Posts tagged psychology

By Makini Brice | July 26, 2012

Scientists were surprised, expecting the areas of the brain to age more slowly, or even delayed, than those of men.

Photo: Microsoft

Even though the gap is closing now in many high-income countries, on average, women tend to live longer lives than men do. Despite – or perhaps because of – women’s physical longevity, women tend to battle cognitive decline in much greater numbers than men do. In fact, women are more likely to suffer from various types of dementia, including the much-maligned Alzheimer’s disease. Now researchers think that they have an answer to the cause of this double-edged sword: stress. Specifically, stress ages women’s brains more quickly than it does men.

Scientists, and every-day observers, have noted that some body parts age at different rates than others do. As people become older, some genes become more active while others become less so. These changes in activity can be monitored through a “transcriptome,” which collects data on all the RNA – the transcripts that carry DNA’s instructions to cells. A multinational team from Australia, China, Germany, and the United States set out to analyze the transcriptomes for 55 different men and women of various ages.

The researchers were fascinated by what they found. According to the abstract of their article published in Aging Cell, “In the superior frontal gyrus (SFG), a part of the prefrontal cortex, we observed manifest differences between the two sexes in the timing of age-related changes, i.e.sexual heterochrony. Intriguingly, age-related expression changes predominantly occurred earlier, or at a faster pace, in females compared to males. These changes included decreased energy production and neural function, and up-regulation of the immune response, all major features of brain aging.”

In other words, researchers found that the brains of women aged more quickly than those of men, especially in the prefrontal cortex. Scientists were surprised, expecting the areas of the brain to age more slowly, or even delayed, than those of men.

In the superior frontal gyrus, researchers found 667 genes that were expressed differently by gender during the aging process. Within that number, 98 percent were associated with faster aging in women.

Scientists were not convinced that the reason lay in biological differences. In fact, since only half of women displayed accelerated aging, they were convinced that the difference was environmental. Researchers theorize that stress is the difference-maker, and that it affects women’s brains more severely than it does men. While a researcher unaffiliated with the study said that the difference could also be caused by inflammation,

Mehmet Somel and his team have conducted similar research on monkeys that confirms their stress theory.

Source: Medical Daily

July 27, 2012 

(Medical Xpress) — Johns Hopkins scientists have discovered a “scaffolding” protein that holds together multiple elements in a complex system responsible for regulating pain, mental illnesses and other complex neurological problems.

Preso1 (green) and mGluR5 (red) appear in the same location inside a neuron.

The finding, published in the May 6 issue of Nature Neuroscience, could give researchers a new target for drugs to treat these often-intractable conditions.

The discovery, detailed in a study led by neuroscience professor Paul Worley, M.D., of the Johns Hopkins University School of Medicine, focuses on a family of proteins called group 1 metabotropic glutamate receptors (mGluRs) that lie on the surfaces of nerve cells. When these receptors lock in glutamate, a chemical that neurons use to communicate, it encourages neurons to fire.

Without a way to turn off these receptors, neurons would remain active indefinitely, keeping pain and other responses going long after they’re useful. Previous research suggested that these mGluRs need to bind to another protein called Homer to shut down, and that this binding is stronger after other molecules called protein kinases modify the receptors. However, Worley explains, thus far it’s been unclear exactly how all these different players come together.

Seeking the mechanism behind this phenomenon, Worley and his colleagues started with a series of experiments to see what other proteins the mGluRs and Homer were binding with in rat brains. Their search turned up a third protein called Preso1, which bound to both mGluRs and Homer. A search in genetic databases shows that the gene responsible for making Preso1 is present in animals ranging from fruit flies to people, highlighting its importance in a wide variety of creatures.

To figure out what Preso1 does, the researchers performed another series of experiments to examine behavior of neurons that produced both mGluRs and Homer. They found that when these neurons also expressed Preso1, the mGluRs bound Homer more efficiently, suggesting that Preso1 might somehow increase modification by protein kinases.

Worley’s team received another clue when they found that protein kinases also bind to Preso1.

Genetically modifying mice so that they don’t make any Preso1, the researchers found that binding between mGluRs and Homer in these animals’ neurons was greatly reduced compared to normal mice.

Additionally, when the researchers injected the modified mice with a chemical that causes pain and inflammation, the animals had a significantly greater and longer-lasting response compared to regular mice. A final experiment showed that neurons taken from the modified animals were significantly more responsive to the neurotransmitter glutamate. When the researchers added Preso1 to the cell cultures, this increased activity disappeared, suggesting that Preso1 is pivotal for mGluRs to signal properly.

Taken together, Worley explains, the findings suggest that Preso1 appears to gather all the important elements in this system — Homer, protein kinases and mGluRs — bringing them all together to coordinate the activation and deactivation of the mGluRs.

With Preso1 so pivotal for regulating group 1 mGluR activity, it could prove a useful new target for drugs to treat a variety of health problems in which these receptors are thought to play a role, including chronic pain, schizophrenia, Alzheimer’s disease, and fragile X syndrome, Worley says.

"Because mGluRs play so many important roles in the brain for so many different mental and neurological health conditions, knowledge of their regulatory mechanisms is extremely important. But we really don’t know how they work in great detail," he says. "You need to know all the players before you can understand the system. Here, we’ve identified an important player that no one had previously known had existed. Preso1 and Homer appear essential for desensitization of mGluR signaling, much like beta-adrenergic receptor kinase and arrestin are important for desensitization of adrenergic and opiate receptors."

Provided by Johns Hopkins University

Source: medicalxpress.com

July 27, 2012

Anyone that has ever had trouble sleeping can attest to the difficulties at work the following day. Experts recommend eight hours of sleep per night for ideal health and productivity, but what if five to six hours of sleep is your norm? Is your work still negatively affected? A team of researchers at Brigham and Women’s Hospital (BWH) have discovered that regardless of how tired you perceive yourself to be, that lack of sleep can influence the way you perform certain tasks.

This finding is published in the July 26, 2012 online edition of The Journal of Vision.

"Our team decided to look at how sleep might affect complex visual search tasks, because they are common in safety-sensitive activities, such as air-traffic control, baggage screening, and monitoring power plant operations," explained Jeanne F. Duffy, PhD, MBA, senior author on this study and associate neuroscientist at BWH. "These types of jobs involve processes that require repeated, quick memory encoding and retrieval of visual information, in combination with decision making about the information."

Researchers collected and analyzed data from visual search tasks from 12 participants over a one month study. In the first week, all participants were scheduled to sleep 10-12 hours per night to make sure they were well-rested. For the following three weeks, the participants were scheduled to sleep the equivalent of 5.6 hours per night, and also had their sleep times scheduled on a 28-hour cycle, mirroring chronic jet lag. The research team gave the participants computer tests that involved visual search tasks and recorded how quickly the participants could find important information, and also how accurate they were in identifying it. The researchers report that the longer the participants were awake, the more slowly they identified the important information in the test. Additionally, during the biological night time, 12 a.m. -6 a.m., participants (who were unaware of the time throughout the study) also performed the tasks more slowly than they did during the daytime.

"This research provides valuable information for workers, and their employers, who perform these types of visual search tasks during the night shift, because they will do it much more slowly than when they are working during the day," said Duffy. "The longer someone is awake, the more the ability to perform a task, in this case a visual search, is hindered, and this impact of being awake is even stronger at night."

While the accuracy of the participants stayed the fairly constant, they were slower to identify the relevant information as the weeks went on. The self-ratings of sleepiness only got slightly worse during the second and third weeks on the study schedule, yet the data show that they were performing the visual search tasks significantly slower than in the first week. This finding suggests that someone’s perceptions of how tired they are do not always match their performance ability, explains Duffy.

Provided by Brigham and Women’s Hospital

Source: medicalxpress.com

July 26, 2012 By Mark Wheeler

UCLA researchers say blocking this molecule may improve and speed recovery

FINDINGS:

Researchers at UCLA have identified a novel molecule in the brain that, after stroke, blocks the formation of new connections between neurons. As a result, it limits the brain’s recovery. In a mouse model, the researchers showed that blocking this molecule—called ephrin-A5—induces axonal sprouting, that is, the growth of new connections between the brain’s neurons, or cells, and as a result promotes functional recovery.

IMPACT:

If duplicated in humans, the identification of this molecule could pave the way for a more rapid recovery from stroke and may allow a synergy with existing treatments, such as physical therapy.

UCLA AUTHOR:

Dr. S. Thomas Carmichael, professor of neurology, and colleagues

JOURNAL:       

The research appears online this week in the journal PNAS.

MORE:

Stroke is the leading cause of adult disability because of the brain’s limited capacity for repair. An important process in recovery after stroke may be in the formation of new connections, termed axonal sprouting. The adult brain inhibits axonal sprouting and the formation of these connections. In previous work the researchers found, paradoxically, that the brain sends mixed signals after a stroke—activating molecules that both stimulate and inhibit axonal sprouting. In this present work, the researchers have identified the effect of one molecule that inhibits axonal sprouting and determined the new connections in the brain that are necessary to form for recovery.

The researchers also developed a new tissue bioengineering approach for delivering drugs to the brain after stroke. This approach uses a biopolymer hydrogel, or a gel of naturally occurring brain proteins, to release neural repair molecules directly to the target region for recovery in stroke—the tissue adjacent  to the center of the stroke.

Last, the paper also shows that the more behavioral activity after stroke, such as the amount an impaired limb is used, the more new connections are directly stimulated to form in the injured brain.  This direct link between movement patterns, like those that occur in neurorehabilitation, and the formation of new brain connections, provides a biological mechanism for the effects of some forms of physical therapy after stroke.

Source: UCLA