New role for zebrafish in human studies

Washington, May 20 (ANI): Zebrafish – an important animal model in disease and environmental studies – could eventually help scientists in revealing the function of a mysterious enzyme linked to the steroid cortisol, and found in the human brain, found a researcher at the University of California, San Diego School of Medicine.

In people and other vertebrates, steroids like cortisol perform a variety of diverse duties, including regulating immune response, bone formation and brain activity.

However, too much cortisol is unhealthy. High levels of the steroid have been linked to type 2 diabetes and may impair the brain”s ability to store memories.

The human body regulates cortisol by employing an enzyme called 11 beta-hydroxysteroid dehydrogenase-type 1 or 11beta-HSD1, which catalyzes the synthesis of cortisol in liver and fat cells.

A related enzyme known as 11 beta-HSD-type3 or 11 beta-HSD3 is expressed in the brain, though its utility remains unknown.

In new findings, Dr. Michael E. Baker has reported that 11 beta-HSD3 (but not 11 beta-HSD1) is present in zebrafish, where it appears to serve an important role in fish endocrine physiology.

This makes the fish a potentially useful analog for cortisol studies, including discovering the purpose and function of 11 beta-HSD3 in human brains, which may be an evolutionary precursor to 11 beta-HSD1.

Interestingly, Baker found that the genomes of mice and rats do not contain 11 beta-HSD3.

This means that inserting the appropriate gene for the enzyme in these animal models could provide additional avenues of investigation.

The study will be published in the latest issue of FEBS Letters. (ANI)

Two new genes linked to autism

Washington, May 3 (ANI): Scientists have identified two additional genes that may be associated with autism.

Study co-author Ning Lei, a researcher at Princeton University and the Institute for Advanced Studies, said that there is no known cause of autism, but mutations of several genes have been linked to autism.

For the study, Dr. Lei and her colleagues analyzed data from the Autism Genetic Resource Exchange (AGRE) on 943 families, most of whom had more than one child diagnosed with autism and had undergone genetic testing.

The researchers compared the prevalence of 25 gene mutations in the AGRE families with a control group of 6,317 individuals without developmental or neuropsychiatric illness.

The researchers identified mutations in four genes within the AGRE families. Two of the genes previously were shown to be associated with autism and often are involved in forming or maintaining neural synapses — the point of connection between individual neurons.

One of the new genes identified was neural cell adhesion molecule 2 (NCAM2). NCAM2 is expressed in the hippocampus of the human brain — a region previously associated with autism.

“While mutations in the NCAM2 gene were found in a small percentage of the children that we studied, it is fascinating that this finding continues a consistent story — that many of the genes associated with autism are involved with formation or function of the neural synapse. Studies such as this provide evidence that autism is a genetically based disease that affects neural connectivity,” Dr. Lei said.

The researchers hypothesize that a substantial percentage of children with autism will be shown to have a mutation in one or more of the many genes necessary for normal function of the synapse.

The study also showed that some parents and siblings of children with autism have the NCAM2 mutation but do not have the disorder themselves.

This suggests that other environmental or genetic factors are involved in causing autism in susceptible individuals.

“These results help the public understand that autism is a very complex disorder, much like cancer and no single gene or gene environment is likely to be causative in most cases,” Dr. Lei said.

The findings have been presented at the Pediatric Academic Societies (PAS) annual meeting in Vancouver, British Columbia, Canada. (ANI)

Migratory birds have smaller brains

Washington, April 30 (ANI): Scientists have shed new light on the evolution of brain size in birds.

It has been known for some time that migratory birds have smaller brains than their resident relatives. Now, a new study by tesearchers at Centre for Ecological Research and Forestry Applications (CREAF, a Universitat Autonoma de Barcelona-affiliated centre) looks into the reasons and concludes that the act of migrating leads to a reduced brain size.

The authors point to the fact that the causes could be due to a need to reduce energetic, metabolic and cognitive costs.

To reach these conclusions, scientists reconstructed the evolutionary history of one of the most numerous orders of birds, the passeriformes, a group that includes swallows, tits and crows.

Understanding brain evolution is something that has interested scientists since the times of Charles Darwin, who considered that the large size of a human brain went hand in hand with the exceptional cognitive capacities of our species.

One of the classic explanations is the protective brain theory, which suggests that a large brain -in comparison to body size- makes learning easier. This protects individuals from changes in the environment, such as those produced by changes in season.

In the case of birds however not all species respond to seasonal changes in the same way. Migratory birds avoid these changes by travelling to less inhospitable places when conditions worsen.

This is the strategy followed by swallows or cuckoos. Resident bird species stay in the same area throughout the year and face strong environmental fluctuations. Tits and crows belong to this group.

Previous studies showed that both strategies are related to differences in brain size. The problem however is that it is often difficult to discern the causes and consequences of the differences observed.

By analysing data from 600 passerine species in regions ranging from tropical to artic, CREAF researchers Daniel Sol and Nuria Garcia, together with scientists from Canada and England, confirm that migratory birds have smaller brains than their resident counterparts.

The question now is whether brain size determines lifestyle (migratory or resident) or whether lifestyle determines the size of the brain.

According to the protective brain theory, being a resident bird makes it easier for the brain to grow and this for example facilitates acquiring alternative food-finding strategies for the winter months.

Nevertheless, the study reveals the complete opposite and points to the fact that being a migratory bird is what makes these birds have smaller brains.

The study has been published in the March edition of the journal PLoS One. (ANI)

How the human brain learns language

Washington, Apr 30 (ANI): There is no single advanced area of the human brain that gives it language capabilities above and beyond those of any other animal species, says a new study from the University of Rochester.

Instead, humans rely on several regions of the brain, each designed to accomplish different primitive tasks, in order to make sense of a sentence.

Depending on the type of grammar used in forming a given sentence, the brain will activate a certain set of regions to process it, like a carpenter digging through a toolbox to pick a group of tools to accomplish the various basic components that comprise a complex task.

“We”re using and adapting the machinery we already have in our brains,” said study coauthor Aaron Newman. “Obviously we”re doing something different [from other animals], because we”re able to learn language unlike any other species. But it”s not because some little black box evolved specially in our brain that does only language, and nothing else.”

The team of brain and cognitive scientists – comprised of Newman (now at Dalhousie University after beginning the work as a postdoctoral fellow at the University of Rochester), Elissa Newport (University of Rochester), Ted Supalla (University of Rochester), Daphne Bavelier (University of Rochester), and Peter Hauser (Rochester Institute of Technology) – published their findings in the latest edition of the journal Proceedings of the National Academies of Science. (ANI)

Human brain reacts differently to different races

Washington, Apr 27 (ANI): When dealing with people outside of one”s own race, the human brain fires differently, a new study has found.

The research out of the University of Toronto Scarborough explored the sensitivity of the “mirror-neuron-system” to race and ethnicity.

The researchers had study participants view a series of videos while hooked up to electroencephalogram (EEG) machines. The participants – all white – watched simple videos in which men of different races picked up a glass and took a sip of water. They watched white, black, South Asian and East Asian men perform the task.

Typically, when people observe others perform a simple task, their motor cortex region fires similarly to when they are performing the task themselves. However, the UofT research team, led by PhD student Jennifer Gutsell and Assistant Professor Dr. Michael Inzlicht, found that participants” motor cortex was significantly less likely to fire when they watched the visible minority men perform the simple task. In some cases when participants watched the non-white men performing the task, their brains actually registered as little activity as when they watched a blank screen.

“Previous research shows people are less likely to feel connected to people outside their own ethnic groups, and we wanted to know why,” says Gutsell. “What we found is that there is a basic difference in the way peoples” brains react to those from other ethnic backgrounds. Observing someone of a different race produced significantly less motor-cortex activity than observing a person of one”s own race. In other words, people were less likely to mentally simulate the actions of other-race than same-race people”

The trend was even more pronounced for participants who scored high on a test measuring subtle racism, says Gutsell.

“The so-called mirror-neuron-system is thought to be an important building block for empathy by allowing people to ”mirror” other people”s actions and emotions; our research indicates that this basic building block is less reactive to people who belong to a different race than you,” says Inzlicht.

The finding is published in the Journal of Experimental Social Psychology. (ANI)

First direct recording of mirror neurons in human brain

Washington, Apr 17 (ANI): For the first time, researchers have made a direct recording of mirror neurons in the human brain.

It is believed that mirror neurons are what make us human-they are the cells in the brain that fire not only when we perform a particular action but also when we watch someone else perform that same action.

Neuroscientists have said that this “mirroring” is the mechanism by which we can “read” the minds of others and empathize with them. It”s how we “feel” someone”s pain, how we discern a grimace from a grin, a smirk from a smile.

But, until now, there was no proof that mirror neurons existed – only suspicion and indirect evidence.

Dr. Itzhak Fried, a UCLA professor of neurosurgery and of psychiatry and biobehavioural sciences, Roy Mukamel, a postdoctoral fellow in Fried”s lab, and their colleagues have recorded both single cells and multiple-cell activity, not only in motor regions of the brain where mirror neurons were thought to exist but also in regions involved in vision and in memory.

They also showed that specific subsets of mirror cells increased their activity during the execution of an action but decreased their activity when an action was only being observed.

“We hypothesize that the decreased activity from the cells when observing an action may be to inhibit the observer from automatically performing that same action. Furthermore, this subset of mirror neurons may help us distinguish the actions of other people from our own actions,” said Mukamel.

The researchers drew their data directly from the brains of 21 patients who were being treated at Ronald Reagan UCLA Medical Center for intractable epilepsy.

The patients had been implanted with intracranial depth electrodes to identify seizure foci for potential surgical treatment.

Electrode location was based solely on clinical criteria; the researchers, with the patients” consent, used the same electrodes to “piggyback” their research.

The researchers found that the neurons fired or showed their greatest activity both when the individual performed a task and when they observed a task.

The mirror neurons making the responses were located in the medial frontal cortex and medial temporal cortex, two neural systems where mirroring responses at the single-cell level had not been previously recorded, not even in monkeys.

This new finding demonstrates that mirror neurons are located in more areas of the human brain than previously thought.

Given that different brain areas implement different functions – in this case, the medial frontal cortex for movement selection and the medial temporal cortex for memory – the finding also suggests that mirror neurons provide a complex and rich mirroring of the actions of other people.

Because mirror neurons fire both when an individual performs an action and when one watches another individual perform that same action, it is believed that this “mirroring” is the neural mechanism by which the actions, intentions and emotions of other people can be automatically understood.

“The study suggests that the distribution of these unique cells linking the activity of the self with that of others is wider than previously believed,” said Fried.

“It”s also suspected that dysfunction of these mirror cells might be involved in disorders such as autism, where the clinical signs can include difficulties with verbal and nonverbal communication, imitation and having empathy for others. So gaining a better understanding of the mirror neuron system might help devise strategies for treatment of this disorder,” said Mukamel.

The study was published in the latest edition of the journal Current Biology. (ANI)

Babies recognise emotions by 7 months

Washington, Mar 27 (ANI): Babies as young as 7 months old can discern a voice”s emotional state, suggests a new study.

The new research found that the brains of infants demonstrate a sensitivity to the human voice and to emotions communicated through the voice that is remarkably similar to what is observed in the brains of adults.

The study, published by Cell Press in the March 25 issue of the journal Neuron, probes the origins of voice processing in the human brain and may provide important insight into neurodevelopmental disorders such as autism.

Dr. Tobias Grossmann from the Centre for Brain and Cognitive Development at the University of London led the study which was performed in Dr. Angela D. Friederici”s laboratory at the Max Planck Institute for Human Cognitive and Brain Sciences in Germany.

The researchers used near-infrared spectroscopy to investigate when during development regions in temporal cortex become specifically sensitive to the human voice. These specific cortical regions have been shown to play a key role in processing spoken language in adults.

Grossmann and colleagues observed that 7-month-olds but not 4-month-olds showed adult-like increased responses in the temporal cortex in response to the human voice when compared to nonvocal sounds, suggesting that voice sensitivity emerges between 4 and 7 months of age.

Another important question addressed in this study was whether activity in infants” voice-sensitive brain regions is modulated by emotional prosody. Prosody, essentially the “music” of speech, can reflect the feelings of the speaker, thereby helping to convey the context of language. In humans, sensitivity to emotional prosody is crucial for social communication.

The researchers observed that a voice-sensitive region in the right temporal cortex showed increased activity when 7-month-old infants listened to words spoken with emotional (angry or happy) prosody. Such a modulation of brain activity by emotional signals is thought to be a fundamental brain mechanism to prioritize the processing of significant stimuli in the environment.

“Our findings demonstrate that voice-sensitive brain regions are already specialized and modulated by emotional information by the age of 7 months and raise the possibility that the critical neurodevelopmental processes underlying impaired voice-processing reported in disorders like autism might occur before 7 months,” explains Dr. Grossmann. “Therefore, in future work the current approach could be used to assess individual differences in infants” responses to voices and emotional prosody and might thus serve as one of potentially multiple markers that can help with an early identification of infants at risk for a neurodevelopmental disorder.” (ANI)

Scientists create new period of brain ‘plasticity’ with transplanted embryonic cells

Washington, Mar 26 (ANI): In a new study, researchers were able to prompt a new period of “plasticity,” or capacity for change, in the neural circuitry of the visual cortex of juvenile mice.

The scientists believe that the approach might some day be used to create new periods of plasticity in the human brain that would allow for the repair of neural circuits following injury or disease.

The strategy involved transplanting a specific type of immature neuron from embryonic mice into the visual cortex of young mice.

It could be used to treat neural circuits disrupted in abnormal foetal or postnatal development, stroke, traumatic brain injury, psychiatric illness and aging.

Like all regions of the brain, the visual cortex undergoes a highly plastic period during early life.

In mice, this critical period of plasticity occurs around the end of the fourth week of life.

The catalyst for the so-called critical period plasticity in the visual cortex is the development of synaptic signalling by neurons that release the inhibitory neurotransmitter GABA.

The neurons receive excitatory signals from other neurons, thus helping to maintain the balance of excitation and inhibition in the visual system.

In the study, the scientists wanted to see if the embryonic neurons, once they had matured into GABA-producing inhibitory neurons, could induce plasticity in mice after the normal critical period had closed.

The team first dissected the immature neurons from their origin in the embryonic medial ganglionic eminence (MGE) of the embryonic mice.

Then they transplanted the MGE cells into the animals’ visual cortex at two different juvenile stages.

The cells, targeted to the visual cortex, dispersed through the region, matured into GABAergic inhibitory neurons, and made widespread synaptic connections with excitatory neurons.

The scientists then carried out a process known as monocular visual deprivation, in which they blocked the visual signals to one eye in each of the animals for four days.

When this process is carried out during the critical period, cells in the visual cortex quickly become less responsive to the eye deprived of sensory input, and become more responsive to the non-deprived eye, creating alterations in the neural circuitry.

This phenomenon, known as ocular dominance plasticity, greatly diminishes as the brain matures past this critical postnatal developmental period.

The researchers found that the transplanted cells’ impact occurred once they had reached the cellular age of inhibitory neurons during the normal critical period.

The finding suggests that the normal critical period of plasticity in the visual cortex is regulated by a developmental program intrinsic to inhibitory neurons, and that embryonic inhibitory neuron precursors can retain and execute this program when transplanted into the postnatal cortex, thereby creating a new period of plasticity.

“The findings suggest it ultimately might be possible to use inhibitory neuron transplantation, or some factor that is produced by inhibitory neurons, to create a new period of plasticity of limited duration for repairing damaged brains. It will be important to determine whether transplantation is equally effective in older animals,” said author Dr. Sunil P. Gandhi, PhD.

The study has been published in the journal Science. (ANI)

How the brain constructs morality

Washington, Mar 25 (ANI): Our ability to respond appropriately to intended harms � that is, with outrage toward the perpetrator � is seated in a brain region associated with regulating emotions, says a new study.

According to MIT neuroscientists, patients with damage to this brain area, known as the ventromedial prefrontal cortex (VMPC), are unable to conjure a normal emotional response to hypothetical situations in which a person tries, but fails, to kill another person. Therefore, they judge the situation based only on the outcome, and do not hold the attempted murderer morally responsible.

The finding offers a new piece to the puzzle of how the human brain constructs morality, says Liane Young, a postdoctoral associate in MIT”s Department of Brain and Cognitive Sciences and lead author of a paper describing the findings in the March 25 issue of the journal Neuron.

“We”re slowly chipping away at the structure of morality,” says Young. “We”re not the first to show that emotions matter for morality, but this is a more precise look at how emotions matter.”

Working with researchers at the University of Southern California, led by Antonio Damasio, Young studied a group of nine patients with damage (caused by aneurisms or tumors) to the VMPC, a plum-sized area located behind and above the eyes.

Such patients have difficulty processing social emotions such as empathy or embarrassment, but “they have a perfectly intact capacity for reasoning and other cognitive functions,” says Young.

The researchers gave the subjects a series of 24 hypothetical scenarios and asked for their reactions. The scenarios of most interest to the researchers were ones featuring a mismatch between the person”s intention and the outcome � either failed attempts to harm or accidental harms.

When confronted with failed attempts to harm, the patients had no problems understanding the perpetrator”s intentions, but they failed to hold them morally responsible. The patients even judged attempted harms as more permissible than accidental harms (such as accidentally poisoning someone) � a reversal of the pattern seen in normal adults.

“They can process what people are thinking and their intentions, but they just don”t respond emotionally to that information,” says Young. “They can read about a murder attempt and judge it as morally permissible because no harm was done.”

This supports the idea that making moral judgments requires at least two processes � a logical assessment of the intention, and an emotional reaction to it. The study also supports the theory that the emotional component is seated in the VMPC. (ANI)

How status quo bias in the brain affects decisions

Washington, Mar 16 (ANI): Examining the neural pathways involved in ”status quo bias” in the human brain, researchers at University College London (UCL) have found that the more difficult the decision we face, the more likely we are not to act.

The study looked at the decision-making of participants taking part in a tennis ”line judgement” game while their brains were scanned using functional MRI (fMRI).

“When faced with a complex decision people tend to accept the status quo, hence the old saying ”When in doubt, do nothing,’” said first author Stephen Fleming, Wellcome Trust Centre for Neuroimaging at UCL.

“Whether it”s moving house or changing TV channel, there is a considerable tendency to stick with the current situation and choose not to act, and we wanted to explore this bias towards inaction in our study and examine the regions of the brain involved,” he added.

The 16 study participants were asked to look at a cross between two tramlines on a screen while holding down a ”default” key. They then saw a ball land in the court and had to make a decision as to whether it was in or out.

On each trial, the computer signalled which was the current default option – ”in” or ”out”.

The participants continued to hold down the key to accept the default and had to release it and change to another key to reject the default.

The results showed a consistent bias towards the default, which led to errors.

As the task became more difficult, the bias became even more pronounced.

The fMRI scans showed that a region of the brain known as the subthalamic nucleus (STN) was more active in the cases when the default was rejected.

In addition, greater flow of information was seen from a separate region sensitive to difficulty (the prefrontal cortex) to the STN.

This indicates that the STN plays a key role in overcoming status quo bias when the decision is difficult.

“Interestingly, current treatments of Parkinson”s disease like deep-brain stimulation (DBS) work by disrupting the subthalamic nucleus to alleviate impaired initiation of action. This is one example of how knowing about disease mechanisms can inform our knowledge of normal decision making, and vice-versa,” added Stephen.

“This study looked at a very simple perceptual decision and there are obviously other powerful factors, such as desires and goals that influence decisions about whether or not to act. So, it would be of interest to investigate how these regions respond when values and needs come into play.”

The study has been published in Proceedings of the National Academy of Sciences (PNAS). (ANI)

How the brain hears music and lyrics

Washington, March 10 (ANI): Does the brain process words and music separately or as one? Well scientists in Germany seem to have found an answer to the hotly debated question.

The research team found that the brain first deals with music and lyrics together and then, after passing through more complex processing, like understanding what lyrics mean, the two are treated separately.

In their research, Daniela Sammler of the Max Planck Institute for Human Cognitive and Brain Sciences in Leipzig, Germany, and colleagues worked out a way to determine when active regions were processing just music and when just lyrics, by studying a functional MRI brain scan of someone listening to songs, reports New Scientist.

The team knew that when neurons process the same stimulus repeatedly, their response to it decreases over time.

They reasoned that if they varied just the tune and kept the lyrics the same, areas showing a decline in activity must be processing lyrics.

And if they varied just the lyrics, areas showing a decline must be processing the tune, while any regions declining when both the tune and lyrics are repeated must be processing both.

The research team wrote four different sets of six songs and played these to 12 volunteers while scanning their brains. In one set, all songs had different melodies and lyrics.

In another, the melodies were different but the lyrics were the same, while in the third set, the opposite was true. The fourth set were identical to each other.

From the fMRI scans the team worked out that one particular part of the brain – the superior temporal sulcus (STS) – was responding to the songs. In the middle of the STS, the lyrics and tune were being processed as a single signal. But in the anterior STS, only the lyrics seemed to be processed.

Sammler said that her team couldn”t find an area specific to processing tunes. This may be because no individual, complex processing occurs for melody, although it might in professional musicians.

She concluded that the brain first deals with music and lyrics together. Then, after passing through the mid-STS more complex processing kicks in, such as understanding what lyrics mean, and the two are treated separately.

“The more they are processed, the more they are separated,” she said.

The study has been published in the Journal of Neuroscience. (ANI)

Scientists identify another necessary step in memory formation

Washington, September 9 (ANI): Scientists at the University of Haifa have identified another component in the chain of actions that take place in the neurons, when the brain is in the process of forming memories.

The researchers say that, together with the results of previous studies, the new findings provide a better understanding of the process of memory formation and storage in the human brain.

In their study report, the researchers point out that the formation of memory to sensory information on the world-new sounds, tastes, sights, and smells-is vital for animal survival.

They say that very little of this information becomes short-term memory, and that only a small part of the information that becomes short-term memory ultimately becomes long-term and stabilized memory.

Previous studies led by Prof. Kobi Rosenblum found an elevation in the expression of the protein PSD-95 to be necessary for the formation of long-term memory.

The present study aimed to find out whether another molecular process – the addition of a phosphor molecule to the NMDA receptor protein (phosphorylation) – is necessary too.

Earlier studies have proven that changes in the NMDA receptor can adjust the neuronal network in the brain, and that during a learning process this receptor undergoes increased phosphorylation.

Before the present research, none of the studies had proved that the increase in phosphorylation of the NMDA is necessary for the process, and that the process would not occur without it.

During the current study, the scientists chose to focus on the formation of new taste memory in rats as a model for sensory memory because it could enable them to track when the process begins, its specific location is in the brain, and the molecular processes that occur during the process.

Verifying the findings of the previous studies, the first stage of the study showed that the new taste learning does indeed involve a process of increased phosphorylation in the NMDA receptors in the area specific to learning taste in the brain.

In order to do so, mature rats were trained to drink water at set times and after a few days some were given saccharine-sweetened water. The saccharine has no caloric value and therefore has no metabolic impact on the body and cannot affect the body’s processes. As expected, the rats that received the newly sweet-tasting water and that began a process of learning, showed an increase in phosphorylation in comparison to those rats that continued drinking regular water.

The second stage of the study showed that obstruction of the phosphorylation process brought about a change in the location of the receptor in relation to the NMDA, and thus was likely to be responsible for inhibiting the formation of long-term memory.

“Our goal is to identify piece after piece of the complex puzzle that is the formation of long-term memory. Once we know how to describe the chain of actions that take place in the brain, we may be able to know where and how to interfere,” said Dr. Dr. Liza Barki-Harrington, a member of the research team.

“The glutamate neural synapses – via the receptors of the NMDA – and dophamin, play a central role in a number of neural pathologies, including processes of addiction and of schizophrenia.

There is good reason to assume that one afflicted with schizophrenia has a sub- or over-functioning of this system, and its loss of balance is one of the causes of the illness. A better understanding of this balance – or loss of balance – in the normal processes will enable future discovery of new objectives for developing medications, which we hope will improve patients’ lives significantly,” added Prof. Rosenblum.

The study has been published in the Journal of Neuroscience. (ANI)

Smart people are sexier

Wellington, Sep 2 (ANI): A person’s sex quotient lies in his or her brain, according to a study that suggests that being smart is sexy, and the smartest males get the most partners.

Through a study on Australian birds, a team of researchers have lent support to the idea that our big human brain evolved because it is a sexually attractive organ, not just a useful one.

According to the above theory, signs of intelligence – such as creating art, music, and humour – could have made the brainiest people luckiest in love.

The theory was hugely discussed in the book ‘The Mating Mind’ by an evolutionary psychologist, Geoffrey Miller, almost a decade ago.

Jason Keagy, of the University of Maryland in the US, said that testing the theory in humans was very difficult, and thus he chose to observe satin bowerbirds at Wallaby Creek in NSW instead.

He claimed that Bowerbirds are intelligent.

“But they’re not as complex as humans,” Stuff.co.nz quoted him as saying.

Keagy could get an accurate record of the male birds’ sexual success by videotaping their every movement.

“They can’t really lie to us,” he said.

Known for their fascination with blue objects, bowerbirds have a strong aversion to red.

In the first IQ test, the researchers placed three red objects under a clear plastic container in their bower, and found that the smartest males could remove the cover and carry away the offending objects in 20 seconds.

“It looks pretty simple, but some weren’t able to do it,” said Keagy.

In a second braintwister, he glued a red object down and observed that some bowerbirds kept on trying in vain to pull it out, while the brighter ones quickly twigged this was impossible and covered it with leaves.

The males who failed the plastic container test were spurned.

“No females were mating with them,” said Keagy.

However, the smartest birds attracted up to 20 female partners a season.

“This is the first evidence [in any species] that individuals with better problem-solving abilities are more sexually attractive,” he said.

He claimed that greater intelligence could allow male bowerbirds to woo more females because they can build more elaborate bowers, are better dancers or are more responsive to subtle cues from the females during courtship.

Alternative theories to the mating mind include that our large brain evolved because it was advantageous for hunting or living in social groups, and cultural creativity was simply a fortuitous by-product of the struggle to survive.

The study has been published in the journal Animal Behaviour. (ANI)

Common drug can function as ‘off switch’ for Parkinson therapy

Washington, Aug 29 (ANI): A common antibiotic can act as an “off switch” for a gene therapy that is being developed for Parkinson’s disease, according to a study on rats conducted by University of Florida researchers.

The findings of the study have explained how new, therapeutic genes that have been irrevocably delivered to the human brain to treat Parkinson’s can be controlled if the genes unexpectedly start causing problems.

Meanwhile, in a review of Parkinson treatments, the researchers have said that earlier experiments using growth factors – naturally occurring substances that cause cells to grow and divide – to rescue dying brain cells may have failed because they occurred too late in the course of the disease.

Taken together, the findings have indicated that gene therapy to enable the brain to retain its ability to produce dopamine- a neurotransmitter that falls in critically short supply in Parkinson’s patients- could be safely attempted during earlier stages of the disease with an added likelihood of success.

“We have worked every day for 10 years to design a construct to the gene delivery vector that enhances the safety profile of gene transfer for Parkinson’s disease,” said Ronald Mandel, a professor of neuroscience at UF.

He added: “With that added measure of safety, we believe we can intervene with gene transfer in patients at earlier stages of the disease. We strongly believe that trials to save dopamine-producing connections in patients with Parkinson’s disease have failed because the therapy went into patients who were in the late stages of the disease and who had too few remaining dopamine-producing connections.”

Often patients are given prescriptions for levodopa (L-dopa), which is converted into dopamine by enzymes in the brain. But such treatment is not effective over time, and does nothing to slow the disease’s progression.

In the meantime, trials in the US to treat Parkinson’s involving direct infusion of growth factors or the transplantation of genes that produce growth factors have had limited success, with some side effects.

Mandel’s research group has concentrated on using an adeno-associated virus to engineer brain cells in animal models with genes that can protect dopamine-producing cells, which then do the vital work of producing glial cell line-derived neurotrophic factor (GDNF).

The naturally occurring protein is important for the survival of dopamine-producing neurons during brain development, and a survival factor when given to adults.

For the current study, the researchers engineered the virus with two genes that must act in concert to produce the protein.

But this precise interaction can be inhibited with dietary doxycycline, an antibiotic that is often prescribed in low doses to treat bacterial growth related to acne.

Depending on the amount of the antibiotic, protein production can be reduced or stopped, which would for the first time give medical investigators the ability to regulate gene therapy after the treatment was delivered.

“With this technique, you could adjust the therapy in the patient. That would be extremely helpful because no one is really certain yet what dosage is required for a protective effect in humans. The process is also much more sensitive than we had imagined it would be. GDNF production can be shut down completely with a dose of doxycycline that is much smaller than what is commonly prescribed,” said Fredric P. Manfredsson, a postdoctoral associate in UF’s department of neuroscience.

The researchers used a number of methods to gauge GDNF production, but one was uncommon and involved the novel observation of the rats’ weight.

The scientists found that they could control the rate of weight gain in the rats with dietary doxycycline, which essentially verified they were controlling the GDNF therapy.

The study has been published in the journal Molecular Therapy. (ANI)

Non-lethal blast waves can cause brain injuries even without direct head impacts

Washington, August 27 (ANI): In a new research, scientists have discovered that non-lethal blast waves can cause human brain injury even without direct head impacts, which could lead to an enhanced understanding of head injuries and improved military helmet design.

Using numerical hydrodynamic computer simulations, Lawrence Livermore scientists Willy Moss and Michael King, along with University of Rochester colleague Eric Blackman, have discovered that non-lethal blasts can induce enough skull flexure to generate potentially damaging loads in the brain, even without direct head impact.

Traumatic brain injury (TBI) results from mechanical loads in the brain, often without skull fracture, and causes complex, long-lasting symptoms.

TBI in civilians is usually caused by direct head impacts resulting from motor vehicle and sports accidents. TBI also has emerged among military combat personnel exposed to blast waves.

As modern body armor has substantially reduced soldier fatalities from explosive attacks, the lower mortality rates have revealed the high prevalence of TBI.

But, TBIs resulting from blast waves without head impacts have not been well understood.

To tackle this puzzle, the research team used three-dimensional hydrodynamic simulations to prove that direct action of the blast wave on the head causes skull flexure, producing mechanical loads in brain tissue comparable to those in an injury-inducing impact, even at non-lethal blast pressures as low as 1 bar above atmospheric pressure.

The Army’s Advanced Combat Helmet replaced the older Personal Armor System for Ground Troops helmet.

Its Kevlar shell provides ballistic and impact protection, and its reduced edge cut, although reducing area of coverage, improves soldiers’ field of vision and hearing.

In particular, the team showed that blast waves affect the brain very differently from direct impacts.

The primary source of injury from direct impacts is the force resulting from the bulk acceleration of the head.

In contrast, a blast wave squeezes the skull, creating pressures as large as an injury-inducing impact and pressure gradients in the brain that are much larger.

This occurs even when the bulk head accelerations induced by a blast wave are much smaller than from a direct impact.

“The blast wave sweeps over the skull like a rolling pin going over dough,” said King, LLNL co-principal investigator.

Although the simulations show that the skull is deformed only about 50 microns, “this is large enough to generate potentially damaging loads in the brain,” according to Moss.

“The possibility that blasts may contribute to traumatic brain injury has implications for injury diagnosis and improved armor design,” he added. (ANI)

Fatness can lead to ‘brain shrinkage’

London, Aug 24 (ANI): A new study from University of California in Los Angeles suggests that piling on the pounds can shrink brains of older people, making them more vulnerable to cognitive problems.

According to Paul Thompson, brains of elderly obese people looked 16 years older than the brains of leaner peers.

The research involving 94 people in their 70s showed that people with higher body mass indexes had smaller brains on average, with the frontal and temporal lobes – important for planning and memory, respectively – particularly affected.

While no one knows whether these people are more likely to develop dementia, a smaller brain is indicative of destructive processes that can develop into dementia.

The team also found that the brains of the 51 overweight people were 6 per cent smaller than those of their normal-weight counterparts, on average, and those of the 14 obese people were 8 per cent smaller.

“The brains of overweight people looked eight years older than the brains of those who were lean, and 16 years older in obese people,” New Scientist quoted Thompson as saying.

Thompson suggests that as increased body fat ups the chances of having clogged arteries, which can reduce blood and oxygen flow to brain cells, the resulting reduction in metabolism could cause brain cell death and the shrinking seen.

He said that exercise protects the very brain regions that had shrunk.

“The most strenuous kind of exercise can save about the same amount of brain tissue that is lost in the obese,” he said.

The findings appear in journal Human Brain Mapping. (ANI)

Scientists identify how meningitis bacteria invade the brain

Washington, Aug 19 (ANI): Scientists in the U.S. have discovered that a specific protein on the surface of a common bacterial pathogen allows the bacteria to leave the bloodstream and enter the brain, initiating the deadly infection known as meningitis.

The new finding may lead to the development of improved vaccines to protect those most vulnerable, including young infants and the elderly.

“Streptococcus pneumoniae, commonly known as pneumococcus, is responsible for half the cases of bacterial meningitis in humans,” said the study’s senior author, Victor Nizet, MD, professor of paediatrics and pharmacy at the University of California, San Diego’s School of Medicine and Skaggs School of Pharmacy and Pharmaceutical Sciences.

Meningitis develops when bacteria penetrate the “blood-brain barrier.”

The blood-brain barrier, comprised of a single layer of highly specialized microvascular endothelial cells, prevents most large molecules from entering into the cerebrospinal fluid, preserving an optimal biochemical environment for brain function.

The research team examined the functions of a protein known as NanA in order to discover how an entire bacterium can breech the blood-brain barrier and gain access to the central nervous system.

NanA is produced by all strains of pneumococcus and displayed prominently on the bacteria’s outer surface.

Through genetic manipulations, the researchers were able to remove the entire NanA protein, or just specific sections of the molecule, from the pathogen.

They found that while normal pneumococci were able to bind, enter and penetrate through human brain microvascular endothelial cells, mutant bacteria lacking the NanA protein -or those expressing only a truncated version of the protein – largely lost these abilities.

Conversely, when the full-length pneumococcal NanA protein was cloned and expressed on the surface of a nonpathogenic laboratory strain, the transformed bacteria gained the ability to bind and enter the same endothelial cells.

Satoshi Uchiyama, MD, a postdoctoral fellow in the Nizet Laboratory and lead author on the study, said: “Our tissue culture studies showed that the NanA protein was both necessary and sufficient for bacterial penetration of the blood brain barrier endothelial cells.”

“After infecting mice intravenously, we also found that far fewer NanA-deficient bacteria left the bloodstream and entered the brain, in comparison to mice infected with the normal pneumococcus,” Uchiyama added.

NanA is best known as an enzyme that cleaves and releases the sugar molecule known as sialic acid, which is present in abundance on the surface of all human cells.

While this enzymatic activity played a small part in promoting NanA-mediated blood-brain barrier interactions, a much stronger role was identified for the outer tip of the protein.

This tip seems to directly attach to the brain microvascular endothelial cells and then stimulate them to take in the pneumococcus.

According to Nizet, because NanA is expressed on the surface of all pneumococcal strains, it is an attractive candidate to include in a universal protein-based vaccine against pneumococcal infection.

The study is available online in the Journal of Experimental Medicine. (ANI)

Our brains may be more flexible than previously thought

London, July 15 (ANI): The human brain seems to be more flexible than previously thought because it can rewire itself within seconds to compensate for a break in incoming data, say researchers.

Daniel Dilks and his colleagues, at the Massachusetts Institute of Technology, say that it is known that the brain is constantly adapting throughout our lives, for example by generating new neurons well into adulthood.

However, they add, they wanted to investigate as to how quickly the brain can adapt, and does it always involve creating new circuits.

For that purpose, say the researchers, they took advantage of the blind spots that occur naturally in our eyes where the optic nerve exits the retina, reports New Scientist magazine.

The brain normally combines images captured by both eyes to fill in the resulting gaps in vision, but the researchers prevented this in 48 volunteers by patching one eye.

Dilks’ team later identified where the blind spot was for each volunteer’s other eye, and then presented an image of a square right next to it.

He says that the volunteers initially saw a square, but reported that within seconds it had morphed into a rectangle, by extending its edge into the blind spot.

According to him, the change in what the volunteers saw was so fast that it must be due to the brain redirecting signals through pre-existing circuits rather than forging new connections.

Based on their observations, the researchers came to the conclusion that the neurons which would normally fill the blind spot using data from the patched eye compensated by stealing data from neighbouring neurons that were “seeing” the square, making it appear like a rectangle.

A research article on their study report has been published in the Journal of Neuroscience. (ANI)

Hearing the music of the brain made possible

London, July 7 (ANI): An American expert has created a technique to turn the human brain’s flickering activity into music.

Philosopher Dan Lloyd at Trinity College in Hartford, Connecticut, believes that listening to scans may give new insights into the differences and similarities between normal and dysfunctional brains.

He points out that brain scans created using functional MRI consist of a series of images in which different areas light up with varying intensity at different times, and that these can be used to determine which parts of the brain are active during a particular task.

Lloyd revealed that to turn such scans into music, he identified regions that become active together, and assigned each of those groups a different pitch.

He later created a software program to analyse a series of scans and generate the notes at those pitches.

The researcher has revealed that each note is played at a volume that corresponds to the intensity of activity.

Upon feeding the software a set of scans of his own brain, taken as he switched between driving a virtual-reality car and resting, Lloyd observed that he could the switch-over in the sounds.

He then gave the software scans taken from volunteers with dementia and schizophrenia, and from healthy volunteers.

He found that the brains of people with schizophrenia switched between low and high activity more erratically than those of healthy subjects, allowing the two types of brain to be distinguished by sound alone.

Even though this difference can be seen by looking at the images, Lloyd’s collaborator Vince Calhoun, at the University of New Mexico in Albuquerque, says that there are variations in the music from people with schizophrenia that are not visually obvious.

“It almost sounds like there is more background warbling,” he says.

The researcher believes that such “unsteady rhythms and cadences” may be indicative of dysfunction in the brain.

Lloyd further observed that the sounds and rhythms in the brains of people with dementia also distinguished from those in the brains of healthy volunteers.

He is now keen on exploring the aesthetic aspects of brain music.

“It’s not quite like composed sound but it’s not random either, it’s ‘almost music’. My students are putting it on their playlists,” he said. (ANI)

Scientists comparing human and canine genomes to find cure for brain cancer

Washington, July 7 (ANI): Researchers at North Carolina State University say that comparing human and canine genomes, they have come to the conclusion that a gene commonly believed to be involved in meningiomas-tumours-which affect the meninges (thin covering) of the human brain, and account for one out of four adult brain tumours-may not be as crucial for tumour formation as previously thought.

“The dog has been man’s best friend for centuries, and now the genome of the dog could well be man’s next best friend,” says Dr. Matthew Breen, professor of genomics at NC State.

“With so much genetic material to consider, one can see why figuring out which genes play a key role in meningiomas is extremely difficult. By looking at tumors seen in both humans and dogs we have a simple way to narrow the search: we compare the affected areas of a human chromosome with related areas on dog chromosomes.

This works because dogs and humans are genetically similar and both get the same kinds of cancers. While we share much of our genetic material, the DNA of a dog is organized differently to our own and this makes it possible to isolate smaller ‘shared’ regions of genetic data rather than looking at an entire chromosome,” he adds.

Breen, NC State colleagues Rachael Thomas and veterinary neurologist Natasha Olby, along with researchers from the University of California-Davis and the Wellcome Trust Sanger Institute in Cambridge, UK shared samples of canine meningiomas for research.

Studies conducted in the past have suggested that a particular tumour-suppressing gene on human chromosome 22, known as NF2, may be a possible contributor to meningioma. It is believed that the deletion of NF2, with its tumour suppressing abilities, may trigger tumour growth.

However, when Breen’s team compared human genome with its canine counterpart, they found that NF2 was rarely affected in dogs with meningioma.

Besides, the research team also looked at gliomas, another kind of brain tumour, and showed common genetic features shared between human and canine tumours that are now under further investigation.

“The data support that dog and human tumors are very similar at the genetic level, so both species will benefit from this research,” Breen says.

“It’s proof of the ‘One Medicine’ concept – the idea that human and animal health relies on a common pool of medical and scientific knowledge and is supported by overlapping technologies and discoveries,” he adds.

A research article on the study has been published in the Journal of Neurooncology. (ANI)