May 9, 2014

Researchers capture handoff of tracked object between brain hemispheres

When tracking a moving object, the two halves of the human brain operate much like runners successfully passing a baton during a relay race, says a University of Oregon researcher.

In a study online ahead of print in Current Biology, electroencephalogram (EEG) measured brainwaves from healthy young adults revealed how information about an attended object — one being watched closely — moves from one brain hemisphere to the other.

Such handoffs are necessary because the human visual system is contralateral; objects on the left side of space are processed by the right hemisphere and vice versa. When objects change sides, the two hemispheres must coordinate so that the tracked object isn’t lost during the exchange.

"Attentional tracking is something we do on a regular basis when driving in traffic or walking through a crowd," said Edward K. Vogel, professor of psychology. "Our world is dynamic. We’re moving. Our eyes are moving. Objects are moving. We need to use our attention to follow objects of interest as they move so that we can predict where they are going.”

People experience a smooth and seamless visual world despite information quickly being transferred back and forth between the hemispheres. “A car in your rearview mirror that moves from one lane to the other doesn’t suddenly disappear and then reappear on the other side,” he said. “The exchange is smooth, in part, because often the hemispheres coordinate a soft handoff.”

That means, he said, that before the object crosses into the other side of space, the new hemisphere picks it up, and the old hemisphere continues to hang on to it until it crosses well into the other side of space. Both hemispheres grab hold of the object during the exchange — much like in a relay race when two runners both briefly have hold of the baton to assure it isn’t dropped.

Eventually, Vogel said, such research may help us better understand individual differences in people’s visual tracking abilities. Some people, for instance, have trouble picking up a moving vehicle seen in a rearview mirror once it enters a blind spot. “This new technique allows us to watch the brain as information about a target is handed off from one side to the other, and it may provide insights into why attention is so limited,” Vogel said.

While psychological studies have often looked at attention and awareness, there has been little focus on how the two hemispheres interact. Interestingly, Vogel said, cellphone companies have long studied a similar problem: how to best transfer a call’s signal while a customer moves from one zone of a cell tower to another.

Cellular carriers using Code Division Multiple Access (CDMA) such as Sprint and Verizon utilize a soft handoff between towers, similar to the new findings. Global System for Mobile (GSM) carriers, such as T-Mobile and ATT, use a hard handoff in which a signal leaving a tower’s coverage is rapidly shut off and then turned on by the next tower — a scenario that tended to, before the technology improved, result in more dropped calls.

"Researchers at the University of Oregon are using cutting-edge techniques to examine important mechanisms of cognitive functioning," said Kimberly Andrews Espy, vice president for research and innovation and dean of the UO Graduate School. "This research by Dr. Vogel and his team provides a window on the process of attentional tracking that furthers our understanding of how the two hemispheres of the brain work together to process visual information."

Filed under cognitive function cerebral hemispheres attentional tracking motion perception neuroscience science

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May 9, 2014

(Image caption: This ribbon diagram shows three ankyrin repeats, a common structure found in receptor proteins that sense either cold or hot temperatures. A Duke team has identified three single-point mutations that can invert temperature-sensitivity, turning a cold-sensor into a heat-sensor. All three of these mutations are located in on a single ankyrin repeat. Credit: Grandl Lab, Duke University)

Small Mutation Changes Brain Freeze to Hot Foot

Ice cream lovers and hot tea drinkers with sensitive teeth could one day have a reason to celebrate a new finding from Duke University researchers. The scientists have found a very small change in a single protein that turns a cold-sensitive receptor into one that senses heat.

Understanding sensation and pain at this level could lead to more specific pain relievers that wouldn’t affect the central nervous system, likely producing less severe side effects than existing medications, said Jorg Grandl, Ph.D., an assistant professor of neurobiology in Duke’s School of Medicine who led the research team.

Temperature-induced pain, also called thermal pain, occurs when the body’s sensory neurons come in contact with temperatures above or below a certain threshold, such as plunging a limb into freezing water.

"We want to understand how either hot or cold temperatures can activate the sensors of hot and cold temperatures in the body," Grandl said.

Previous research has identified transient receptor potential (TRP) ion channels as being highly sensitive to either cold or hot temperatures. TRP ion channels are porous proteins that play a role in initiating electrical signals by controlling the flow of charged ions across the cell membrane.

It’s still unclear how temperatures make this happen, but the Grandl team’s research reveals that single-letter changes in DNA, called point mutations, are sufficient to make cold-sensitive TRP ion channels become sensitive to hot temperatures instead.

"There is strong interest in understanding temperature-sensitive molecules from a functional perspective because they are promising targets for developing analgesic compounds to treat chronic pain," said Grandl, who is also a member of the Duke Institute for Brain Sciences. "It is something we currently do not treat well. So, one promising strategy is to stop pain where it is initially sensed — at that first molecule that functions as a sensor of pain."

In a study appearing online early May 8 in the journal Neuron, Grandl’s team focused on TRPA1, an ion channel best known as a sensor for pain caused by environmental irritants and pungent chemicals, such as mustard oil, the active compound found in wasabi.

Grandl’s colleagues, postdoctoral fellow Sairam Jabba and research technician Raman Goyal, investigated whether single-point mutations could change cold-activated mouse TRPA1 into heat-activated. They formed this hypothesis because, in some other animals, including Drosophila fruit-flies and rattlesnakes, TRPA1 is naturally heat-activated.

To identify these structures, the team created a library of 12,000 mutant clones of the cold-activated mouse TRPA1 ion channel and randomly inserted one or two point mutations into each clone. After placing single clones into the individual slots of a 384-well plate and heating it from 25 degrees Celsius to 45 C in a matter of seconds, they were able to measure the thermal sensitivity of each mutant protein.

This screening pinpointed seven clones that showed strong activation when exposed to heat. Gene sequencing of these clones revealed 12 mutations that could potentially be responsible for changing the mouse TRPA1 from cold-activated to heat-activated. Out of these 12 mutations, Jabba and Goyal identified three mutations powerful enough to individually make that switch in TRPA1.

The mutations all turned out to be located within a single small domain of the ion channel protein known as ankyrin repeat six, indicating this domain plays a role in determining cold or heat activation. Ankyrin repeats are often responsible for managing protein-to-protein interactions, but their precise function in TRPA1 had not been previously known.

Interestingly, these single-point mutations didn’t change the ion channels’ responses to chemicals, such as mustard oil.

"This was very surprising and it demonstrates that making a single-point mutation produced a profound change in the temperature sensitivity of the protein, but it did not affect the chemical sensitivity," Grandl said. "It shows these mechanisms are to some degree distinct."

Grandl said that taken together, the findings also suggest that the effectiveness of such a small mutation might have been key to a single ancestral ion channel evolving into the wide diversity of temperature-activated ion channels we see today.

Filed under ion channels temperature thermal pain sensory neurons mutations neuroscience science

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May 9, 2014

Study helps explain why MS is more common in women

A newly identified difference between the brains of women and men with multiple sclerosis (MS) may help explain why so many more women than men get the disease, researchers at Washington University School of Medicine in St. Louis report.

In recent years, the diagnosis of MS has increased more rapidly among women, who get the disorder nearly four times more than men. The reasons are unclear, but the new study is the first to associate a sex difference in the brain with MS.

(Image caption: An image of tissue from a female brain (left) affected by multiple sclerosis (MS) shows that the brain has much higher levels of a blood vessel receptor (shown in red) than a male brain affected by MS (right). The difference could help explain why so many more women get MS. Credit: Robyn Klein)

The findings appear May 8 in The Journal of Clinical Investigation.

Studying mice and people, the researchers found that females susceptible to MS produce higher levels of a blood vessel receptor protein, S1PR2, than males and that the protein is present at even higher levels in the brain areas that MS typically damages.

“It was a ‘Bingo!’ moment – our genetic studies led us right to this receptor,” said senior author Robyn Klein, MD, PhD. “When we looked at its function in mice, we found that it can determine whether immune cells cross blood vessels into the brain. These cells cause the inflammation that leads to MS.”

An investigational MS drug currently in clinical trials blocks other receptors in the same protein family but does not affect S1PR2. Klein recommended that researchers work to develop a drug that disables S1PR2.

MS is highly unpredictable, flaring and fading at irregular intervals and producing a hodgepodge of symptoms that includes problems with mobility, vision, strength and balance. More than 2 million people worldwide have the condition.

In MS, inflammation caused by misdirected immune cells damages a protective coating that surrounds the branches of nerve cells in the brain and spinal column. This leads the branches to malfunction and sometimes causes them to wither away, disrupting nerve cell communication necessary for normal brain functions such as movement and coordination.

For the new research, Klein studied a mouse model of MS in which the females get the disease more often than the males. The scientists compared levels of gene activity in male and female brains. They also looked at gene activity in the regions of the female brain that MS damages and in other regions the disorder typically does not harm.

They identified 20 genes that were active at different levels in vulnerable female brain regions. Scientists don’t know what 16 of these genes do. Among the remaining genes, the increased activity of S1PR2 stood out because researchers knew from previous studies that the protein regulates how easy it is for cells and molecules to pass through the walls of blood vessels.

Additional experiments showed that S1PR2 opens up the blood-brain barrier, a structure in the brain’s blood vessels that tightly regulates the materials that cross into the brain and spinal fluid. This barrier normally blocks potentially harmful substances from entering the brain. Opening it up likely allows the inflammatory cells that cause MS to get into the central nervous system.

When the researchers tested brain tissue samples obtained from 20 patients after death, they found more S1PR2 in MS patients’ brains than in people without the disorder. Brain tissue from females also had higher levels of S1PR2 than male brain tissue. The highest levels of S1PR2 were found in the brains of two female patients whose symptoms flared and faded irregularly, a pattern scientists call relapsing and remitting MS.

Klein is collaborating with chemists to design a tracer that will allow scientists to monitor S1PR2 levels in the brains of people while they are living. She hopes this will lead to a fuller understanding of how S1PR2 contributes to MS.

“This is an exciting first step in resolving the mystery of why MS rates are dramatically higher in women and in finding better ways to reduce the incidence of this disorder and control symptoms,” said Klein, associate professor of medicine. Klein also is an associate professor of pathology and immunology and of neurobiology and anatomy.

(Source: news.wustl.edu)

Filed under MS sex differences S1PR2 immune cells blood-brain barrier brain tissue neuroscience science

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May 9, 2014

Study confirms mitochondrial deficits in children with autism

Children with autism experience deficits in a type of immune cell that protects the body from infection. Called granulocytes, the cells exhibit one-third the capacity to fight infection and protect the body from invasion compared with the same cells in children who are developing normally.

The cells, which circulate in the bloodstream, are less able to deliver crucial infection-fighting oxidative responses to combat invading pathogens because of dysfunction in their tiny energy-generating organelles, the mitochondria.

The study is published online in the journal Pediatrics.

“Granulocytes fight cellular invaders like bacteria and viruses by producing highly reactive oxidants, toxic chemicals that kill microorganisms. Our findings show that in children with severe autism the level of that response was both lower and slower,” said Eleonora Napoli, lead study author and project scientist in the Department of Molecular Biosciences in the UC Davis School of Veterinary Medicine. “The granulocytes generated less highly reactive oxidants and took longer to produce them.”

The researchers also found that the mitochondria in the granulocytes of children with autism consumed far less oxygen than those of the typically developing children — another sign of decreased mitochondrial function.

Mitochondria are the main intracellular source of oxygen free radicals, which are very reactive and can harm cellular structures and DNA. Cells can repair typical levels of oxidative damage. However, in the children with autism the cells produced more free radicals and were less able to repair the damage, and as a result experienced more oxidative stress. The free radical levels in the blood cells of children with autism were 1 ½ times greater than those without the disorder.

The study was conducted using blood samples of children enrolled in the Childhood Risk of Autism and the Environment (CHARGE) Study and included 10 children with severe autism age 2 to 5 and 10 age-, race- and sex-matched children who were developing typically.

In an earlier study the research team found decreased mitochondrial fortitude in another type of immune cell, the lymphocytes. Together, the findings suggest that deficiencies in the cells’ ability to fuel brain neurons might lead to some of the cognitive impairments associated with autism. Higher levels of free radicals also might contribute to autism severity.

“The response found among granulocytes mirrors earlier results obtained with lymphocytes from children with severe autism, underscoring the cross-talk between energy metabolism and response to oxidative damage,” said Cecilia Giulivi, professor in the Department of Molecular Biosciences in the UC Davis School of Veterinary Medicine and the study’s senior author.

“It also suggests that the immune response seems to be modulated by a nuclear factor named NRF2,” that controls antioxidant response to environmental factors and may hold clues to the gene-environment interaction in autism, Giulivi said.

(Image credit)

Filed under autism mitochondria oxidative stress granulocytes NRF2 immune response neuroscience science

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May 9, 2014

Mouse study offers new clues to cognitive decline

New research suggests that certain types of brain cells may be “picky eaters,” seeming to prefer one specific energy source over others. The finding has implications for understanding the cognitive decline seen in aging and degenerative diseases such as Alzheimer’s and multiple sclerosis.

(Image caption: Neural stem cells differentiate into three different cell types: neurons (purple), oligodendrocytes (red), which produce axon insulation, and astrocytes (green), which also support neurons. Cell nuclei are shown in blue. Credit: Liana Roberts Stein)

Studying mice, investigators from Washington University School of Medicine in St. Louis showed that a specific energy source called NAD is important in cells responsible for maintaining the overall structure of the brain and for performing complex cognitive functions. NAD (nicotinamide adenine dinucleotide) is a molecule that harvests energy from nutrients in food and converts it into a form cells can use.

The work appears in two journal articles — in the May 8 issue of The EMBO Journal, a publication of the European Molecular Biology Organization, and in a recent issue of The Journal of Neuroscience.

“We are interested in understanding how cells make NAD and what implications that has for cellular function, especially in the context of aging and longevity,” said Shin-ichiro Imai, MD, PhD, professor of developmental biology and of medicine and senior author of both papers. “We know, for example, NAD levels decrease with age in tissues such as muscle and fat. We wanted to find out if the same is true in the brain.”

The investigators looked at two types of brain cells: adult neural stem cells, responsible for maintaining supplies of neurons and their supporting cells, and forebrain neurons, vital for performing complex cognitive tasks.

In The EMBO Journal, they reported that NAD levels decreased with age in the mouse hippocampus, a vital region of the brain for cognition. The researchers then used genetic techniques to find out what would happen when NAD manufacturing is turned off in the adult neural stem cells of the mouse brain.

“Neural stem cells are very metabolically expensive, so you might expect them to be particularly vulnerable to loss of an energy source,” said first author Liana Roberts Stein, PhD, postdoctoral researcher in Imai’s lab. “There are other energy sources for brain cells, such as glucose, but no one had ever looked at where NAD is coming from in these cells.”

According to the researchers, there are four pathways of NAD synthesis, and the scientists focused on just one. They wanted to find out whether this particular pathway — a longtime focus of Imai’s lab — is important for these cells or if the other routes could compensate.

The pathway begins with the B vitamin nicotinamide. Cells take dietary nicotinamide and, with a helper protein called Nampt, manufacture a molecule called NMN, which then is processed further to make NAD. When Stein eliminated Nampt from neural stem cells, several significant changes took place.

Levels of NAD dropped, and the neural stem cells stopped dividing; they stopped renewing themselves; and they stopped being able to create important cells that insulate axons, the “wires” that carry electrical signals throughout the brain. With less insulation, these signals slow down, impairing brain function.

Imai and Stein pointed out possible therapeutic implications of this finding, especially in light of what is known about cognitive decline in aging and certain diseases.

“Scientists have shown that with age there actually isn’t a large decrease in the total neuron population,” Stein said. “But there is quite a substantial decrease in white matter, which is primarily composed of cells that function in axon insulation. This pathway also could be relevant in conditions involving loss of cells that make this insulation, like multiple sclerosis.”

Imai and Stein also found they could prevent the loss of the neural stem cells missing Nampt by giving the mice NMN, the next molecule in the chain of events leading to NAD.

“We gave the mice NMN in their drinking water for 12 months,” Stein said. “And at the higher dose, we saw a rescue of the neural stem cell pool in aged mice.”

Imai called this finding exciting because it supports the possibility of a future NMN supplement.

“We think that NMN could convey a similar effect in people,” Imai said. “A future clinical trial for NMN will tell us if it has any efficacy in humans.”

In addition to maintaining stem cell populations and keeping the brain supplied with all its cell types, the investigators showed that NAD also is vital for the process of cognition itself.

Reporting in The Journal of Neuroscience, they showed that neurons of the mouse forebrain depend heavily on NAD in normal cognitive function. Instead of deleting Nampt in stem cells, this time Stein deleted it only in neurons of the forebrain. All other cells were normal, including those that make axon insulation.

Without Nampt and its eventual product, NAD, in forebrain neurons, the behavior of the mice changed dramatically, according to the investigators.

“The mice were really hyperactive, with a twofold increase in activity levels,” Stein said. “They also showed a loss of anxiety-like behaviors. These mice didn’t seem to sense or fear potentially threatening situations and showed fairly drastic memory defects.”

Stein pointed out that these neurons are in a region of the brain known to be particularly vulnerable to neurodegenerative conditions from Alzheimer’s disease to stroke.

“It’s possible that these neurons’ dependence on Nampt is responsible for their extreme susceptibility to these conditions,” she said. “It would be interesting to model some of these diseases in mice and see if supplementing NMN provides any benefit to their behavior or memory.”

“We haven’t done that study yet,” Imai added. “But this is the direction the entire field is going.”

(Source: news.wustl.edu)

Filed under cognitive decline stem cells brain cells aging NAD hippocampus nicotinamide neuroscience science

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May 9, 2014

(Image caption: In Greek mythology, Clotho – the eponym for the anti-aging factor klotho – is the Fate who spins the thread of life. Here, the goddess spins the metaphorical thread of life that is DNA, influencing lifespan and cognition. Illustration by Michael Griffin Kelley)

Better Cognition Seen with Gene Variant Carried by 1 in 5 People

A scientific team led by the Gladstone Institutes and UC San Francisco has discovered that a common form of a gene already associated with long life also improves learning and memory, a finding that could have implications for treating age-related diseases like Alzheimer’s.

The researchers found that people who carry a single copy of the KL-VS variant of the KLOTHO gene perform better on a wide variety of cognitive tests. When the researchers modeled the effects in mice, they found it strengthened the connections between neurons that make learning possible – what is known as synaptic plasticity – by increasing the action of a cell receptor critical to forming memories.

The discovery is a major step toward understanding how genes improve cognitive ability and could open a new route to treating diseases like Alzheimer’s. Researchers have long suspected that some people may be protected from the disease because of their greater cognitive capacity, or reserve. Since elevated levels of the klotho protein appear to improve cognition throughout the lifespan, raising klotho levels could build cognitive reserve as a bulwark against the disease.

“As the world’s population ages, cognitive frailty is our biggest biomedical challenge,” said Dena Dubal, MD, PhD, assistant professor of neurology, the David A. Coulter Endowed Chair in Aging and Neurodegeneration at UCSF and lead author of the study, published May 8 in Cell Reports. “If we can understand how to enhance brain function, it would have a huge impact on people’s lives.”

First to Link Between Klotho Variant and Better Cognition

Klotho was discovered in 1997 and named after the Fate from Greek mythology who spins the thread of life.

The investigators found that people who carry a single copy of the KL-VS variant of the KLOTHO gene, roughly 20 percent of the population, have more klotho protein in their blood than non-carriers. Besides increasing the secretion of klotho, the KL-VS variant may also change the action of the protein and is known to lessen age-related cardiovascular disease and promote longevity.

The team’s report is the first to link the KL-VS variant, or allele, to better cognition in humans, and buttresses these findings with genetic, electrophysiological, biochemical and behavioral experiments in mice.

The researchers tested the associations between the allele and age-related human cognition in three separate studies involving more than 700 people without dementia between the ages of 52 and 85. Altogether, it took about three years to conduct the work.

“These surprising results pave a promising new avenue of research,” said Roderick Corriveau, PhD, program director at NIH’s National Institute of Neurological Disorders and Stroke (NINDS). “Although preliminary, they suggest klotho could be used to bump up cognition for people suffering from dementia.”

Learning Better at All Stages of Life

Having the KL-VS allele did not seem to protect people from age-related cognitive decline. But overall the effect was to boost cognition, so that the middle-aged study participants began their decline from a higher point.

“Based on what was known about klotho, we expected it to affect the brain by changing the aging process,” said senior author Lennart Mucke, MD, who directs neurological research at the Gladstone Institutes and is a professor of neurology and the Joseph B. Martin Distinguished Professor of Neuroscience at UCSF. “But this is not what we found, which suggested to us that we were on to something new and different.”

To get a closer look at how the gene variant operates, the researchers used mice that were engineered to produce more of the mouse version of klotho and found that these mice learned better at all stages of life. Put through mazes, these transgenic mice were more likely to try different routes, an indication that they had superior working memory. In a test of spatial learning and memory, the mice with extra klothoperformed twice as well.

Researchers then analyzed the mouse brain tissue and found that the mice with elevated klotho had twice as many GluN2B subunits within synaptic connections. GluN2B is part of the N-methyl-D-aspartate receptor, or NMDAR, a key receptor involved in synaptic plasticity.

The researchers found more GluN2B-containing receptors in the hippocampus and frontal cortex, brain regions that support cognitive functions. When the researchers gave the mice a drug that blocks the action of these receptors, the klotho-enhanced mice lost their cognitive advantage.

Filed under cognition cognitive performance KLOTHO gene longevity GluN2B synaptic plasticity neuroscience science

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May 8, 2014

Temper trap: the genetics of aggression and self-control

Everyone knows someone with a quick temper – it might even be you. And while scientists have known for decades that aggression is hereditary, there is another biological layer to those angry flare-ups: self-control.

In a paper published earlier this year in the Journal of Cognitive Neuroscience, my colleagues and I found that people who are genetically predisposed toward aggression try hard to control their anger, but have inefficient functioning in brain regions that control emotions.

In other words, self-control is, in part, biological.

466 notes

May 8, 2014

Psilocybin inhibits the processing of negative emotions in the brain

When emotions are processed in a negatively biased manner in the brain, an individual is at risk to develop depression. Psilocybin, the bioactive component of the Mexican magic mushroom, seems to intervene positively in the emotion-processing mechanism. Even a small amount of the natural substance attenuates the processing of negative emotions and brightens mood as shown by UZH researchers using imaging methods.

Emotions like fear, anger, sadness, and joy enable people to adjust to their environment and react flexibly to stress and strain and are vital for cognitive processes, physiological reactions, and social behaviour. The processing of emotions is closely linked to structures in the brain, i.e. to what is known as the limbic system. Within this system the amygdala plays a central role – above all it processes negative emotions like anxiety and fear. If the activity of the amygdala becomes unbalanced, depression and anxiety disorders may develop.

Researchers at the Psychiatric University Hospital of Zurich have now shown that psilocybin, the bioactive component in the Mexican magic mushroom, influences the amygdala, thereby weakening the processing of negative stimuli. These findings could “point the way to novel approaches to treatment” comments the lead author Rainer Krähenmann on the results which have now been published in the renowned medical journal “Biological Psychiatry”.

Psilocybin inhibits the processing of negative emotions in the amygdala

The processing of emotions can be impaired by various causes and elicit mental disorders. Elevated activity of the amygdala in response to stimuli leads to the neurons strengthening negative signals and weakening the processing of positive ones. This mechanism plays an important role in the development of depression and anxiety disorders. Psilocybin intervenes specifically in this mechanism as shown by Dr. Rainer Krähenmann’s research team of the Neuropsychopharmacology and Brain Imaging Unit led by Prof. Dr. Franz Vollenweider.

Psilocybin positively influences mood in healthy individuals. In the brain, this substance stimulates specific docking sites for the messenger serotonin. The scientists therefore assumed that psilocybin exerts its mood-brightening effect via a change in the serotonin system in the limbic brain regions. This could, in fact, be demonstrated using functional magnetic resonance imaging (fMRI). “Even a moderate dose of psilocybin weakens the processing of negative stimuli by modifying amygdala activity in the limbic system as well as in other associated brain regions”, continues Krähenmann. The study clearly shows that the modulation of amygdala activity is directly linked to the experience of heightened mood.

Next study with depressive patients

According to Krähenmann, this observation is of major clinical importance. Depressive patients in particular react more to negative stimuli and their thoughts often revolve around negative contents. Hence, the neuropharmacologists now wish to elucidate in further studies whether psilocybin normalises the exaggerated processing of negative stimuli as seen in neuroimaging studies of depressed patients - and may consequently lead to improved mood in these patients.

Rainer Krähenmann considers research into novel approaches to treatment very important, because current available drugs for the treatment of depression and anxiety disorders are not effective in all patients and are often associated with unwanted side effects.

(Source: mediadesk.uzh.ch)

Filed under psilocybin emotions amygdala serotonin depression neuroscience science

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May 8, 2014

New study examines premature menopause and effects on later life cognition

Premature menopause is associated with long-term negative effects on cognitive function, suggests a new study published today (7 May) in BJOG: An International Journal of Obstetrics and Gynaecology (BJOG).

The average age of menopause is around 50 years in the Western World. Premature menopause refers to menopause at or before 40 years of age, this could be due to a bilateral ovariectomy, (surgically induced menopause)or non-surgical loss of ovarian function (sometimes referred to as ‘natural’ menopause).

The study, based on a sample of 4868 women, used cognitive tests and clinical dementia diagnosis at baseline and after two, four and seven years and aimed to determine whether premature menopause can have an effect on later-life cognitive function. The effects of the type of menopause, whether natural or surgical, and use of hormone treatment were also examined.

Of the 4,868 women in this study, natural menopause was reported by 79% of the women, 10% as a surgical menopause and 11% of women reported menopause due to other causes, such as radiation or chemotherapy. Around 7.6% of the women in the study had a premature menopause and a further 12.8% an early menopause (between the ages of 41 and 45 years). Over a fifth of the women used hormone treatment during the menopause.

Results show that in comparison to women who experienced menopause after the age of 50, those with a premature menopause had a more than 40% increased risk of poor performance on tasks assessing verbal fluency and visual memory and was associated with a 35% increased risk of decline in psychomotor speed (coordination between the brain and the muscles that brings about movement) and overall cognitive function over 7 years. There was no significant association with the risk of dementia.

Furthermore, both premature ovarian failure and premature surgical menopause were associated with a more than two-fold risk of poor verbal fluency. In terms of visual memory, premature ovarian failure was associated with a significantly increased risk of poor performance, and there was a similar trend for premature surgical menopause.

When the potential modifying effect of using hormone treatment at the time of premature menopause was examined, there was some evidence that it may be beneficial for visual memory, but it could increase the risk of poor verbal fluency.

Dr Joanne Ryan, Postdoctoral Research Fellow, Neuropsychiatry: Epidemiological and Clinical Research, Hospital La Colombiere, Montpellier, said:

“Both premature surgical menopause and premature ovarian failure, were associated with long-term negative effects on cognitive function, which are not entirely offset by menopausal hormone treatment.

“In terms of surgical menopause, our results suggest that the potential long-term effects on cognitive function should form part of the decision-making process when considering ovariectomy in younger women.”

Pierre Martin Hirsch, BJOG deputy editor-in-chief added:

“With the ageing population it is important to have a better understanding of the long term effects of a premature menopause on later-life cognitive function and the potential benefit from using menopausal hormone treatment.

“This study adds to the existing evidence base to suggest premature menopause can have a significant impact on cognitive function in later life which healthcare professionals must be aware of.”

(Source: eu.wiley.com)

Filed under menopause premature menopause cognitive function dementia cognition neuroscience science

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May 8, 2014

Scientists link honeybees’ changing roles throughout their lives to brain chemistry

Scientists have been linking an increasing range of behaviors and inclinations from monogamy to addiction to animals’, including humans’, underlying biology. To that growing list, they’re adding division of labor — at least in killer bees. A report published in ACS’ Journal of Proteome Research presents new data that link the amounts of certain neuropeptides in these notorious bees’ brains with their jobs inside and outside the hive.

Mario Sergio Palma and colleagues explain that dividing tasks among individuals in a group is a key development in social behavior among Hymenoptera insects, which include bees, ants, sawflies and wasps. One of the starkest examples of this division of labor is the development of “castes,” which, through nutrition and hormones, results in long-lived queens that lay all the thousands of eggs in a colony and barren workers that forage for food and protect the hive. Bee researchers had already observed that honeybees, including Africanized Apis mellifera, better known as “killer” bees, divide tasks by age. As workers get older, their roles change from nursing and cleaning the hive to guarding and foraging. Palma’s team wanted to see whether peptides in the brain were associated with the bees’ shifting duties.

They found that the amounts of two substances varied by time and location in the brains of the honeybees in a way that mirrored the timing of their changing roles. “Thus, these neuropeptides appear to have some functions in the honeybee brain that are specifically related to the age-related division of labor,” the scientists conclude.

(Source: acs.org)

Filed under honeybee killer bee neuropeptides ontogeny mass spectrometry neuroscience science