Mechanism that prepares newborn’s brain for information processing found

May 15, 2010 By Leave a Comment

Washington, May 15 (ANI): A mechanism in the memory centre of newborn that adjusts the maturation of the brain for the information processing required later in life has been found by researchers at the University of Helsinki.

The study was published this week in an American science magazine The Journal of Neuroscience.

The brain cells in the brain of a newborn are still quite loosely interconnected. In the middle of chaos, they are looking for contact with each other and are only later able to operate as interactive neural networks.

Many cognitive operations, such as attention, memory, learning and certain states of sleep are based on rhythmic interactions of neural networks. For a long time the researchers have been interested in finding the stage in the development of the brain in which the functional characteristics and interconnections are sufficiently developed for these subtle brain functions.

Key players in this maturation process include a type of nerve cells called interneurones, and recent research sheds light on their functional development. The researchers have noticed that the activeness of the interneurones change dramatically during early development. In the memory centre of the brain they found a mechanism which adjusts changes in the activeness of interneurones.

The interneurones nerve cells are kind of controller cells. In the nervous system of a newborn they promote the creation of nerve cell contacts, and on the other hand they prevent premature rhythmic activity of neural networks. During development the controlling role will change, and the result is that the neural network becomes more efficiently rhythmic. This can be seen, for example, in the strengthening of the EEG signal during sleep.

The mechanism adjusting the activity of the interneurones is related to the development phase which prepares the brain to process and handle information needed later in life. The finding may also offer more detailed means to intervene in the electric disorders of developing neural networks, such as epilepsy. (ANI)

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Schizophrenia drugs turn up volume of brain”s key signaling system

May 13, 2010 By Leave a Comment

Washington, May 13 (ANI): Schizophrenia drugs raise the volume of a key signalling system in the brain, a new research has found.

Eric J. Aamodt and colleagues say: “This is the first example of a common but specific molecular effect produced by all antipsychotic drugs in any biological system.”

Writing in the current edition of ACS Chemical Neuroscience, a monthly journal, the team explains that scientists know little about how antipsychotic drugs work, aside from the drugs” effects on one signalling chemical called dopamine.

New studies, for instance, suggested that medications like olanzapine, quetiapine, and clozapine also affect other signalling systems in the brain.

These systems, including one termed the Akt signalling pathway, influence behaviour by regulating communication between brain cells.

To fill those gaps in knowledge, the scientists turned to genetically modified forms of a worm, C. elegans, often used as a stand-in for people in such research.

The tiny creatures were wired to glow green to show activity of Akt, a signal that is too quiet in schizophrenic brains.

They found that all of the 13 antipsychotic drugs tested, representative of all major categories of antipsychotic medications, helped the worms maintain their characteristic green glow.

The results highlight the importance of Akt signalling in schizophrenia, suggesting that medications or other approaches that increase Akt signalling might help to alleviate the symptoms of schizophrenia.

Other labs have identified certain dietary measures that may also increase Akt signalling. (ANI)

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Schizophrenia genes linked to brain signalling

May 11, 2010 By Leave a Comment

Washington, May 11 (ANI): Genetics researchers analysed the genomes of patients with schizophrenia and found numerous copy number variations—deletions or duplications of DNA sequences—that increase the risk of developing the neurodegenerative disease.

Significantly, many of these variations occur in genes that affect signaling among brain cells.

“When we compared the genomes of patients with schizophrenia to those of healthy subjects, we found variations in genes that regulate brain functions, several of which are already known to be perturbed in patients with this disorder. Although much research remains to be done, detecting genes on specific pathways is a first step to identifying more specific targets for improved drug treatments,” said study leader Dr. Hakon Hakonarson, director of the Center for Applied Genomics at The Children”s Hospital of Philadelphia.

A devastating psychiatric disorder that affects an estimated 1.5 percent of the population, schizophrenia may include hallucinations, disorganized speech, abnormal thought processes and other symptoms.

The researchers compared DNA samples from a total of 1,735 adult patients with schizophrenia to DNA from 3,485 healthy adult subjects, using highly automated genotyping tools.

They used a whole-genome approach, covering the full set of genetic material from each individual, following their first analysis with a replication study.

The study team found copy number variations (CNVs) in or near genes that play important roles in the brain.

Among those genes were CACNA1B and DOC2A, both of which carry the codes for proteins that use calcium signals to help control how neurotransmitters are released in the brain.

Two other genes, RET and RIT2, are members of another signalling gene family known to be involved in brain development.

The researchers found that the genes and signalling systems linked to schizophrenia had some overlap with those for autism and for attention-deficit hyperactivity disorder. In fact, the current study found deletions in the same region of chromosome 16 as that found in a CNV study of autism spectrum disorders that Hakonarson led in 2009.

“Although different brain regions may be affected in these different neuropsychiatric disorders, these overlaps suggest that there may be common features in their underlying pathogenesis. These genes affect synaptic function, so deletions or duplications in those genes may alter how brain circuits are formed,” said Hakonarson.

The research appears in the Proceedings of the National Academy of Sciences. (ANI)

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Power of touch helps paternal mice to bond with offspring

May 11, 2010 By Leave a Comment

London, May 11 (ANI): Scientists have shown that paternal mice bond with their offspring through the power of touch.

In the study, it was shown that paternal mice that physically interact with their babies grow new brain cells and form lasting memories of their babies.

The researchers found that when paternal mice interact with their newborn babies, new brain cells develop in the olfactory bulb, the part of the brain responsible for sense of smell, and in the hippocampus, which is responsible for memory.

Weeks after the fathers are separated from their babies they still demonstrate that bond and are able to distinguish their offspring from unrelated mice.

If fathers are prevented from physical interactions with their babies, no new neurons or memories are formed and they cannot recognize their offspring.

Previous research has shown that adult humans also have the capacity to generate new brain cells in the olfactory bulb and the hippocampus and that human fathers exhibit more affection and attachment and fewer ignoring behaviours toward children whose smell they can identify.

“What we have found has implications for long-term mental health. Our work shows that social interactions foster healthy brains and healthy brains foster positive social interactions, demonstrating a positive feedback loop. Our findings support the idea that physical interactions between fathers and their offspring may be a critical component for developing healthy relationships and a healthy society,” said neuroscientist Samuel Weiss, director of the Hotchkiss Brain Institute at the Faculty of Medicine.

The study is published on-line this week in the prestigious international journal, Nature Neuroscience. (ANI)

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Differences in brain’s language circuits linked to dyslexia

May 11, 2010 By Leave a Comment

Washington, May 11 (ANI): Despite getting an appropriate education and demonstrating intellectual ability in other areas, kids children with dyslexia often struggle with reading, writing, and spelling. Now, scientists have found the reason behind it.

They have found that these children”s difficulties with written language may be linked to structural differences within an important information highway in the brain known to play a role in oral language.

Vanderbilt University researchers Sheryl Rimrodt and Laurie Cutting and colleagues at Johns Hopkins University and Kennedy Krieger Institute used an emerging MRI technique, called diffusion tensor imaging (DTI), to discover evidence linking dyslexia to structural differences in an important bundle of white matter in the left-hemisphere language network.

White matter is made up of fibers that can be thought of as the wiring that allows communication between brain cells; the left-hemisphere language network is made up of bundles of these fibres and contains branches that extend from the back of the brain (including vision cells) to the front parts that are responsible for articulation and speech.

“When you are reading, you are essentially saying things out loud in your head. If you have decreased integrity of white matter in this area, the front and back part of your brain are not talking to one another. This would affect reading, because you need both to act as a cohesive unit,” said Cutting.

Rimrodt and Cutting used the DTI technique to map the course of an important white matter bundle in this network and discovered that it ran through a frontal brain region known to be less well organised in the dyslexic brain.

They also found that fibers in that frontal part of the tract were oriented differently in dyslexia.

Rimrodt sai:, “To find a convergence of MRI evidence that goes beyond identifying a region of the brain that differs in dyslexia to linking that to an identifiable structure and beginning to explore physical characteristics of the region is very exciting. It brings us a little bit closer to understanding how dyslexia happens.”

The findings are published in the June 2010 issue of Elsevier”s Cortex. (ANI)

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Endometrial stem cells could repair Parkinson”s related brain cell damage

May 7, 2010 By Leave a Comment

Washington, May 7 (ANI): In a study on mice, researchers found that stem cells derived from the endometrium (uterine lining) could repair brain cells damaged by Parkinson”s disease, according to Yale School of Medicine researchers.

Although these are preliminary results, the findings increase the likelihood that endometrial tissue could be harvested from women with Parkinson”s disease and used to re-grow brain areas that have been damaged by the disease, according to lead author Dr. Hugh S. Taylor.

Because of their ability to divide into new cell types, stem cells could be the key to treating many different kinds of diseases, like Parkinson”s, in which the body”s own cells are damaged or depleted.

Parkinson”s is caused by a breakdown of dopamine-producing nerve cells in the brain stem. Dopamine is a neurotransmitter that stimulates the motor neurons that in turn control muscles.

When dopamine production is reduced, the nerves fail to control movement or maintain coordination.

In their study, the researchers collected and cultured endometrial tissue from nine women, and verified that they could be transformed into dopamine-producing nerve cells like those in the brain.

“The dopamine levels in the mice increased once we transferred the endometrial stem cells into their brains. This is encouraging because women have a ready supply of stem cells that are easily obtained, can differentiate into other cell types. They may have great potential for treating multiple diseases,” said Taylor.

Highlighting the benefits of using endometrial stem cells, Taylor said the ethical concerns surrounding the use of embryonic stem cells are eliminated when using adult stem cells.

Taylor also pointed out that endometrial stem cells are one of the best sources for generating neurons because they appear to be less likely to be rejected than stem cells from other sources.

“This is just the tip of the iceberg of what we will be able to do with these cells. We believe these neurons are only the first of many cell types derived from endometrium that will be used to treat a variety of diseases,” said Taylor.

The findings are published in the Journal of Cellular and Molecular Medicine. (ANI)

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Dark chocolate may provide protection against brain injury from stroke

May 6, 2010 By Leave a Comment

Washington, May 6 (ANI): A compound in dark chocolate may protect the brain after a stroke by increasing cellular signals already known to shield nerve cells from damage, Johns Hopkins researchers have discovered.

Ninety minutes after feeding mice a single modest dose of epicatechin, a compound found naturally in dark chocolate, the scientists induced an ischemic stroke by essentially cutting off blood supply to the animals” brains.

They found that the animals that had preventively ingested the epicatechin suffered significantly less brain damage than the ones that had not been given the compound.

While most treatments against stroke in humans have to be given within a two- to three-hour time window to be effective, epicatechin appeared to limit further neuronal damage when given to mice 3.5 hours after a stroke. Given six hours after a stroke, however, the compound offered no protection to brain cells.

Sylvain Doré, Ph.D., associate professor of anesthesiology and critical care medicine and pharmacology and molecular sciences at the Johns Hopkins University School of Medicine, says his study suggests that epicatechin stimulates two previously well-established pathways known to shield nerve cells in the brain from damage.

When the stroke hits, the brain is ready to protect itself because these pathways — Nrf2 and heme oxygenase 1 — are activated. In mice that selectively lacked activity in those pathways, the study found, epicatechin had no significant protective effect and their brain cells died after a stroke.

The study appears online in the Journal of Cerebral Blood Flow and Metabolism. (ANI)

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Uncontrolled brain activity linked to epilepsy

April 26, 2010 By Leave a Comment

London, April 26 (ANI): An American study has shed new light on the mechanism behind epilepsy attacks in the brain.

Neuroscientist Douglas A. Coulter, the co-author of the research study, from The Children”s Hospital of Philadelphia, said: “By better understanding the detailed events that occur in epilepsy, we are gaining knowledge that could ultimately lead to better treatments for epilepsy, and possibly for other neurological diseases.

“Temporal lobe epilepsy, in particular, often resists current treatments.”

For the research, Coulter and colleagues, collaborated with a team led by co-senior author Philip G. Haydon, of Tufts University School of Medicine.

In epilepsy, excessive signalling between neurons, a major type of brain cell that communicates electrical signals across gaps called synapses, can lead to epileptic seizures.

However, another class of brain cells called glia can regulate those signals. Among the glia are star-shaped cells called astrocytes-the particular focus of this research.

Haydon, the Annetta and Gustav Grisard professor and chair of the department of neuroscience at Tufts, said: “This study shows that changes in astrocytes are key to brain dysfunction and opens the potential for novel therapeutic strategies in epilepsy.

The researchers focused on an abnormal condition called reactive astrocytosis, known to occur in many neurological diseases.

The astrocytes swell to a large size and change expression levels of a number of proteins.

The impact of reactive astrocytosis on brain function is difficult to investigate because it usually occurs in the context of brain inflammation and abnormal changes in surrounding cells.

The researchers solved this problem by using a virus to selectively cause reactive astrocytosis without triggering broader inflammation and brain injury, in a mouse model.

They were able to focus on how the altered astrocytes affected specific synapses in neurons in the brain”s hippocampus.

Studying the neuronal circuitry in brain slices from the mice, the study team found that changes in reactive astrocytes profoundly reduced the inhibitory control over brain signals.

Healthy brain function requires a delicate balance between excitation – the firing of brain signals – and inhibition, which limits those signals.

An enzyme called glutamine synthetase is a key actor in a biological cycle that regulates the balance.

The current study found that reactive astrocytosis reduces the supply of that enzyme, which in turn decreases inhibition and allows neurons to fire out of control.

Coulter said: “We already know that inhibition is a powerful force in the brain.

“In epilepsy, inhibition is not working properly, and uncontrolled signaling leads to epileptic seizures. Because both disrupted inhibition and reactive astrocytosis are known to occur in other neurologic conditions, including many psychiatric disorders, traumatic brain injury, and neurodegenerative disorders such as Parkinson”s disease, our findings may have wide implications.”

Significantly, the researchers were able to dampen neuronal excitability in the animals” brain slices by adding glutamine, an amino acid that is depleted as a result of reduced glutamine synthetase activity.

The study has appeared in the journal Nature Neuroscience. (ANI)

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Gene that ties stress to obesity and diabetes identified

April 20, 2010 By Leave a Comment

Washington, April 20 (ANI): Scientists have discovered a gene that ties stress to obesity and diabetes.

Dr. Alon Chen of the Weizmann Institute”s Neurobiology Department and his research team have now discovered that changes in the activity of a single gene in the brain not only cause mice to exhibit anxious behavior, but also lead to metabolic changes that cause the mice to develop symptoms associated with type 2 diabetes.

All of the body”s systems are involved in the stress response, which evolved to deal with threats and danger.

Behavioural changes tied to stress include heightened anxiety and concentration, while other changes in the body include heat-generation, changes the metabolism of various substances and even changes in food preferences.

The research team suspected that a protein known as Urocortin-3 (Ucn3) ties all of these things together. This protein is produced in certain brain cells – especially in times of stress – and it”s known to play a role in regulating the body”s stress response.

These nerve cells have extensions that act as ”highways” that speed Ucn3 on to two other sites in the brain: One, in the hypothalamus – the brain”s center for hormonal regulation of basic bodily functions – oversees, among other things, substance exchange and feelings of hunger and satiety; the other is involved in regulating behavior, including levels of anxiety.

Nerve cells in both these areas have special receptors for Ucn3 on their surfaces, and the protein binds to these receptors to initiate the stress response.

The researchers developed a new, finely-tuned method for influencing the activity of a single gene in one area in the brain, using it to increase the amounts of Ucn3 produced in just that location.

They found that heightened levels of the protein produced two different effects: The mice”s anxiety-related behavior increased, and their bodies underwent metabolic changes, as well.

With excess Ucn3, their bodies burned more sugar and fewer fatty acids, and their metabolic rate sped up.

These mice began to show signs of the first stages of type 2 diabetes: A drop in muscle sensitivity to insulin delayed sugar uptake by the cells, resulting in raised sugar levels in the blood. Their pancreas then produced extra insulin to make up for the perceived ”deficit.”

“We showed that the actions of single gene in just one part of the brain can have profound effects on the metabolism of the whole body,” Chen said.

These findings were published online this week in the Proceedings of the National Academy of Sciences (PNAS). (ANI)

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Why some people are more susceptible to stress than others

March 31, 2010 By Leave a Comment

Washington, March 31 (ANI): Scientists have found new clues to why some people are more susceptible to stress than others.

In a study of mice, researchers at UT Southwestern Medical Center determined that weeks after experiencing a stressful event, animals that were more susceptible to stress exhibited enhanced neurogenesis – the birth of new nerve cells in the brain.

Specifically, the cells that these animals produced after a stressful event survived longer than new brain cells produced by mice that were more resilient.

In addition, when researchers prevented neurogenesis in both stress-susceptible and resilient mice, the animals previously susceptible to stress became more resilient.

“This work shows that there is a period of time during which it may be possible to alter memories relevant to a social situation by manipulating adult-generated nerve cells in the brain,” said Dr. Amelia Eisch, associate professor of psychiatry at UT Southwestern and senior author of the study.

“This could eventually lead to a better understanding of why, in humans, there is an enormous variety of responses to stressful situations,” Eisch added.

The study appears in the Proceedings of the National Academy of Sciences. (ANI)

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How the brain constructs morality

March 30, 2010 By Leave a Comment

Washington, Mar 30 (ANI): MIT neuroscientists have influenced people”s moral judgments by disrupting specific brain region, a development that helps reveal how the brain constructs morality.

To make moral judgments about other people, we often need to infer their intentions – an ability known as “theory of mind.”

Previous studies have shown that a brain region known as the right temporo-parietal junction (TPJ) is highly active when we think about other people”s intentions, thoughts and beliefs. In the new study, the researchers disrupted activity in the right TPJ by inducing a current in the brain using a magnetic field applied to the scalp. They found that the subjects” ability to make moral judgments that require an understanding of other people”s intentions was impaired.

The researchers, led by Rebecca Saxe, MIT assistant professor of brain and cognitive sciences, report their findings in the Proceedings of the National Academy of Sciences the week of March 29.

The study offers “striking evidence” that the right TPJ, located at the brain”s surface above and behind the right ear, is critical for making moral judgments, says Liane Young, lead author of the paper. It”s also startling, since under normal circumstances people are very confident and consistent in these kinds of moral judgments, says Young, a postdoctoral associate in MIT”s Department of Brain and Cognitive Sciences.

“You think of morality as being a really high-level behavior,” she says. “To be able to apply (a magnetic field) to a specific brain region and change people”s moral judgments is really astonishing.”

To reach the conclusion, the researchers used a non-invasive technique known as transcranial magnetic stimulation (TMS) to selectively interfere with brain activity in the right TPJ. A magnetic field applied to a small area of the skull creates weak electric currents that impede nearby brain cells” ability to fire normally, but the effect is only temporary.

In one experiment, volunteers were exposed to TMS for 25 minutes before taking a test in which they read a series of scenarios and made moral judgments of characters” actions on a scale of 1 (absolutely forbidden) to 7 (absolutely permissible).

In a second experiment, TMS was applied in 500-milisecond bursts at the moment when the subject was asked to make a moral judgment. For example, subjects were asked to judge how permissible it is for someone to let his girlfriend walk across a bridge he knows to be unsafe, even if she ends up making it across safely. In such cases, a judgment based solely on the outcome would hold the perpetrator morally blameless, even though it appears he intended to do harm.

In both experiments, the researchers found that when the right TPJ was disrupted, subjects were more likely to judge failed attempts to harm as morally permissible. Therefore, the researchers believe that TMS interfered with subjects” ability to interpret others” intentions, forcing them to rely more on outcome information to make their judgments. (ANI)

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Some women have ‘bad mum’ switch

March 26, 2010 By Leave a Comment

Melbourne, Mar 26 (ANI): Some women are born with a bad mother switch, says a new study.

Researchers at Richmond University in Virginia said that women develop a set of “maternal neurons” that operate like “bad mother/good mother” switches in the brain.

Using brain-scanning techniques, they have identified a cluster of brain cells, created during pregnancy and “switched on” after birth, that appear to correlate with good or bad parenting behaviours.

“We believe that a certain number of these ”maternal neurons” need to be ”switched on” for good mothering to take place,” News.com.au quoted Professor Craig Kinsley, whose research has so far been limited to rodents and small mammals, as saying.

“Our research showed that the mothers with fewer than this number of ‘maternal neurons’ tended to neglect or abuse their offspring, while those animals with the lowest numbers actually savaged or killed their own young,” he added.

Similar techniques could soon be used to identify human mothers with the capacity to abuse their children.

A team at Yale University is already using brain scans to study the areas of the brain that drive good and bad mothering.

“We have identified certain areas of the brain where there is a correlation between the level of neuron activity and measures of ‘adequate’ and ‘inadequate’ parenting,” said Professor James Swain.

However, not everyone is supporting the idea.

“There is no single factor that determines maternal behaviour,” said Professor Alison Fleming.

“The idea that a woman’s brain is ‘hard-wired’ in such a way that she will abuse her children and that it is not within her power to refrain from doing wrong is based on a misunderstanding of neuro-anatomy. All behaviour is dictated by the brain, but the brain is formed in interaction with our environment,” he added.

Fleming is also concerned that the new research into maternal neurons could be used to argue diminished responsibility for those who abuse their children.

But Kinsley disagrees, saying: “We are all a slave to our brain function. An abusive mother has something malfunctioning in the brain so, in that respect, her behavior is beyond her control.” When it comes to studying the brain, questions of “bad” and “good” need to be replaced with notions of “broken” and “fixed”, he said.

“But it’s not a question of whether we excuse a certain behaviour. The aim of our research is to identify brain malfunctions so we can work towards fixing them.” (ANI)

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New Alzheimer’s-related genes identified

September 7, 2009 By Leave a Comment

London, Sept 7 (ANI): A group of British scientists have identified two new genes that are linked with Alzheimer’s disease.

After analysing the gene pool of more than 19,000 older European and U.S. residents, researchers from the School of Medicine at Cardiff in the UK and Washington University School of Medicine in St. Louis have discovered the genes APOJ, also known as clustrin, on chromosome 8, and PICALM, on chromosome 11.

A team of French colleagues have also uncovered a third gene called APOE4, the only one previously linked to the more common late-onset form of the disease.

“There’s good evidence that these new genes may be novel risk factors, the first discovered since APOE in 1993,” Nature magazine quoted Washington University researcher and co-author Alison M. Goate as saying.

“So it’s a very important observation because this study is the first to provide such significant evidence of novel genetic risk factors for the most common form of Alzheimer’s disease,” she added.

Co-author Dr. John C. Morris, of Washington University, said: “The power of the new Genome Wide Association Study methods is that with large datasets we can now identify genes that earlier techniques were unable to confirm. These new genes associated with Alzheimer’s disease provide new clues about how the illness develops.”

Prof Julie Williams, Chief Scientific Adviser to the Alzheimer’s Research Trust, said: “Both CLU and PICALM highlight new pathways that lead to Alzheimer’s disease. The CLU gene produces clusterin which normally acts to protect the brain in a variety of ways. Variation in this gene could remove this protection and contribute to Alzheimer’s development.”

She added: “PICALM is important at synapses – connections between brain cells – and is involved in the transport of molecules into and inside of nerve cells, helping form memories and other brain functions.

We know that the health of synapses is closely related to memory performance in Alzheimer’s disease, thus changes in genes which affect synapses are likely to have a direct effect on disease development.”

Goate believes that many more genes may be involved in Alzheimer’s risk.

A research article on the study has been published in the journal Nature Genetics. (ANI)

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Eyes alert us to approaching objects before brain notices

September 7, 2009 By Leave a Comment

London, September 7 (ANI): Swiss scientists have discovered a kind of eye cells that can alert people to any objects drawing near, without taking the brain’s help.

Botond Roska and his colleagues at the Friedrich Miescher Institute for Biomedical Research in Basel believe that this ability may have evolved to speed escape from predators.

As to the significance of this finding, the researchers say that scientists have thus far known that the only cells that are sensitive to approaching objects exist in the brain.

While investigating mouse eye cells, the researchers noticed that one type behaved unusually in response to movement.

Upon further analysis, they observed that this one kind of retinal cell fired only when an object approached.

Based on that observation, the researchers came to the conclusion that people might have similar cells, which alert them to approaching objects faster than the brain cells do.

“It’s an alarm system that’s as close to the front end of the organism as possible. If you left it to the brain to respond, it might be too late,” New Scientist magazine quoted Roska as saying.

He has revealed that his next step will be to find out how the approach-sensitive cells evoke a reaction in the brain.

Russell Foster, a neuroscientist at the University of Oxford, said: “This is exciting work. How the nerve cells of the visual system work out that an object is approaching represents a very old question in neuroscience.”

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

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

August 29, 2009 By Leave a Comment

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)

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Epilepsy linked to disruption of brain development during early childhood

August 25, 2009 By Leave a Comment

London, August 24 (ANI): Scientists at Beth Israel Deaconess Medical Center (BIDMC) say that a form of partial epilepsy, which is associated with auditory and other sensory hallucinations, may result from the disruption of brain development during early childhood.

The researchers claim that their findings provide the first genetic link between childhood brain development and a seizure disorder that lasts throughout adulthood, and also identify a new pathway that controls how neuron circuits are “pruned” and matured.

“During early childhood – roughly between the ages of one and five – the brain undergoes a period of major circuit remodeling,” Nature magazine quoted senior author Dr. Matthew Anderson, a principal investigator in the Departments of Neurology and Pathology at BIDMC, as saying.

“Our discovery that a familial form of temporal lobe epilepsy can develop at this point demonstrates the fragility of the brain during this critical period,” he added.

In their study report, the researchers have revealed that their findings focus on the development of synapses, the connections between brain cells.

“At birth, the brain is loaded with excitatory synapses which help make nerve cells ‘fire,’” says Anderson, who is also an Assistant Professor of Neurology and Pathology at Harvard Medical School.

“However, if these excess synapses are not adequately ‘pruned,’ they can overgrow, leading to excessive transmission of excitatory signals and the development of pathological conditions, including learning disabilities and autism in addition to epilepsy,” he adds.

Anderson has revealed that his study involved a genetically engineered mouse model, and and brain slice patch-clamp electrophysiology techniques.

He said that his team found that a mutant form of the LGI1 (leucine-rich glioma-inactivated 1) gene was preventing the normal brain development.

“The first clue was our discovery that LGI1 is not expressed until the exact time when excitatory synapses are matured. We subsequently learned that the mLGI1 gene was indeed prohibiting excitatory synapses from being adequately pruned, leading to an increased excitability of circuits in the brain which left it prone to excessive synchronous discharges that are characteristic of epilepsy,” said Anderson.

Autosomal dominant lateral temporal lobe epilepsy (ADLTE) is characterized by frequent partial seizures-two to five per month-that are associated with auditory or other sensory auras.

Tonic-clonic seizures also occur in the majority of ADLTE patients, but are infrequent, developing only about once a year.

“These partial seizures can have a significant impact on a patient’s quality of life. Because patients can be disoriented and excessively tired following a seizure event, their day-to-day lives can sometimes be seriously disrupted. And when it comes to driving and other activities, there is still a real danger associated with this condition,” notes Anderson.

“One important reason to identify genetic causes of epilepsy is the hope that these discoveries will eventually lead to new therapies. By identifying this new pathway, we may have found a new target for future drug development,” he adds.

A research article describing Anderson’s study has been published in the journal Nature Medicine. (ANI)

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Fatness can lead to ‘brain shrinkage’

August 25, 2009 By Leave a Comment

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)

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Bird flu virus strain leaves survivors at increased Parkinson’s disease risk

August 20, 2009 By Leave a Comment

Washington, August 20 (ANI): An animal study conducted by experts at St. Jude Children’s Research Hospital has suggested that at least one strain of the H5N1 avian influenza virus leaves survivors at significantly increased risk for Parkinson’s disease, and possibly other neurological problems later in life.

In their study report, the researchers write that mice that survived infection with an H5N1 flu strain were found to be more likely than uninfected mice to develop brain changes associated with neurological disorders like Parkinson’s and Alzheimer’s diseases.

Parkinson’s and Alzheimer’s involve loss of brain cells crucial to a variety of tasks, including movement, memory and intellectual functioning.

The researchers say that their study has shown that the H5N1 flu strain causes a 17 percent loss of the same neurons lost in Parkinson’s as well as accumulation in certain brain cells of a protein implicated in both diseases.

“This avian flu strain does not directly cause Parkinson’s disease, but it does make you more susceptible,” said Dr. Richard Smeyne, associate member in St. Jude Developmental Neurobiology.

“Around age 40, people start to get a decline in brain cells. Most people die before they lose enough neurons to get Parkinson’s. But we believe this H5N1 infection changes the curve. It makes the brain more sensitive to another hit, possibly involving other environmental toxins,” Smeyne added.

Smeyne revealed that the study focused on a single strain of the H5N1 flu virus, the A/Vietnam/1203/04 strain, and that the threat posed by other viruses, including the current H1N1 pandemic flu virus, was still being studied.

During the study, the researchers infected some mice with an H5N1 flu strain isolated in 2004 from a patient in Vietnam, which is still considered to be the most virulent of the avian flu viruses.

About two-thirds of the mice developed flu symptoms, primarily weight loss. After three weeks, there was no evidence of H5N1 in the nervous systems of the mice that survived.

However, the inflammation triggered by the infection within the brain continued for months, and it was found to be quite similar to inflammation associated with inherited forms of Parkinson’s.

Although the tremor and movement problems disappeared as flu symptoms eased, the researchers reported that 60 days later, mice had lost roughly 17 percent of dopamine-producing cells in SNpc, a structure found in the midbrain.

They also found evidence that the avian flu infection led to over-production of a protein found in the brain cells of individuals with both Alzheimer’s and Parkinson’s diseases.

“The virus activates this protein,” Smeyne said.

The study has been reported in the online early edition of the Proceedings of the National Academy of Sciences. (ANI)

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MRI methods can show bone marrow stem cells’ viability as brain-repairing therapy

August 20, 2009 By Leave a Comment

Washington, August 20 (ANI): Researchers at Tel Aviv University have offered new hope for people with incurable neurodegenerative diseases like Huntington’s, Alzheimer’s, and Parkinson’s by showing that the viability of stem cells created from a patient’s own bone marrow can be determined using MRI tracking methods.

Dr. Yoram Cohen, of TAU’s School of Chemistry, claims that he has been able to track the progress of the innovative cells called mesenchymal stem cells within the brain.

He says that initial studies indicate that it is possible to identify unhealthy or damaged tissues, migrate to them, and potentially repair or halt cell degeneration.

“By monitoring the motion of these cells, you get information about how viable they are, and how they can benefit the tissue. We have been able to prove that these stem cells travel within the brain, and only travel where they are needed. They read the chemical signalling of the tissue, which indicate areas of stress. And then they go and try to repair the situation,” he says.

During the study, Dr. Cohen and his colleagues tracked the activity of the live cells within the brain using the in-vivo MRI at the Strauss Centre for Computational Neuro-Imaging, with a view to establishing their viability as a therapy for neurodegenerative disease.

The researchers used magnetic iron oxide nanoparticles to label the stem cells, so that they could be identified as clear black dots on an MRI picture after being injected into the brain.

The stem cells were then injected into the brain of an animal that had an experimental model of Huntington’s disease, which suffered from a similar neuropathology as the one seen in human patients.

On MRI, it was possible to watch the stem cells migrating towards the diseased area of the brain.

“Cells that go toward a certain position that needs to be rescued are the best indirect proof that they are live and viable. If they can migrate towards the target, they are alive and can read chemical signalling,” says Dr. Cohen.

He believes that the benefits of using differentiated mesenchymal cells (MSC) may be numerous.

“Bone marrow-derived MSCs bypass ethical and production complications, and in the long run, the cells are less likely to be rejected because they come from the patients themselves. This means you don’t need immunosuppressant therapy,” he says.

Dr. Cohen has revealed that the next step in his research will be to develop a real-life therapy for those suffering from neurodegenerative diseases.

A researcher article on his study has been published in the journal Stem Cells. (ANI)

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How toxic various sizes of Alzheimer’s clusters can be to brain’s nerve cells

August 12, 2009 By Leave a Comment

Washington, August 12 (ANI): In a breakthrough that may pave the way for an effective treatment for Alzheimer’s disease, scientists at the University of California-Los Angeles (UCLA) have created various sizes of clusters in their lab, which exactly match the clusters of the amyloid ß-protein (Aß) protein that form in the brains of those affected with the disease.

The researchers say that their work has shown that the ability of these grape-like clusters to kill nerve cells in the brain, scientifically known as toxicity, increases dramatically as they increase in size.

They say that though the larger clusters are more toxic than smaller ones, the larger formations are relatively rare.

Given that smaller versions are numerous, the researchers say, they are an inviting target for the development of new therapeutic drugs.

“We now have the best understanding yet of what types of toxic A-beta structures we should target with new classes of therapeutic drugs,” said senior author David Teplow, a professor of Neurology at UCLA.

The researchers have found that the larger the cluster, the greater the toxicity, but they also found that the increase in toxicity with these clusters is not linear.

“Clusters that contain two Aß molecules are more toxic than a single Aß molecule, and those with three molecules are more toxic that those with two,” said Teplow.

He pointed out that clusters composed of two Aß molecules are three-fold more toxic than the simple monomer compound, but those made of three molecules and four four molecules are more than 10-fold more toxic than are monomers.

This suggests that the larger, more toxic clusters should be the target for scientists trying to stop Alzheimer’s.

But Teplow notes that the relative amounts of the smaller clusters are far greater than that of the bigger clusters, and are, in total, more toxic.

So in an Alzheimer’s brain, the larger clusters are relatively rare, he said.

“Think of the molecules being wrapped in very weak Velcro. So a number of molecules can bind together to form large clusters, but they break apart very easily,” he said.

Having developed a process in the lab to be able to make pure forms of these Aß clusters of specific size will enable detailed study of their structures to show where every atom is.

“This will make development of drugs much easier and likely more successful,” he said. (ANI)

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