ERA-Net NEURON Announces Winners of the First Excellent Paper in Neuroscience Award

July 7, 2010 By Leave a Comment

AMSTERDAM–(Business Wire)–
ERA-Net NEURON, an initiative of the European Commission aimed at advancing
transnational European research in the field of disease-related neuroscience,
announced today the winners of the Excellent Paper in Neuroscience award for
young scientists for the year 2009. The two winners, awarded each a prize of
€3,000, are Dr. Heidi O. Nousiainen from the National Institute for Health and
Welfare, Biomedicum, Finland and Dr. Asya Rolls from the Weizmann Institute of
Science, Israel. The award ceremony took place during the 7th Forum of European
Neuroscience Societies (FENS) yesterday in Amsterdam. Dr. Heidi Nousiainen was
invited to the Conference as the special ERA-Net NEURON Young Investigator
lecturer.

“The first Excellent Paper in Neuroscience Award is awarded to outstanding
scientific publications by young researchers in the field of disease related
neurosciences,” said Dr. Marlies Dorlöchter, coordinator of ERA-Net NEURON. “The
two winners, chosen out of seven candidates, have made significant contributions
towards our understanding of disease and injury of the nervous system as well as
the development of novel therapies. Their achievements emphasize the high
quality neuroscience research undertaken in Europe.”

About the Chosen Papers

Dr. Heidi O. Nousiainen received the award on her publication in Nature Genetics
(2008)1 describing and identifying the gene underlying two fatal nervous system
diseases (LCCS1 and LAAHD) that are characterized by marked atrophy of spinal
cord motoneurons and fetal immobility, and who are lethal already during fetal
development or shortly after birth. Dr. Nousiainen discovered that the disease
causing gene is GLE1 which encodes for a protein that has been shown to
participate in mRNA export from the nucleus as well translation of mRNA into
protein. This discovery adds a new and important member to the increasing number
of RNA processing molecules linked to neurodegenerative diseases. This study
provides significant new information about the molecular background of fetal
motoneuron disease, but at the same time also gives insight into the mechanisms
that are essential for the normal development as well as maturation and
functioning of motoneurons.

Dr. Asya Rolls received the award on her publication in PLoS Medicine (2008)2
for elucidating the role of scar tissue formation in spinal cord repair after
injury. It has been accepted for quite some time that lack of nerve regeneration
in the central nervous system is due to formation of a deleterious scar tissue.
Dr. Rolls addressed the question of why should the body invest so much energy in
scar formation after traumatic spinal cord injury (SCI) only to inhibit spinal
cord repair. She showed that initial formation of the scar, and in particular a
protein called CSPG, is part of an `SOS` response crucial for recovery. In fact,
inhibiting the formation of CSPG at the early stages of spinal cord injury
actually harms the recovery process. On the other hand, CSPG inhibition during
the later subacute phase, improves functional recovery and can benefit
regeneration. This study thus identified an endogenous repair mechanism of the
body and may have considerable implications for the treatment of SCI.

About ERA-Net NEURON

ERA-Net NEURON, an initiative funded by the European Commission, has been set up
to establish sustained co-operation between national funding bodies and to
coordinate their research programs on disease-related neuroscience. Coordinated
by Dr. Marlies Dorlöchter from Germany, the participating ERA-Net NEURON partner
countries and funding institutions include: Austria, The Austrian Science Fund
(FWF); Canada, The funding agency for health research in Québec (FRSQ); Finland,
Academy of Finland (AKA); France, The National Agency for Research (ANR), the
French National Centre for Scientific Research (CNRS) and the National Institute
for Health and Medical Research (INSERM); Germany, Project Management Agency in
the German Aerospace Centre (PT-DLR) for the Federal Ministry of Education and
Research (BMBF); Israel, The Chief Scientist Office, Ministry of Health
(CSO-MOH); Italy, Ministry of Health (MOH); Luxemburg, National Research Fund
(FNR); Poland – National Centre for Research and Development (NCBiR); Romania,
Ministry of Education and Research (ANCS-MEdR) and National Centre for
Programmes Management (CNMP); Spain – Ministry of Education and Science (MICINN)
and Fund for Health Research (ISCIII-FIS); Sweden, Swedish Research Council
(SRC); and United Kingdom, Medical Research Council. For further information,
please visit www.neuron-eranet.org.

1 Heidi O Nousiainen H.O., Marjo Kestilä M., Pakkasjärvi N., Honkala H., Kuure
S., Tallila J., Vuopala K., Ignatius J., Herva R. and Peltonen L. (2008).
Mutations in mRNA export mediator GLE1 result in a fetal motoneuron disease.
Nature Genetics, 2:155-7

2 Rolls A., Shechter R., London A., Segev Y., Jacob-Hirsch J., N., Rechavi G.,
Schwartz M. (2008). Two Faces of Chondroitin Sulfate Proteoglycan in Spinal Cord
Repair: A Role in Microglia/Macrophage Activation. PLoS Medicine, 5:1262-1277

ERA-Net NEURON
Tsipi Haitovsky, Media Liaison
+972-52-598-9892
tsipih@netvision.co.il

Copyright Business Wire 2010

Filed Under: International News Tagged With: , , , , , , , , , , , , , , , , , , ,

How sex hormones control ‘masculinization’ of the brain

April 29, 2010 By Leave a Comment

Washington, Apr 29 (ANI): A new study has uncovered some information about how sex hormones control masculinization of the brain during development and drive gender related behaviors in adult males.

Published by Cell Press in the April 29 issue of the journal Neuron, the study demonstrates that direct action of testosterone, the prototypical male hormone, is unnecessary for masculinizing the brain and behavior.

Testosterone and estrogen are thought to play an essential role in organizing and activating gender-specific patterns of behavior in sexually reproducing animals.

Testosterone is produced by the testes and directly activates the androgen receptor (AR) in target tissues such as muscle. Estrogen is produced by the ovaries and is nearly undetectable in the circulation of males of most species. However, circulating testosterone in males can be converted into estrogen in the brain, and this testosterone-derived estrogen has been shown to control many male behaviors.

“It was known that testosterone and estrogen are essential for typical male behaviors in many vertebrate species,” explains the study”s senior author, Dr. Nirao M. Shah from the Department of Anatomy at the University of California, San Francisco. “However, how these two hormones interact to control masculinization of the brain and behavior remained to be established.”

Dr. Shah and colleagues found that during the neonatal testosterone surge there is very little AR expressed in the developing brain, making it unlikely that testosterone signaling via AR plays a major role in masculinizing neural pathways. Importantly, they went on to show that the male pattern of AR expression in the brain was dependent on testosterone-derived estrogen signaling.

The researchers then used a genetic approach to knock out the AR in the mouse nervous system and observed that these mutants still exhibited male type mating, fighting, and territorial marking behaviors. However, these mutant males had striking reductions in specific components of these masculine behaviors. These results show that testosterone signaling via AR does not control masculine differentiation of the brain and behavior but regulates the frequency and extent of male typical behaviors.

“Our findings in conjunction with previous work suggest a model for the control of male pattern behaviors in which estrogen masculinizes the neural circuits for mating, fighting, and territory marking, and testosterone and estrogen signaling generate the male typical levels of these behaviors,” concludes Dr. Shah. “It will be interesting in future studies to identify the molecular and circuit level mechanisms that are controlled by these hormones.” (ANI)

Filed Under: International News Tagged With: , , , , , , , , , , , , , , , , , , ,

Intelligent, creative computers come closer to reality

April 26, 2010 By Leave a Comment

London, Apr 26 (ANI): Taking a leap towards intelligent and creative computers, researchers have now created a brain-like process of circuit evolution in an organic molecular layer that can solve complex problems.

The advance by the international research team from Japan and Michigan Technological University is the first time a brain-like “evolutionary circuit” has been realized.

This computer is massively parallel—the world””s fastest supercomputers can only process bits one at a time in each of their channels. Their circuit allows instantaneous changes of 300 bits.

Their processor can produce solutions to problems for which algorithms on computers are unknown, like predictions of natural calamities and outbreaks of disease.

To prove this unique feature, the researchers have mimicked two natural phenomena in the molecular layer—heat diffusion and the evolution of cancer cells.

The monolayer has intelligence— it can solve many problems on the same grid.

Their molecular processor heals itself if there is a defect, reports Nature.

This remarkable self-healing property comes from the self-organizing ability of the molecular monolayer.

No existing man-made computer has this property, but our brain does: if a neuron dies, another neuron takes over its function.

The work is described in the Nature Physics paper. (ANI)

Filed Under: International News Tagged With: , , , , , , , , , , , , , , , , , ,

Network problem harms brain in Alzheimer’s disease!

March 29, 2010 By Leave a Comment

Mon, Mar 29 12:02 PM

In what could pave the way for new strategies for early diagnosis and effective treatment of Alzheimer’s, scientists have found that the disease makes parts of the brain shrink “as messages fail to get through”.

The findings, published in the ‘Neurology’ journal, suggest a build-up of deposits of the protein amyloid-beta in a region of the brain known as temporal inferior cortex which is connected to the hippocampus involved in memory.

Alzheimer’s disease is characterised by two factors –a build-up of amyloid-beta plaques in the brain, and a loss of neurons.

Lead scientist Dr Cassandra Szoeke of CSIRO said the puzzle for them was that the parts of the brain that had shrunk (atrophied) due to neuron loss were not the same as those showing increased deposits of amyloid-beta.

Using MRI scans to study Alzheimer’s disease affected brain tissue, the scientists found that shrinking (atrophy) of the hippocampus was associated with plaque deposits in the temporal inferior cortex.

The results indicate that the increased accumulation of amyloid in temporal inferior cortex disrupts connections with the hippocampus, causing the neurons to die, say the scientists.

“By helping to better understand the mechanisms involved in the progression of the disease, the study may guide the development of new strategies for early diagnosis,” Dr Szoeke said.
Agencies

Filed Under: International News Tagged With: , , , , , , , , , , , , , , , , , , ,

How the brain constructs morality

March 25, 2010 By Leave a Comment

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)

Filed Under: International News Tagged With: , , , , , , , , , , , , , , , , , , ,

What makes the first impression last?

March 25, 2010 By Leave a Comment

London, Mar 25 (ANI): Scientists at Cedars-Sinai Medical Center and the California Institute of Technology have found how the memory of a first impression lasts in the brain.

They have suggested that when memory-related neurons in the brain fire in sync with certain brain waves, the resulting image recognition and memories are stronger than if this synchronization does not occur.

Synchronization is influenced by “theta waves,” which are associated with relaxation, daydreaming and drowsiness, but also with learning and memory formation.

While it has long been understood that a relaxed mind is one that is ready to receive new information, the study pinpoints a mechanism by which this state of mind allows neurons to work together to improve memory retention.

Further exploration of these events could have implications for developing new therapies to treat learning disabilities and some types of dementia, according to the authors.

“Theta oscillations are known to be involved in memory formation, and previous studies have identified correlations between memory strength and the activity of certain neurons, but the relationships between these events have not been understood. Our research shows that when memory-related neurons are well coordinated to theta waves during the learning process, memories are stronger,” said Dr. Adam N. Mamelak.

“We have yet to discover all factors that influence theta oscillations and the coordination of spike timing, but this study establishes a direct relationship between events at the circuit level of the brain – individual neuron spike timing relative to the local brain wave environment – and their effects on human behavior,” said Dr. Ueli Rutishauser.

He said that the study also found that while the predictability of memory strength was determined by spike timing relative to theta oscillations, it was not influenced by other related factors, such as the neuron-firing rate or the amplitude of the theta oscillations.

This study was conducted with eight volunteers who suffer from epilepsy and were undergoing intracranial EEGs.

The authors note that steps were taken to ensure that the patients” underlying medical condition did not affect the outcome of the study.

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

Filed Under: International News Tagged With: , , , , , , , , , , , , , , , , , , ,

Soon, robot controlled by human brain cells

September 10, 2009 By Leave a Comment

London, Sept 10 (ANI): Scientists from University of Reading are working on developing a robot that would be controlled by human brain cells.

Lead researchers Kevin Warwick and Ben Whalley have already used rat brain cells to control a simple wheeled robot.

During the study, the researchers grew around 300,000 rat neurons in a nutrient broth and device producing spikes of electrical activity were connected to the output of the robot’s distance sensors.

The neurons could successfully steer the robot around a small enclosure.

Based on the findings rat models, the researchers are now working on steering the robot with the help of human brain cells.

The researchers believe that understanding how the neuron culture responds to stimulation could lead to deeper insights of neurological conditions such as epilepsy.

For instance, the way large numbers of neurons sometimes spike in unison – a phenomenon known as “bursting” – may be similar to what happens during an epileptic seizure.

The research team suggests if the behavior could be altered by changing the culture chemically, electrically or physically, it might pave way for potential therapies.

To make the system a better model of human disease, a culture of human neurons will be connected to the robot once the current work with rat cells is completed.

They will analyze the differences in the behavior of robots controlled by rat and human neurons.

“We’ll be trying to find out if the learning aspects and memory appear to be similar,” New Scientist quoted Warwick as saying. (ANI)

Filed Under: Science News Tagged With: , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , ,

Forgotten memories still exist in the brain

September 10, 2009 By Leave a Comment

Washington, Sept 10 (ANI): A new research by UC Irvine neuroscientists suggests that memories exist even when forgotten.

With the help of advanced brain imaging techniques, the study’s scientists discovered that a person’s brain activity while remembering an event is very similar to when it was first experienced, even if specifics can’t be recalled.

“If the details are still there, hopefully we can find a way to access them,” said Jeff Johnson, postdoctoral researcher at UCI’s Center for the Neurobiology of Learning and Memory and lead author of the study, appearing Sept. 10 in the journal Neuron.

“By understanding how this works in young, healthy adults, we can potentially gain insight into situations where our memories fail more noticeably, such as when we get older,” he said.

“It also might shed light on the fate of vivid memories of traumatic events that we may want to forget,” he added.

In collaboration with scientists at Princeton University, Johnson and colleague Michael Rugg, CNLM director, used functional magnetic resonance imaging to study the brain activity of students.

Inside an fMRI scanner, the students were shown words and asked to perform various tasks: imagine how an artist would draw the object named by the word, think about how the object is used, or pronounce the word backward in their minds. The scanner captured images of their brain activity during these exercises.

About 20 minutes later, the students viewed the words a second time and were asked to remember any details linked to them. Again, brain activity was recorded.

Utilizing a mathematical method called pattern analysis, the scientists associated the different tasks with distinct patterns of brain activity. When a student had a strong recollection of a word from a particular task, the pattern was very similar to the one generated during the task.

When recollection was weak or nonexistent, the pattern was not as prominent but still recognizable as belonging to that particular task.

“The pattern analyzer could accurately identify tasks based on the patterns generated, regardless of whether the subject remembered specific details,” Johnson said.

“This tells us the brain knew something about what had occurred, even though the subject was not aware of the information,” the expert added. (ANI)

Filed Under: Science News Tagged With: , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , ,

Nicotine plays “tricks” on the brain

September 10, 2009 By Leave a Comment

Washington, Sept 10 (ANI): Nicotine, the addictive component in cigarettes, “tricks” the brain into creating memory associations between environmental cues and smoking behavior, say researchers at Baylor College of Medicine.

The study has been published in the journal Neuron.

“Our brains normally make these associations between things that support our existence and environmental cues so that we conduct behaviors leading to successful lives. The brain sends a reward signal when we act in a way that contributes to our well being,” said Dr. John A. Dani, professor of neuroscience at BCM and co-author of the study.

“However, nicotine commandeers this subconscious learning process in the brain so we begin to behave as though smoking is a positive action,” the expert added.

Dani said that environmental events linked with smoking can become cues that prompt the smoking urge. Those cues could include alcohol, a meal with friends, or even the drive home from work.

To understand why the associations are so strong, Dani and Dr. Jianrong Tang, instructor of neuroscience at BCM and co-author of the report, decided to record brain activity of mice as they were exposed to nicotine, the addictive component of tobacco.

The mice were allowed to roam through an apparatus with two separate compartments. In one compartment, they received nicotine. In the other, they got a benign saline solution. Later, the researchers recorded how long the mice spent in each compartment. They also recorded brain activity within the hippocampus, an area of the brain that creates new memories.

“The brain activity change was just amazing. Compared to injections of saline, nicotine strengthened neuronal connections – sometimes up to 200 percent. This strengthening of connections underlies new memory formation,” Dani said.

Consequently, mice learned to spent more time in the compartment where the nicotine was administered compared to the one where saline was given to them.

“We found that nicotine could strengthen neuronal synaptic connections only when the so called reward centers sent a dopamine signal. That was a critical process in creating the memory associations even with bad behavior like smoking,” the expert said. (ANI)

Filed Under: Science News Tagged With: , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , ,

How addictive drugs influence learning and memory

September 10, 2009 By Leave a Comment

Washington, Sep 10 (ANI): In a new study on mice, researchers have found why and how the use of addictive drugs take control of reward signals and influence neural processes associated with learning and memory.

The study could help explain how drug-associated memories, such as the place of drug use, drive and perpetuate the addiction.

It is known that the neurochemical dopamine, a key player in the brain’s reward system, is involved in the process of addiction.

Research has indicated that dopamine participates in neural processes associated with learning, such as the strengthening of neuronal connections, called synaptic potentiation.

Evidence has also implicated the hippocampus, a deep-brain structure that is critical for formation of new memories, in the development of drug addiction.

“Although addictive drugs like nicotine have been shown to influence the induction of synaptic potentiation, there has been little or no research in freely moving animals that monitors ongoing induction of synaptic potentiation by a biologically relevant drug dose,” explains senior author Dr. John Dani from the Department of Neuroscience at the Baylor College of Medicine in Houston, Texas.

The researchers recorded from the brains of freely moving mice while applying physiologically relevant concentrations of nicotine, the addictive component in tobacco.

The researchers found that nicotine induced synaptic potentiation correlated with the mice learning to prefer a place associated with the nicotine dose.

Importantly, these effects required a local dopamine signal within the hippocampus.

The finding reinforces the view that dopamine enables memory for specific events.

Overall, the results point to some intriguing possibilities about how drug-associated memories might contribute to behaviors associated with addiction.

“An animal’s memories or feelings about the environment are updated when the dopamine signal labels a particular event as important, new, and salient. Normally these memories help us to perform successful behaviors, but in our study, those memories were linked to the addictive drug.

When specific environmental events occur, such as the place or people associated with drug use, they are capable of cuing drug-associated memories or feelings that motivate continued drug use or relapse,” concluded Dani.

The study has been published in the latest issue of the journal Neuron. (ANI)

Filed Under: Science News Tagged With: , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , ,

Newly found natural odours could pave way for developing mosquito repellents

August 27, 2009 By Leave a Comment

London, Aug 27 (ANI): In a lab study on fruit flies, entomologists led by an Indian origin scientist at the University of California, Riverside, have discovered a novel class of compounds that could help in developing inexpensive and safe mosquito repellents for combating West Nile virus and other deadly tropical diseases.

Under stress, fruit flies emit carbon dioxide (CO2) that serves as a warning to other fruit flies that danger or predators could be nearby.

The fruit flies are able to detect the CO2 and escape because their antennae are equipped with specialized neurons that are sensitive to the gas.

But fruits and other important food sources for fruit flies also emit CO2 as a by-product of respiration and ripening.

Researchers started to wonder how does fruit flied find their way to these foods, despite having an inherent tendency to avoid CO2.

However, Anandasankar Ray, an assistant professor in the Department of Entomology, and Stephanie Turner, his graduate student, have now identified a new class of odorants – chemical compounds with smells – present in ripening fruit that prevent the CO2-sensitive neurons in the antennae from functioning.

They discovered that particularly two odours, hexanol and 2,3- butanedione, are strong inhibitors of the CO2-sensitive neurons in the fruit fly.

The research has strong implications for control of deadly diseases transmitted by Culex mosquitoes such as West Nile virus disease and filariasis, an infectious tropical disease affecting the lymphatic system.

“CO2 emitted in human breath is the main attractant for the Culex mosquito to find people, aiding the transmission of these deadly diseases. In our experiments we identified hexanol, and a related odor, butanal, as strong inhibitors of CO2-sensitive neurons in Culex mosquitoes. These compounds can now be used to guide research in developing novel repellents and masking agents that are economical and environmentally safe methods to block mosquitoes’ ability to detect CO2 in our breath, thereby dramatically reducing mosquito-human contact,” Nature quoted Ray as saying.

Inhibitory odours not only play an important role in modifying insect behaviour, but the study found that some of these odours even have a long-term effect.

For example, the researchers found that some odours silenced the CO2 neuron in the fruit fly well beyond the period of application.

“To our surprise, we found that exposure to a long-term CO2 response inhibitor can exert a profound and specific effect on the behavior of the insect, even after the inhibitor is no longer in the environment.

This means this odorant could potentially be used to keep mosquitoes at bay for longer periods of time, benefiting people in areas where mosquito-transmitted diseases are prevalent,” said Ray.

The results of the study appear in Nature. (ANI)

Filed Under: Science News Tagged With: , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , ,

Indian-origin boffin offers potential new spinal muscular atrophy treatment

July 29, 2009 By Leave a Comment

Washington, July 28 (ANI): A team of researchers led by Indian origin scientist has come up with a potential new treatment for spinal muscular atrophy, the second-leading cause of infant mortality in the world.

Ravindra Singh, associate professor in biomedical sciences at Iowa State University’s College of Veterinary Medicine said that more than 95 percent of the sufferers have a mutated or deleted gene called Survival Motor Neuron 1 (SMN1) that doesn’t correctly do its job of creating functional SMN proteins.

He suggested that replacing poor-performing gene with another gene could help treat the disease.

Humans need a certain level of SMN protein to ward off Spinal Muscular Atrophy.

When SMN1 fails to create functioning proteins, Spinal Muscular Atrophy is the result.

There is a gene already in humans that looks very much like SMN1, so much so that it’s called SMN2. The SMN2 gene doesn’t seem to serve any function that researchers can identify.

Singh has discovered a way of using SMN2 to produce the working SMN protein. When SMN2 makes enough SMN, it compensates for the mutated or malfunctioning SMN1 gene.

However, SMN2 doesn’t produce normal protein because of the presence of a specific intronic sequence in the gene or DNA.

To make SMN2 behave as SMN1, Singh has introduced a small antisense oligonucleotide that blocks this specific intronic sequence.

When the intronic sequence is blocked, SMN2 produces normal proteins and acts, in effect, like SMN1.

“The significance of our work is that we have this stuff called junk DNA in SMN2,” said Singh.

“We found that we could get SNM2 to behave as SMN1 by introducing a small oligonucleotide. It is a very simple experiment if you think about it,” he added.

The resulting proteins are normal just like a regular cell – free from Spinal Muscular Atrophy.

“Our cells are healthy and survive. From that point of view, this is a major achievement,” he added.

The study appears online in Landes Bioscience.(ANI)

Filed Under: Science News Tagged With: , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , ,

Anticipating an award as satisfying as actually receiving it

July 16, 2009 By Leave a Comment

Washington, July 16 (ANI): No one likes to be held in suspense when it comes to receiving rewards. And now, a new research has claimed that knowing that you’re in line for a particular prize is as satisfying as actually receiving it.

The study demonstrates that single neurons in the reward centre of the brain process not only primitive rewards but also more abstract, cognitive rewards related to the quest for information about the future.

The study has been published by Cell Press in the July 16 issue of the journal Neuron.

“The desire to know what the future holds is a powerful motivator in everyday life, but we know little about how this desire is created by neurons in the brain,” says lead study author Dr. Ethan S. Bromberg-Martin from the National Institutes of Health in Bethesda, Maryland.

Dr. Bromberg-Martin and co-author, Dr. Okihide Hikosaka, investigated whether dopamine-releasing neurons associated with processing basic primitive rewards, such as food and water, are also involved in processing more abstract rewards.

The researchers focused on a form of cognitive reward that involves anticipation of a substantial future gain.

In the study, a simple decision task allowed rhesus monkeys to choose whether to view informative pictures that would tell them the size of upcoming water rewards.

The researchers recorded the activity of dopamine reward neurons while the monkeys performed the task.

The monkeys showed a strong preference for information about upcoming rewards and preferred to receive the information as soon as possible, even though the information had no effect on the final reward outcome.

Importantly, the dopamine neurons that signalled the monkey’s expectation of water rewards also signalled the expectation of advance information in a manner that was correlated with the strength of the animal’s preference.

“The monkeys and dopamine neurons treated information about rewards as if it was a reward itself,” explains Dr. Bromberg-Martin.

The authors conclude that the same dopamine neurons that signal primitive rewards like food and water also signal the cognitive reward of advance information. (ANI)

Filed Under: Science News Tagged With: , , , , , , , , , , , , , , , , , , ,

New drug helps rescue memory loss in mice with Alzheimer’s disease

July 15, 2009 By Leave a Comment

Washington, July 15 (ANI): A drug similar to the one used in clinical trials for treatment of rheumatoid arthritis and psoriasis has been found to be effective against Alzheimer’s disease, say researchers.

The drug called PMX205 has been found to prevent inflamed immune cells from gathering in brain regions with Alzheimer’s lesions called amyloid plaques.

Cell inflammation in these areas accelerates neuron damage, exacerbating the disease.

“We used a multidisciplinary approach combining an understanding of immunology and neurobiology to uncover a completely different target than other therapies,” said Andrea Tenner, lead author of the study that led to the findings, and a molecular biology and biochemistry professor at UCI.

During the study, the researchers fed the mice, genetically altered to develop age-related Alzheimer’s-like symptoms, with PMX205 mixed in drinking water for 12 weeks.

The treatment occurred at an age when plaques were accumulating in their brains.

The researchers then gave the treated mice learning and memory tests and examined their brains for evidence of the disease.

The study showed that Alzheimer’s mice that were not given the drug performed significantly worse on the test than normal mice.

But – in all but one case – the treated Alzheimer’s mice performed almost as well as the normal mice.

Those with the rescued cognitive ability had more than 50 percent fewer Alzheimer’s lesions and inflammatory immune cells than the untreated diseased mice.

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

Filed Under: Uncategorized Tagged With: , , , , , , , , , , , , , , , , , , , ,

Scientists identify alcohol-binding site in the brain

June 29, 2009 By Leave a Comment

London, June 29 (ANI): Scientists at the Salk Institute for Biological Studies have a step closer to understanding how alcohol alters the way brain cells work.

The researchers say that they have identified a binding site for alcohol in an ion channel that plays a key role in several brain functions associated with drugs of abuse and seizures.

They believe that their results could lead to the development of novel treatments for alcoholism, drug addiction, and epilepsy.

Ethanol, the alcohol in intoxicating beverages, is known to alter the communication between brain cells.

“There’s been a lot of interest in the field to find out how alcohol acts in the brain,” Nature magazine quoted Dr. Paul A. Slesinger, an associate professor in the Peptide Biology Laboratory at the Salk Institute, as saying.

“One of several views held that ethanol works by interacting directly with ion channel proteins, but there were no studies that visualized the site of association,” added the lead researcher.

He says that his study has shown that alcohols directly interact with a specific nook contained within a channel protein.

According to him, this ion channel plays a key role in several brain functions associated with drugs of abuse and seizures.

In their previous research, Slesinger’s team focused on the neural function of these ion channels, called GIRK channels, which open up during periods of chemical communication between neurons and dampen the signal, creating the equivalent of a short circuit.

“When GIRKs open in response to neurotransmitter activation, potassium ions leak out of the neuron, decreasing neuronal activity,” says UCSD Biology graduate student and first author Prafulla Aryal.

While alcohols have been previously shown to open up GIRK channels, no study ever determined whether this was a direct effect or whether this was the by-product of other molecular changes in the cell.

The researchers say that the identification of the location of a physical alcohol-binding site important for GIRK channel activation could point to new strategies for treating related brain diseases.

They believe that this protein structure may be used to develop a drug that antagonizes the actions of alcohol for the treatment of alcohol dependence.

“(Alternatively) If we could find a novel drug that fits the alcohol-binding site and then activate GIRK channels, this would dampen overall neuronal excitability in the brain and perhaps provide a new tool for treating epilepsy,” says Slesinger.

A research article describing the study has been published in the journal Nature Neuroscience. (ANI)

Filed Under: Science News Tagged With: , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , ,

How neuronal activity is timed in brain’s memory-making circuits

May 30, 2009 By Leave a Comment

London, May 30 (ANI): Researchers at the California Institute of Technology (Caltech) have challenged the long-held assumption that theta oscillations-a type of prominent brain rhythm that orchestrates neuronal activity in the hippocampus-remain “in sync” across this key area for the formation of new memories.

In a new study, the researchers have found that instead of being in sync, theta oscillations actually sweep along the length of the hippocampus as travelling waves.

“It was assumed that activity in the hippocampus is synchronized throughout. But when we looked simultaneously at many different anatomical locations across the hippocampus, we found instead a systematic delay in neuronal activity from site to site. Instead of the whole structure oscillating at once, we see travelling waves that propagate across the hippocampus in a consistent direction, along its long axis,” Nature magazine quoted Evgueniy Lubenov, a postdoctoral scholar at the Center for Biological Circuit Design at Caltech, as saying.

Athanassios Siapas, associate professor of computation and neural systems and Bren Scholar at Caltech, added: “In other words, the hippocampus has a series of local time zones, just like we have on Earth.”
During the study, the researchers analysed the theta oscillations generated as rats move around and explore their environment.

The observed how and when rats’ neurons fired relative to their positions and to the phase of the theta oscillations.

They did so using multiple electrodes with recording sites, which enabled them to simultaneously isolate the spiking of many individual neurons.

“Each of these neurons fires only in a restricted region of space. Furthermore, the spikes don’t just happen any time-they pay attention to the phase of the ongoing theta oscillation. If you have access to the phase at which the neuron fired, you have additional information about where the rat was in space,” Lubenov said.

Upon combining the data about neuronal firing, oscillation phase and rat location, the researchers observed that neuronal activity indeed sweeps across the hippocampus in a wave, with its peak appearing in one region, then another, then another, rather than hitting the entire hippocampus in one synchronized pulse.

“This changes our notion of how spatial information is represented in the rat brain. It was believed that the firing of hippocampal neurons encodes the physical location of the rat in its environment-in other words, a point of physical space. Our findings suggest that what is encoded is actually a portion of the rat’s trajectory-that is, a segment of physical space,” Lubenov said.

Siapas added: “Such segments may be the elementary unit of hippocampal computation. Assume the path a rat takes in an environment is represented and stored as a sequence of point locations. If the rat visits the same location more than once, the representation becomes ambiguous. Representing the rat trajectory as a sequence of segments oriented in space resolves such ambiguities.”

The researchers say that the significance of their findings lies in the fact that they may prove helpful in understanding how information is transmitted from the hippocampus to other areas of the brain.

“Different portions of the hippocampus are connected to different areas in other parts of the brain. The fact that hippocampal activity forms a traveling wave means that these target areas receive inputs from the hippocampus in a specific sequence rather than all at once,” said Siapas.

The researcher also dismissed the suggestion that this behaviour is found only in rat brains, insisting that theta oscillations are ubiquitous in mammalian brains.

“I would expect the traveling-wave nature of theta oscillations to be a general finding, applicable to humans as well,” he said.

And while it is not known whether human hippocampal cells function as place cells, as they do in rats, “it may turn out to be the case that the human hippocampus plays a role in providing spatial cues that are important to episodic memory,” Lubenov said.

What we do know is that, by showing that theta oscillations travel across the hippocampus, the Caltech team will likely change the way neuroscientists think about how the hippocampus works. (ANI)

Filed Under: Science News Tagged With: , , , , , , , , , , , , , , , , , , , ,

Scientists identify ‘molecule trio’ that kills neurons in Parkinson’s

May 2, 2009 By Leave a Comment

Washington, Apr 30 (ANI): In a novel study, researchers at Columbia University Medical Centre have identified a trio of molecules that are responsible for killing brain cells in Parkinson’s patients.

They have showed that three molecules – the neurotransmitter dopamine, a calcium channel, and a protein called alpha-synuclein – act together to kill the neurons.

The symptoms of Parkinson’s – including uncontrollable tremors and difficulty in moving arms and legs – are blamed on the loss of neurons from the substantia nigra region of the brain.

“Though the interactions among the three molecules are complex, the flip side is that we now see that there are many options available to rescue the cells,” said Dr Eugene Mosharov, associate research scientist and study’s author.

The researchers showed that neurons die because calcium channels lead to an increase of dopamine inside the cell; excess dopamine then reacts with alpha-synuclein to form inactive complexes; and then the complexes gum up the cell’s ability to dispose of toxic waste that builds up in the cell over time. The waste eventually kills the cell.

The neurons will survive if just one of the three factors is missing, said the researchers.

“It may be possible to save neurons and stop Parkinson’s disease by interfering with just one of the three factors,” Dr. Mosharov added.

The researchers hope that a drug already in clinical trials – which blocks the culprit calcium channel – may work to slow or stop the progression of the disease.

The study is published in journal Neuron. (ANI)

Filed Under: Science News Tagged With: , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , ,

How the brain handles words

May 2, 2009 By Leave a Comment

Washington, Apr 30 (ANI): How the brain gives meaning to letters on a page has been a mystery for scientists. Now, a new study has tried to solve the puzzle.

Neuroscientists at Georgetown University Medical Center have found that an area known to be important for reading in the left visual cortex contains neurons that are specialized to process written words as whole word units.

Although some theories of reading as well as neuropsychological and experimental data have argued for the existence of a neural representation for whole written real words (an “orthographic lexicon”), evidence for this has been elusive.

“Reading relies on neural representations that are experience dependent,” says senior author Maximilian Riesenhuber, PhD, of the GUMC Laboratory for Computational Cognitive Neuroscience.

“Evolution did not provide each of us with a little dictionary in our heads,” the expert added.

Because the findings, published in the April 30 issue of Neuron, shed light on how written words are processed in the brain, they also provide clues as to how reading disorders such as dyslexia could arise, Riesenhuber says.

“Previous studies have shown that this brain area is affected in reading disorders such as dyslexia, but it is unclear what the mechanisms involved are. Our data suggest that looking at the neuronal selectivity in this area might provide new insight. For instance, we would expect reading difficulties if neurons never become well tuned to words, making reading a slow, arduous process, just like it would be if reading all nonwords,” the expert added.

The GUMC researchers – Riesenhuber, first author Laurie S. Glezer, MA, and Xiong Jiang, PhD – set up a series of experiments with the participation of volunteers. They showed the participants pairings of words, and used functional Magnetic Resonance Imaging (fMRI) to measure brain blood flow in an area in the left visual cortex called the “visual word form area” while the participants performed a reading task.

Most other studies using fMRI to examine the “visual word form area” have used the averaged neuronal response in which many word stimuli are presented and the change in activity is measured, but this approach does not tease out the response neurons have to individual words, Riesenhuber says. However, by using the technique of fMRI rapid adaptation, in which the stimuli are shown in pairs, it is possible to measure the selectivity of neurons for individual words.

In their experiments, the researchers looked at the response between two visually similar normal words that shared all letters but one (i.e. ‘boat’ and ‘coat’) and found that the neural response to this condition “looked just like when participants saw two words that shared no letters, for example ‘coat’ and ‘fish’,” says Glezer.

“This shows that the neurons in this area of the brain are very selective for individual words. Even though the two words shared all letters but one, there is no overlap in the neural representation, just like when the two words are completely different,” the expert said.

The researchers then looked at the brain’s response to sets of nonwords in which the stimuli look like real words but have never been seen before (i.e. tarm). They found that the response to nonwords was not selective, with similar nonwords appearing to have overlapping neural representations. (ANI)

Filed Under: Science News Tagged With: , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , ,

How proteins travel in the brain

April 23, 2009 By Leave a Comment

London, Apr 22 (ANI): While proteins are known to be at the centre of every life process, and carry out all sorts of work by going to the cell, what guides these basic molecules towards their target cells in the brain has been unknown, until now.

Don Arnold- a molecular and computational biologist at USC College-and colleagues have now solved the mystery for key proteins in the brain.

“There’s no little man sitting there, putting the protein in the right place. Proteins have to have in them encoded information that tells them where to go in the cell,” Nature quoted Arnold as saying.

Neurons have separate structures for receiving signals (dendrites) and for sending them (axons).

The electrical properties of both types of neurons depend on different proteins.

But the proteins travel in bubbles, or vesicles, powered by motors known as kinesins that travel along tiny molecular paths.

Even though the paths point to both axons and dendrites, dendritic proteins end up in dendrites, and axonal proteins go to the axons.

The researchers discovered a crude but effective sorting mechanism, in which firstly kinesins blindly carry both types of proteins towards the axon.

But, dendritic proteins enable the vesicles transporting them to bind to a second motor, known as myosin, that walks them back into the dendrite.

The filter ensures that only axonal proteins make it into the axon, while the others are caught by the second motor and diverted to the dendrite.

“This mechanism fishes these things out of the axon,” said Arnold.

Once in the dendrite, the proteins either land in a place where they can do their electrical work or they move back towards the axon, only to be fished out again.

Arnold said that the process looks inefficient, “but it is very effective.”

The discovery could allow finer control over neurons for basic research or for treatment of neurological disorders.

Also, scientists could target only dendrites or axons in a neuron for studying its outgoing or incoming impulses.

Apart from these applications, the study contributes a lot to the understanding of the brain and of protein transport in general.

“It’s a very basic question, something people have been wondering about for a long time,” said Arnold.

The study is appearing online this week in Nature Neuroscience. (ANI)

Filed Under: Science News Tagged With: , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , ,

Jet lag upsets body clocks in 2 neural centres to disrupt sleep

April 17, 2009 By Leave a Comment

Washington, April 17 (ANI): Scientists at the University of Washington have moved a step closer to developing more effective treatments for jet lag, by finding out that this problem disrupts sleep by upsetting internal clocks in two separate but linked groups of neurons in a structure in the brain called the suprachiasmatic nucleus.

The researchers have revealed that this structure lies below the hypothalamus at the base of the brain.

According to them, one group is synchronized with deep sleep that results from physical fatigue, and the other controls the dream state of rapid eye movement (REM) sleep.

The bottom neurons receive light information directly from the eyes and govern rhythms in tune with periods of light and dark, while the top neurons do not receive direct light information and so govern rhythms as a more independent internal biological clock.

Horacio de la Iglesia, a UW associate professor of biology, points out that some of the body’s rhythms seem to be “more loyal” to the bottom neurons, and others are much more in tune with the top neurons.

Normally the two neuron groups are synchronized with each other, but disruptions like jet travel across time zones or shift work can throw the cycles out of kilter.

Deep sleep is most closely tied to light-dark cycles, and typically adjusts to a new schedule in a couple of days. However, REM sleep is more tied to the light-insensitive dorsal neurons, and can be out of sync for a week or more.

“When we impose a 22-hour light-dark cycle on animals, the ventral center can catch up but the dorsal doesn’t adapt and defaults to its own inner cycle,” de la Iglesia said.

In the rats he tests while conducting lab experiments, that normal cycle is 25 hours.

Upon imposing the artificial 22-hour light-dark schedule, the researcher observed that the rats’ deep sleep quickly adapted to the 22-hour cycle, but their REM sleep continued to follow a 25-hour cycle.

The researcher said that REM sleep, consequently, did not occur in a normal progression following deep sleep.

“We found that after exposing rats to a shift of the light-dark timing that simulates a trip from Paris to New York, REM sleep needed 6 to 8 days to catch up with non-REM, or deep, sleep, the sleep you usually experience in the first part of the night,” de la Iglesia said.

The study showed that the two types of sleep overlap immediately after the simulated jet lag occurs, and that there is a greater likelihood of the animals entering REM sleep earlier than they should.

According to de la Iglesia, this may help understand why travellers and shift workers may take several days to adapt to their new schedules.

“It also could explain why jet lag is associated with lower learning performance. We think the disruption of the normal circadian sequence of sleep states is very detrimental to learning,” he said.

“One of the problems is that you are doing things at times that your body isn’t prepared to do them. One group of neurons tells your body it is Paris time and another says that it is New York time. You are internally desynchronized,” he added.

The researcher believes that this study may be useful in fine-tuning pharmaceutical and other therapies.

“We can go back to the treatments that are believed to be effective and see where they might be acting in the circuitry of these neuron centres, then refine them to be more effective,” he said.

A researcher article on the study has been published online in the journal Current Biology. (ANI)

Filed Under: Uncategorized Tagged With: , , , , , , , , , , , , , , , , , , ,
« Older Posts