenazine, were each tested individually and in different combinations.

With the exception of Phenazine, these compounds have known benefits for treating neurodegenerative diseases. Parker and his team showed that each of these compounds reduces paralysis and neurodegeneration and that each acts on different parts of the ER pathway to achieve neuroprotection. More importantly, the researchers found that using these compounds in different combinations can enhance their therapeutic effects.

“These results are quite encouraging,” says Dr Parker, “and have given us a much better understanding of ER’s role in ALS as well as showing the way for improved treatments”. Parker’s team plans to test and confirm these findings with more complex animal models, a necessary step in developing medication that can be of benefit to human beings.

(Source: nouvelles.umontreal.ca)

Filed under neurodegenerative diseases Lou Gehrig's disease ALS neuronal dysfunction cell death endoplasmic reticulum neuroscience science

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Going Places: Rat Brain ‘GPS’ Maps Routes to Rewards

Research has implications for understanding memory and imagination

While studying rats’ ability to navigate familiar territory, Johns Hopkins scientists found that one particular brain structure uses remembered spatial information to imagine routes the rats then follow. Their discovery has implications for understanding why damage to that structure, called the hippocampus, disrupts specific types of memory and learning in people with Alzheimer’s disease and age-related cognitive decline. And because these mental trajectories guide the rats’ behavior, the research model the scientists developed may be useful in future studies on higher-level tasks, such as decision-making.

The details of their work were published online in the journal Nature on April 17.

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“For the first time, we believe we have evidence that before a rat returns to an important place, it actually plans out its path,” says David Foster, Ph.D., assistant professor of neuroscience at the Johns Hopkins University School of Medicine. “The rat finds that location in its mind’s eye and knows how to get there.”

Foster and his team found that, at least for the purposes of navigation, the “mind’s eye” is located in the hippocampus, which is composed of two banana-shaped segments under the cerebral cortex on both sides of the brain. It is best known for creating memories. In people with Alzheimer’s, it is one of the first parts of the brain to sustain damage.

The Foster lab experiments focused on a group of neurons in the hippocampus called place cells because they are known to fire when animals are at a given location within a given environment. What was not known, Foster says, was how and when the brain uses that information.

By miniaturizing an existing technology, Foster and a postdoc in his lab, Brad Pfeiffer, Ph.D., were able to implant 20 microwires into each side of the hippocampus of four rats. The tiny wires let them record electrical activity from as many as 250 individual place cells at the same time, more than ever achieved before.

Over a two-week training period, the rats became familiar with the testing area which was surrounded by a variety of objects, so that the rats could tell where they were in relation to the objects outside. The space was 2 meters square with 36 tiny “dishes” placed at regular intervals in a grid. A single dish at a time would be filled with the rats’ reward: liquid chocolate.

The rats’ navigation tests involved as many as 40 sets of alternating “odd” and “even” trials per day. The odd trials required the rats to “forage” through the arena to find a chocolate-filled dish in a random location; the even trials required the rats to return each time to a “home” dish to receive their reward. While the rats fulfilled their tasks, the researchers recorded the firing of their place cells.

They found that as a rat travels randomly through the box without knowing where it needs to go, different combinations of place cells fire at each location along its path. The same set of cells fires every time the rat travels the same spot. These unique combinations of firings “mark” each spot in the rat’s brain and can be reconstructed into what seems like a virtual map, when needed.

When a rat is about to go to a specific location, e.g., “home,” place cells in its hippocampus fire in a sequence that creates a predictive path, which the rat then follows, somewhat like Hansel and Gretel following an imagined bread crumb trail.

Foster says that “unlike a Hansel and Gretel bread crumb trail, which only allows you to leave by the same route by which you entered, the rats’ memories of their surroundings are flexible and can be reconstructed in a way that allows them to ‘picture’ how to quickly get from point A to point B.” In order to do this, he says, the rats must already be familiar with the terrain between point A and point B, but, like a GPS, they don’t have to have previously started at point A with the goal of reaching point B.

Foster says the elderly can get lost easily, and research on aged mice shows that their place cells can fail to distinguish between different environments. His team’s research suggests that defective place cells would also affect a person’s ability to “look ahead” in their imaginations to predict a way home. Similarly, he says, higher-order brain functions, like problem solving, also require people to “look ahead” and imagine themselves in a different scenario.

“The hippocampus seems to be directing the movement of the rats, making decisions for them in real time,” says Foster. “Our model allows us to see this happening in a way that’s not been possible before. Our next question is, what will these place cells do when we put obstacles in the rats’ paths?”

Filed under cerebral cortex hippocampus cognitive decline spatial information rats neuroscience science

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Listening to leptin: Researchers identify and block protein that interferes with appetite-suppressing hormone Ever since the appetite-regulation hormone called leptin was discovered in 1994, scientists  have sought to understand the mechanisms that control its action. It was known that leptin was made by fat cells, reduced appetite and interacted with insulin , but the precise molecular details of its function —details that might enable the creation of a new treatment for obesity — remained elusive. Now, University of Texas Medical Branch at Galveston researchers have revealed a significant part of one of those mechanisms, identifying a protein that can interfere with the brain’s response to leptin. They’ve also created a compound that blocks the protein’s action — a potential forerunner to an anti-obesity drug. In experiments with mice fed a high-fat diet, scientists from UTMB and the University of California, San Diego explored the role of the protein, known as Epac1, in blocking leptin’s activity in the brain. They found that mice genetically engineered to be unable to produce Epac1 had lower body weights, lower body fat percentages, lower blood-plasma leptin levels and better glucose tolerance than normal mice. When the researchers used a specially developed “Epac inhibitor” to treat brain-slice cultures taken from normal laboratory mice, they found elevated levels of proteins associated with greater leptin sensitivity. Similar results were seen in the genetically engineered mice that lacked the Epac1 gene. In addition, normal mice treated with the inhibitor had significantly lower levels of leptin in their blood plasma — an indication that Epac1 also affected their leptin levels. “We found that we can increase leptin sensitivity by creating mice that lack the genes for Epac1 or through a pharmacological intervention with our Epac inhibitor,” said UTMB professor Xiaodong Cheng, lead author of a paper on the study that recently appeared on the cover of Molecular and Cellular Biology. “The knockout mice gave us a way to tease out the function of the protein, and the inhibitor served as a pharmacological probe that allowed us to manipulate these molecules in the cells.” Cheng and his colleagues suspected a connection between Epac1 and leptin because Epac1 is activated by cyclic AMP, a signaling molecule linked to metabolism and leptin production and secretion. Cyclic AMP is tied to a multitude of other cell signaling processes, many of which are targeted by current drugs. Cheng believes that understanding how it acts through Epac1 (and another form of the protein called Epac2) will also generate new pharmaceutical possibilities — possibly including a drug therapy that will help fight obesity and diabetes. “We refer to these Epac inhibitors as pharmacological probes, and while they are still far away from drugs, pharmaceutical intervention is always our eventual goal,” Cheng said. “We were the first to develop Epac inhibitors, and now we’re working very actively with Dr. Jia Zhou, a UTMB medicinal chemist, to modify them and improve their properties. In addition, we are collaborating with colleagues at the NIH National Center for Advancing Translational Sciences in searching for more potent and selective pharmacological probes for Epac proteins.”

Listening to leptin: Researchers identify and block protein that interferes with appetite-suppressing hormone

Ever since the appetite-regulation hormone called leptin was discovered in 1994, scientists  have sought to understand the mechanisms that control its action. It was known that leptin was made by fat cells, reduced appetite and interacted with insulin , but the precise molecular details of its function —details that might enable the creation of a new treatment for obesity — remained elusive.

Now, University of Texas Medical Branch at Galveston researchers have revealed a significant part of one of those mechanisms, identifying a protein that can interfere with the brain’s response to leptin. They’ve also created a compound that blocks the protein’s action — a potential forerunner to an anti-obesity drug.

In experiments with mice fed a high-fat diet, scientists from UTMB and the University of California, San Diego explored the role of the protein, known as Epac1, in blocking leptin’s activity in the brain. They found that mice genetically engineered to be unable to produce Epac1 had lower body weights, lower body fat percentages, lower blood-plasma leptin levels and better glucose tolerance than normal mice.

When the researchers used a specially developed “Epac inhibitor” to treat brain-slice cultures taken from normal laboratory mice, they found elevated levels of proteins associated with greater leptin sensitivity. Similar results were seen in the genetically engineered mice that lacked the Epac1 gene. In addition, normal mice treated with the inhibitor had significantly lower levels of leptin in their blood plasma — an indication that Epac1 also affected their leptin levels.

“We found that we can increase leptin sensitivity by creating mice that lack the genes for Epac1 or through a pharmacological intervention with our Epac inhibitor,” said UTMB professor Xiaodong Cheng, lead author of a paper on the study that recently appeared on the cover of Molecular and Cellular Biology. “The knockout mice gave us a way to tease out the function of the protein, and the inhibitor served as a pharmacological probe that allowed us to manipulate these molecules in the cells.”

Cheng and his colleagues suspected a connection between Epac1 and leptin because Epac1 is activated by cyclic AMP, a signaling molecule linked to metabolism and leptin production and secretion. Cyclic AMP is tied to a multitude of other cell signaling processes, many of which are targeted by current drugs. Cheng believes that understanding how it acts through Epac1 (and another form of the protein called Epac2) will also generate new pharmaceutical possibilities — possibly including a drug therapy that will help fight obesity and diabetes.

“We refer to these Epac inhibitors as pharmacological probes, and while they are still far away from drugs, pharmaceutical intervention is always our eventual goal,” Cheng said. “We were the first to develop Epac inhibitors, and now we’re working very actively with Dr. Jia Zhou, a UTMB medicinal chemist, to modify them and improve their properties. In addition, we are collaborating with colleagues at the NIH National Center for Advancing Translational Sciences in searching for more potent and selective pharmacological probes for Epac proteins.”

Filed under leptin obesity appetite regulation Epac1 protein Epac inhibitor neuroscience science

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Family history of Alzheimer’s associated with abnormal brain pathology

Close family members of people with Alzheimer’s disease are more than twice as likely as those without a family history to develop silent buildup of brain plaques associated with Alzheimer’s disease, according to researchers at Duke Medicine.

The study, published online in the journal PLOS ONE on April 17, 2013, confirms earlier findings on a known genetic variation that increases one’s risk for Alzheimer’s, and raises new questions about other genetic factors involved in the disease that have yet to be identified.

An estimated 25 million people worldwide have Alzheimer’s disease, and the number is expected to triple by 2050. More than 95 percent of these individuals have late-onset Alzheimer’s, which usually occurs after the age of 65. Research has shown that Alzheimer’s begins years to decades before it is diagnosed, with changes to the brain measurable through a variety of tests.

Family history is a known risk factor and predictor of late-onset Alzheimer’s disease, and studies suggest a two- to four-fold greater risk for Alzheimer’s in individuals with a mother, father, brother or sister who develop the disease. These first-degree relatives share roughly 50 percent of their genes with another member of their family. Common genetic variations, including changes to the APOE gene, account for around 50 percent of the heritability of Alzheimer’s, but the disease’s other genetic roots are still unexplained.

“In this study, we sought to understand whether simply having a positive family history, in otherwise normal or mildly forgetful people, was enough to trigger silent buildup of Alzheimer’s plaques and shrinkage of memory centers,” said senior author P. Murali Doraiswamy, professor of psychiatry and medicine at Duke.

Duke neuroscience research trainee Erika J. Lampert, Doraiswamy and colleagues analyzed data from 257 adults, ages 55 to 89, both cognitively healthy and with varying levels of impairment. The participants were part of the Alzheimer’s Disease Neuroimaging Initiative, a national study working to define the progression of Alzheimer’s through biomarkers.

The researchers looked at participants’ age, gender and family history of the disease, with a positive family history defined as having a parent or sibling with Alzheimer’s. This information was compared with cognitive assessments and other biological tests, including APOE genotyping, MRI scans measuring hippocampal volume, and studies of three different pathologic markers (Aβ42, t-tau, and t-tau/Aβ42 ratio) found in cerebrospinal fluid.

As expected, the researchers found that a variation in the APOE gene associated with a greater risk and earlier onset of Alzheimer’s was overrepresented in participants with a family history of the disease. However, other biological differences were also seen in those with a family history, suggesting that unidentified genetic factors may influence the disease’s development before the onset of dementia.

Nearly half of all healthy people with a positive family history would have met the criteria for preclinical Alzheimer’s disease based on measurements of their cerebrospinal fluid, but only about 20 percent of those without a family history would have met such criteria.

“We already knew that family history increases one’s risk for developing Alzheimer’s, but we now are showing that people with a positive family history may also have higher levels of Alzheimer’s pathology earlier, which could be a reason why they experience a faster cognitive decline than those without a family history,” Lampert said.

The findings may influence the design of future studies developing new diagnostic tests for Alzheimer’s, as researchers may choose to exclude those with a positive family history – a group that has historically volunteered to participate in studies to better understand the disease – as healthy controls, given that they are more likely to develop Alzheimer’s pathology.

“Our study shows the power of a simple one-minute questionnaire about family history to predict silent brain changes,” Doraiswamy said. “In the absence of full understanding of all genetic risks for late-onset Alzheimer’s, family history information can serve as a risk stratification tool for prevention research and personalizing care.” He encouraged those with a known positive family history to seek out clinical trials specific to preventing the disease.

(Source: dukehealth.org)

Filed under alzheimer's disease family history APOE gene memory dementia neuroscience science

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Scientists reverse memory loss in animal brain cells Neuroscientists at The University of Texas Health Science Center at Houston (UTHealth) have taken a major step in their efforts to help people with memory loss tied to brain disorders such as Alzheimer’s disease. Using sea snail nerve cells, the scientists reversed memory loss by determining when the cells were primed for learning. The scientists were able to help the cells compensate for memory loss by retraining them through the use of optimized training schedules. Findings of this proof-of-principle study appear in the April 17 issue of The Journal of Neuroscience. “Although much works remains to be done, we have demonstrated the feasibility of our new strategy to help overcome memory deficits,” said John “Jack” Byrne, Ph.D., the study’s senior author, as well as director of the W.M. Keck Center for the Neurobiology of Learning and Memory and chairman of the Department of Neurobiology and Anatomy at the UTHealth Medical School. This latest study builds on Byrne’s 2012 investigation that pioneered this memory enhancement strategy. The 2012 study showed a significant increase in long-term memory in healthy sea snails called Aplysia californica, an animal that has a simple nervous system, but with cells having properties similar to other more advanced species including humans. Yili Zhang, Ph.D., the study’s co-lead author and a research scientist at the UTHealth Medical School, has developed a sophisticated mathematical model that can predict when the biochemical processes in the snail’s brain are primed for learning. Her model is based on five training sessions scheduled at different time intervals ranging from 5 to 50 minutes. It can generate 10,000 different schedules and identify the schedule most attuned to optimum learning. “The logical follow-up question was whether you could use the same strategy to overcome a deficit in memory,” Byrne said. “Memory is due to a change in the strength of the connections among neurons. In many diseases associated with memory deficits, the change is blocked.” To test whether their strategy would help with memory loss, Rong-Yu Liu, Ph.D., co-lead author and senior research scientist at the UTHealth Medical School, simulated a brain disorder in a cell culture by taking sensory cells from the sea snails and blocking the activity of a gene that produces a memory protein. This resulted in a significant impairment in the strength of the neurons’ connections, which is responsible for long-term memory. To mimic training sessions, cells were administered a chemical at intervals prescribed by the mathematical model. After five training sessions, which like the earlier study were at irregular intervals, the strength of the connections returned to near normal in the impaired cells. “This methodology may apply to humans if we can identify the same biochemical processes in humans. Our results suggest a new strategy for treatments of cognitive impairment.  Mathematical models might help design therapies that optimize the combination of training protocols with traditional drug treatments,” Byrne said. He added, “Combining these two could enhance the effectiveness of the latter while compensating at least in part for any limitations or undesirable side effects of drugs. These two approaches are likely to be more effective together than separately and may have broad generalities in treating individuals with learning and memory deficits.” (Image courtesy: UC Berkeley)

Scientists reverse memory loss in animal brain cells

Neuroscientists at The University of Texas Health Science Center at Houston (UTHealth) have taken a major step in their efforts to help people with memory loss tied to brain disorders such as Alzheimer’s disease.

Using sea snail nerve cells, the scientists reversed memory loss by determining when the cells were primed for learning. The scientists were able to help the cells compensate for memory loss by retraining them through the use of optimized training schedules. Findings of this proof-of-principle study appear in the April 17 issue of The Journal of Neuroscience.

“Although much works remains to be done, we have demonstrated the feasibility of our new strategy to help overcome memory deficits,” said John “Jack” Byrne, Ph.D., the study’s senior author, as well as director of the W.M. Keck Center for the Neurobiology of Learning and Memory and chairman of the Department of Neurobiology and Anatomy at the UTHealth Medical School.

This latest study builds on Byrne’s 2012 investigation that pioneered this memory enhancement strategy. The 2012 study showed a significant increase in long-term memory in healthy sea snails called Aplysia californica, an animal that has a simple nervous system, but with cells having properties similar to other more advanced species including humans.

Yili Zhang, Ph.D., the study’s co-lead author and a research scientist at the UTHealth Medical School, has developed a sophisticated mathematical model that can predict when the biochemical processes in the snail’s brain are primed for learning.

Her model is based on five training sessions scheduled at different time intervals ranging from 5 to 50 minutes. It can generate 10,000 different schedules and identify the schedule most attuned to optimum learning.

“The logical follow-up question was whether you could use the same strategy to overcome a deficit in memory,” Byrne said. “Memory is due to a change in the strength of the connections among neurons. In many diseases associated with memory deficits, the change is blocked.”

To test whether their strategy would help with memory loss, Rong-Yu Liu, Ph.D., co-lead author and senior research scientist at the UTHealth Medical School, simulated a brain disorder in a cell culture by taking sensory cells from the sea snails and blocking the activity of a gene that produces a memory protein. This resulted in a significant impairment in the strength of the neurons’ connections, which is responsible for long-term memory.

To mimic training sessions, cells were administered a chemical at intervals prescribed by the mathematical model. After five training sessions, which like the earlier study were at irregular intervals, the strength of the connections returned to near normal in the impaired cells.

“This methodology may apply to humans if we can identify the same biochemical processes in humans. Our results suggest a new strategy for treatments of cognitive impairment.  Mathematical models might help design therapies that optimize the combination of training protocols with traditional drug treatments,” Byrne said.

He added, “Combining these two could enhance the effectiveness of the latter while compensating at least in part for any limitations or undesirable side effects of drugs. These two approaches are likely to be more effective together than separately and may have broad generalities in treating individuals with learning and memory deficits.”

(Image courtesy: UC Berkeley)

Filed under alzheimer's disease memory loss animal model nerve cells aplysia memory neuroscience science

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Detecting Autism From Brain Activity Neuroscientists from Case Western Reserve University School of Medicine and the University of Toronto have developed an efficient and reliable method of analyzing brain activity to detect autism in children. Their findings appear today in the online journal PLOS ONE. The researchers recorded and analyzed dynamic patterns of brain activity with magnetoencephalography (MEG) to determine the brain’s functional connectivity – that is, its communication from one region to another. MEG measures magnetic fields generated by electrical currents in neurons of the brain. Roberto Fernández Galán, PhD, an assistant professor of neurosciences at Case Western Reserve and an electrophysiologist seasoned in theoretical physics led the research team that detected autism spectrum disorder (ASD) with 94 percent accuracy. The new analytic method offers an efficient, quantitative way of confirming a clinical diagnosis of autism. “We asked the question, ‘Can you distinguish an autistic brain from a non-autistic brain simply by looking at the patterns of neural activity?’ and indeed, you can,” Galán said. “This discovery opens the door to quantitative tools that complement the existing diagnostic tools for autism based on behavioral tests.” In a study of 19 children—nine with ASD—141 sensors tracked the activity of each child’s cortex. The sensors recorded how different regions interacted with each other while at rest, and compared the brain’s interactions of the control group to those with ASD. Researchers found significantly stronger connections between rear and frontal areas of the brain in the ASD group; there was an asymmetrical flow of information to the frontal region, but not vice versa. The new insight into the directionality of the connections may help identify anatomical abnormalities in ASD brains. Most current measures of functional connectivity do not indicate the interactions’ directionality. “It is not just who is connected to whom, but rather who is driving whom,” Galán said. Their approach also allows them to measure background noise, or the spontaneous input driving the brain’s activity while at rest. A spatial map of these inputs demonstrated there was more complexity and structure in the control group than the ASD group, which had less variety and intricacy. This feature offered better discrimination between the two groups, providing an even stronger measure of criteria than functional connectivity alone, with 94 percent accuracy. Case Western Reserve’s Office of Technology Transfer has filed a provisional patent application for the analysis’ algorithm, which investigates the brain’s activity at rest. Galán and colleagues hope to collaborate with others in the autism field with emphasis on translational and clinical research. (Image: SPL)

Detecting Autism From Brain Activity

Neuroscientists from Case Western Reserve University School of Medicine and the University of Toronto have developed an efficient and reliable method of analyzing brain activity to detect autism in children. Their findings appear today in the online journal PLOS ONE.

The researchers recorded and analyzed dynamic patterns of brain activity with magnetoencephalography (MEG) to determine the brain’s functional connectivity – that is, its communication from one region to another. MEG measures magnetic fields generated by electrical currents in neurons of the brain.

Roberto Fernández Galán, PhD, an assistant professor of neurosciences at Case Western Reserve and an electrophysiologist seasoned in theoretical physics led the research team that detected autism spectrum disorder (ASD) with 94 percent accuracy. The new analytic method offers an efficient, quantitative way of confirming a clinical diagnosis of autism.

“We asked the question, ‘Can you distinguish an autistic brain from a non-autistic brain simply by looking at the patterns of neural activity?’ and indeed, you can,” Galán said. “This discovery opens the door to quantitative tools that complement the existing diagnostic tools for autism based on behavioral tests.”

In a study of 19 children—nine with ASD—141 sensors tracked the activity of each child’s cortex. The sensors recorded how different regions interacted with each other while at rest, and compared the brain’s interactions of the control group to those with ASD. Researchers found significantly stronger connections between rear and frontal areas of the brain in the ASD group; there was an asymmetrical flow of information to the frontal region, but not vice versa.

The new insight into the directionality of the connections may help identify anatomical abnormalities in ASD brains. Most current measures of functional connectivity do not indicate the interactions’ directionality.

“It is not just who is connected to whom, but rather who is driving whom,” Galán said.

Their approach also allows them to measure background noise, or the spontaneous input driving the brain’s activity while at rest. A spatial map of these inputs demonstrated there was more complexity and structure in the control group than the ASD group, which had less variety and intricacy. This feature offered better discrimination between the two groups, providing an even stronger measure of criteria than functional connectivity alone, with 94 percent accuracy.

Case Western Reserve’s Office of Technology Transfer has filed a provisional patent application for the analysis’ algorithm, which investigates the brain’s activity at rest. Galán and colleagues hope to collaborate with others in the autism field with emphasis on translational and clinical research.

(Image: SPL)

Filed under brain activity autism ASD magnetoencephalography autistic brain neuroscience science

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Why Don’t Men Understand Women? Altered Neural Networks for Reading the Language of Male and Female Eyes Men are traditionally thought to have more problems in understanding women compared to understanding other men, though evidence supporting this assumption remains sparse. Recently, it has been shown, however, that meńs problems in recognizing women’s emotions could be linked to difficulties in extracting the relevant information from the eye region, which remain one of the richest sources of social information for the attribution of mental states to others. To determine possible differences in the neural correlates underlying emotion recognition from female, as compared to male eyes, a modified version of the Reading the Mind in the Eyes Test in combination with functional magnetic resonance imaging (fMRI) was applied to a sample of 22 participants. We found that men actually had twice as many problems in recognizing emotions from female as compared to male eyes, and that these problems were particularly associated with a lack of activation in limbic regions of the brain (including the hippocampus and the rostral anterior cingulate cortex). Moreover, men revealed heightened activation of the right amygdala to male stimuli regardless of condition (sex vs. emotion recognition). Thus, our findings highlight the function of the amygdala in the affective component of theory of mind (ToM) and in empathy, and provide further evidence that men are substantially less able to infer mental states expressed by women, which may be accompanied by sex-specific differences in amygdala activity.

Why Don’t Men Understand Women? Altered Neural Networks for Reading the Language of Male and Female Eyes

Men are traditionally thought to have more problems in understanding women compared to understanding other men, though evidence supporting this assumption remains sparse. Recently, it has been shown, however, that meńs problems in recognizing women’s emotions could be linked to difficulties in extracting the relevant information from the eye region, which remain one of the richest sources of social information for the attribution of mental states to others. To determine possible differences in the neural correlates underlying emotion recognition from female, as compared to male eyes, a modified version of the Reading the Mind in the Eyes Test in combination with functional magnetic resonance imaging (fMRI) was applied to a sample of 22 participants. We found that men actually had twice as many problems in recognizing emotions from female as compared to male eyes, and that these problems were particularly associated with a lack of activation in limbic regions of the brain (including the hippocampus and the rostral anterior cingulate cortex). Moreover, men revealed heightened activation of the right amygdala to male stimuli regardless of condition (sex vs. emotion recognition). Thus, our findings highlight the function of the amygdala in the affective component of theory of mind (ToM) and in empathy, and provide further evidence that men are substantially less able to infer mental states expressed by women, which may be accompanied by sex-specific differences in amygdala activity.

Filed under emotions emotion recognition limbic system amygdala empathy men women psychology neuroscience science

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The Shrinking of the Hobbit’s Brain Where do Hobbits come from? No, not the little humanoids in the J. R. R. Tolkien books, but Homo floresiensis, the 1-meter-tall human with the chimp-sized brain that lived on the Indonesian island of Flores between 90,000 and 13,000 years ago. There are two main hypotheses: either the creature downsized from H. erectus, a human ancestor that lived in Africa and Asia and that is known to have made it to Flores about 800,000 years ago and may have shrunk when it got there—a case of so-called “insular dwarfism” often seen in other animals that get small when they take up residence on islands. Or it evolved from an even earlier, smaller-brained ancestor, such as the early human H. habilis or an australopithecine like Lucy, that somehow made it to Flores from Africa. The insular dwarfism hypothesis had fallen out of favor recently, however, because many researchers thought that the Hobbit’s brain, often estimated at 400 cubic centimeters in volume, was too small to have evolved from the larger H. erectus brain, which was at least twice as big. But a new study, published online today in the Proceedings of the Royal Society B, finds from CT scans of the Hobbit’s brain that it was actually about 426 cubic centimeters in volume. The team calculates that this is big enough to make the island dwarfism hypothesis considerably more plausible once the body size differences between the Hobbit and H. erectus—which was nearly twice as tall—are adjusted for.

The Shrinking of the Hobbit’s Brain

Where do Hobbits come from? No, not the little humanoids in the J. R. R. Tolkien books, but Homo floresiensis, the 1-meter-tall human with the chimp-sized brain that lived on the Indonesian island of Flores between 90,000 and 13,000 years ago. There are two main hypotheses: either the creature downsized from H. erectus, a human ancestor that lived in Africa and Asia and that is known to have made it to Flores about 800,000 years ago and may have shrunk when it got there—a case of so-called “insular dwarfism” often seen in other animals that get small when they take up residence on islands. Or it evolved from an even earlier, smaller-brained ancestor, such as the early human H. habilis or an australopithecine like Lucy, that somehow made it to Flores from Africa. The insular dwarfism hypothesis had fallen out of favor recently, however, because many researchers thought that the Hobbit’s brain, often estimated at 400 cubic centimeters in volume, was too small to have evolved from the larger H. erectus brain, which was at least twice as big. But a new study, published online today in the Proceedings of the Royal Society B, finds from CT scans of the Hobbit’s brain that it was actually about 426 cubic centimeters in volume. The team calculates that this is big enough to make the island dwarfism hypothesis considerably more plausible once the body size differences between the Hobbit and H. erectus—which was nearly twice as tall—are adjusted for.

Filed under brain size homo floresiensis CT scans insular dwarfism evolution neuroscience science

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Drug Could Improve Working Memory of People with Autism People with an Autism Spectrum Disorder (ASD) often have trouble communicating and interacting with others because they process language, facial expressions and social cues differently. Previously, researchers found that propranolol, a drug commonly used to treat high blood pressure, anxiety and panic, could improve the language abilities and social functioning of people with an ASD. Now, University of Missouri investigators say the prescription drug also could help improve the working memory abilities of individuals with autism. Working memory represents individuals’ ability to hold and manipulate a small amount of information for a short period; it allows people to remember directions, complete puzzles and follow conversations. Neurologist David Beversdorf and research neuropsychologist Shawn Christ found that propranolol improves the working memory performance of people with an ASD. “Seeing a tiger might signal a fight or flight response. Nowadays, a stressor such as taking an exam could generate the same response, which is not helpful,” said Beversdorf, an associate professor in the Departments of Radiology and Neurology in the MU School of Medicine. “Propranolol works by calming those nervous responses, which is why some people benefit from taking the drug to reduce anxiety.” Propranolol increased working memory performance in a sample of 14 young adult patients of the MU Thompson Center for Autism and Neurodevelopmental Disorders but had little to no effect on a group of 13 study participants who do not have autism. The researchers do not recommend that doctors prescribe propranolol solely to improve working memory in individuals with an ASD, but patients who already take the prescription drug might benefit. “People with an Autism Spectrum Disorder who are already being prescribed propranolol for a different reason, such as anxiety, might also see an improvement in working memory,” said Christ, an associate professor in the Department of Psychological Sciences in the MU College of Arts and Science. Future research will incorporate clinical trials to assess further the relationship between cognitive and behavioral functioning and connectivity among various regions of the brain. The study, “Noradrenergic Moderation of Working Memory Impairments in Adults with Autism Spectrum Disorder,” was published in the Journal of the International Neuropsychological Society. Kimberly Bodner, a psychological sciences doctoral student at MU, and Sanjida Saklayen from the Ohio State University College of Medicine co-authored the study.

Drug Could Improve Working Memory of People with Autism

People with an Autism Spectrum Disorder (ASD) often have trouble communicating and interacting with others because they process language, facial expressions and social cues differently. Previously, researchers found that propranolol, a drug commonly used to treat high blood pressure, anxiety and panic, could improve the language abilities and social functioning of people with an ASD. Now, University of Missouri investigators say the prescription drug also could help improve the working memory abilities of individuals with autism.

Working memory represents individuals’ ability to hold and manipulate a small amount of information for a short period; it allows people to remember directions, complete puzzles and follow conversations. Neurologist David Beversdorf and research neuropsychologist Shawn Christ found that propranolol improves the working memory performance of people with an ASD.

“Seeing a tiger might signal a fight or flight response. Nowadays, a stressor such as taking an exam could generate the same response, which is not helpful,” said Beversdorf, an associate professor in the Departments of Radiology and Neurology in the MU School of Medicine. “Propranolol works by calming those nervous responses, which is why some people benefit from taking the drug to reduce anxiety.”

Propranolol increased working memory performance in a sample of 14 young adult patients of the MU Thompson Center for Autism and Neurodevelopmental Disorders but had little to no effect on a group of 13 study participants who do not have autism. The researchers do not recommend that doctors prescribe propranolol solely to improve working memory in individuals with an ASD, but patients who already take the prescription drug might benefit.

“People with an Autism Spectrum Disorder who are already being prescribed propranolol for a different reason, such as anxiety, might also see an improvement in working memory,” said Christ, an associate professor in the Department of Psychological Sciences in the MU College of Arts and Science.

Future research will incorporate clinical trials to assess further the relationship between cognitive and behavioral functioning and connectivity among various regions of the brain.

The study, “Noradrenergic Moderation of Working Memory Impairments in Adults with Autism Spectrum Disorder,” was published in the Journal of the International Neuropsychological Society. Kimberly Bodner, a psychological sciences doctoral student at MU, and Sanjida Saklayen from the Ohio State University College of Medicine co-authored the study.

Filed under autism ASD working memory propranolol cognitive functioning neuroscience science

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Stimulating the Brain Blunts Cigarette Craving

Cigarette smoking is the leading cause of preventable deaths globally. Unfortunately smoking cessation is difficult, with more than 90% of attempts to quit resulting in relapse.

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(Image: Jupiterimages)

There are a growing number of available methods that can be tried in the effort to reduce smoking, including medications, behavioral therapies, hypnosis, and even acupuncture. All attempt to alter brain function or behavior in some way.

A new study published in Biological Psychiatry now reports that a single 15-minute session of high frequency transcranial magnetic stimulation (TMS) over the prefrontal cortex temporarily reduced cue-induced smoking craving in nicotine-dependent individuals.

Nicotine activates the dopamine system and reward-related regions in the brain. Nicotine withdrawal naturally results in decreased activity of these regions, which has been closely associated with craving, relapse, and continued nicotine consumption.

One of the critical reward-related regions is the dorsolateral prefrontal cortex, which can be targeted using a brain stimulation technology called transcranial magnetic stimulation. Transcranial magnetic stimulation is a non-invasive procedure that uses magnetic fields to stimulate nerve cells. It does not require sedation or anesthesia and so patients remain awake, reclined in a chair, while treatment is administered through coils placed near the forehead.

Dr. Xingbao Li and colleagues at Medical University of South Carolina examined cravings triggered by smoking cues in 16 nicotine-dependent volunteers who received one session each of high frequency or sham repetitive transcranial magnetic stimulation applied over the dorsolateral prefrontal cortex. This design allowed the researchers to ferret out the effects of the real versus the sham stimulation, similar to how placebo pills are used in evaluating the effectiveness and safety of new medications.

They found that craving induced by smoking cues was reduced after participants received real stimulation. They also report that the reduction in cue-induced craving was positively correlated with level of nicotine dependence; in other words, the TMS-induced craving reductions were greater in those with higher levels of nicotine use.

Dr. John Krystal, Editor of Biological Psychiatry, commented, “One of the elegant aspects of this study is that it suggests that specific manipulations of particular brain circuits may help to protect smokers and possibly people with other addictions from relapsing.”

"While this was only a temporary effect, it raises the possibility that repeated TMS sessions might ultimately be used to help smokers quit smoking. TMS as used in this study is safe and is already FDA approved for treating depression. This finding opens the way for further exploration of the use of brain stimulation techniques in smoking cessation treatment," said Li.

(Source: alphagalileo.org)

Filed under smoking tobacco smoking transcranial magnetic stimulation prefrontal cortex brain stimulation neuroscience science

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