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duminică, 5 august 2012

ADHD Linked With Slower Brain Development

According to a study conducted by the National Institutes of Health, children with attention-deficit/hyperactivity disorder (ADHD) experience a developmental delay in frontal regions of the brain.

The study is published in Biological Psychiatry.

The team examined 234 children with ADHD and 231 normally developing children. Each child's brain was scanned up to four times from age 10 to 17. The team then used advanced neuroimaging technology in order to map the trajectories of surface area development at over 80,000 points across the brain.

The surface area of the cerebral cortex - the folded gray tissue that makes up the outermost part of the brain - grows during childhood. However, the researchers discovered that this process was delayed in frontal brain regions in children with ADHD.

According to the researchers, the normally developing children attained 50% peak area in the right prefrontal cortex at a mean of 12.7 years compared with 14.6 years for children with ADHD.

Dr. Phillip Shaw, a clinician studying ADHD at the National Institute of Mental Health explained: "As other components of cortical development are also delayed, this suggests there is a global delay in ADHD in brain regions important for the control of action and attention."

Dr. John Krystal, Editor of Biological Psychiatry, said: "These data highlight the importance of longitudinal approaches to brain structure. Seeing a lag in brain development, we now need to try to understand the causes of this developmental delay in ADHD."

Dr. Shaw explained that the study finding "guides us to search for genes that control the timing of brain development in the disorder, opening up new targets for treatment."

Further research expanding these measures into adulthood will also be vital. Such data would help determine whether or when a degree of normalization occurs, or if these delays translate into long-lasting cortical deficits.

Written by Grace Rattue
Copyright: Medical News Today
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posted by Alexander Nestoiter on 3 Aug 2012 at 7:30 pm

Review this statement from the article very carefully: "According to the researchers, the normally developing children attained 50% peak area in the right prefrontal cortex at a mean of 12.7 years compared with 14.6 years for children with ADHD."
This means that children attain 50% peak in the average of 12.7 years. Children with ADHD attain this point in the average of 14.6 years. The study was conducted on kids from 10 to 17 years of age. As you can see something is off with their figures.
What is even more bothersome, is that while they studied kids 10-17 years of age, they now pass the results of the study to all kids, including those who are only 4 years old.
Not in this article, but in others, they urge parents to monitor their kids for any signs of the broad ADD/ADHD spectrum of symptoms, get the kids diagnosed, and, of course, seek treatment = pills.

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Allergy Sufferers Have Lower Risk Of Brain Tumors

A new study has added to the growing body of evidence implying that there's a link between allergies and reduced risk of a serious type of cancer that starts in the brain.

According to this particular study, published in the Journal of the National Cancer Institute, the reduced risk seems to be stronger among women than men, however men have a lower tumor risk with certain allergies.

Scientists have believed having allergies or similar factors reduces the risk for this cancer, and this study has strengthened that theory. Experts have never known whether allergies lower the risk of cancer or if, before diagnosis, these tumors (glioma) interfere with the hypersensitive immune response to allergens, because they have the potential to suppress the immune system in order to grow.

Stored blood samples that were taken from patients decades before they were diagnosed with glioma were analyzed by the researchers. The researchers found that there was a 50% reduced risk of developing glioma 20 years later for men and women who had blood samples containing allergy-related antibodies, compared to people without signs of allergies.

Judith Schwartzbaum, associate professor of epidemiology at Ohio State University, investigator in the University's Comprehensive Cancer Center, and leading author of the study, said:

"This is our most important finding. The longer before glioma diagnosis that the effect of allergies is present, the less likely it is that the tumor is suppressing allergies. Seeing this association so long before tumor diagnosis suggests that antibodies or some aspect of allergy is reducing tumor risk.
It could be that in allergic people, higher levels of circulating antibodies may stimulate the immune system, and that could lower the risk of glioma. Absence of allergy is the strongest risk factor identified so far for this brain tumor, and there is still more to understand about how this association works."

Studies, until now, have not been able to analyze blood samples collected longer than 20 years before tumor diagnosis. Previous studies examining the relationship between allergies and brain tumor risk have used self-report questionnaires on patients' histories with glioma.

The study also showed that women had at least a 50% lower risk for the most severe and common type of these tumors, known as glioblastoma, if their blood samples tested positive for specific allergy antibodies. These results were not seen in men. On the other hand, men had a 20% reduced risk of this tumor if they tested positive for both specific antibodies and antibodies of unknown function than men who tested negative.

In the United States, glioblastomas constitute about 60% of adult tumors that start in the brain, which affects 3 in 100,000 people. Patients may seek treatments such as radiation, surgery, and chemotherapy. On average, these patients survive for about one year, with fewer than 25% surviving up to 2 years and just 10% surviving up to 5 years.

The Janus Serum Bank in Norway granted the research team access to specimens. This bank contains samples collected over the last 40 years from people during their annual medical checkups or from volunteer blood donors. Since 1953, Norway has registered all recent cancer cases in the country, and personal identification numbers allows cross-referencing those cases with blood samples that have been previously collected.

The experts were able to analyze stored samples from 594 citizens who were diagnosed with glioma, including 374 that were diagnosed with glioblastoma, between 1974 and 2007. These samples were matched for age, sex, and date of blood collection with 1,777 samples from people who did not have glioma in order to compare.

The team was looking for levels of two types of proteins, IgE, or immunoglobulin E, while they were measuring the blood samples. This is a class of antibodies that are made from white blood cells that mediate immune responses to allergens. Two classes of IgE take part in the allergic response: allergen-specific IgE- identifies specific components of an allergentotal IgE- identifies these components but also includes antibodies with unknown functionsThe researchers observed each sample and determined whether the serum had elevated levels of IgE specific to the most common allergens in Norway as well as IgE. Specific Respiratory allergens were: tree pollen and plantsdog and horse danderdust mitesmoldA statistical analysis was then conducted in order to approximate the association between the risk of developing glioma and elevated concentrations of allergen-specific IgE and total IgE.

A 54% reduced risk of glioblastoma was associated with the women who tested positive for elevated levels of allergen-specific IgE compared to the women who tested negative. This association was not seen in men.

The relation between total IgE levels and risk of glioma was the same for both sexes. For men and women combined, a 25% reduced risk of glioma was associated with testing positive for elevated total IgE.

The analysis for effects on glioblastoma risk alone showed a similar decreased risk for both men and women combined whose blood samples tested positive for elevated levels of IgE. However, this finding was considered borderline in terms of statistical significance because it was not a significant enough number, meaning there is still the possibility that the association could be caused by chance.

"There is definitely a difference in the effect of allergen-specific IgE between men and women. And even results for total IgE suggest there still may be a difference between the sexes. The reason for this difference is unknown," explained Schwartzbaum.

This research has shown evidence for the likelihood that the immune system of people with respiratory allergies could help fight against this type of cancer. The author explained that being able to examine this association over 4 decades between blood sampling and tumor diagnosis gave him and his team better insight.

For example, a 46% reduced risk for developing glioma 20 years later was associated with a positive test for elevated concentrations of total IgE compared to samples that tested negative. That reduced risk was only about 25% in samples that tested positive for high levels of total IgE taken between 2 and 15 years before diagnosis.

Schwartzbaum explained:

"There may be a trend- the closer the samples get to the time of diagnosis, the less help the IgE is in decreasing the risk of glioma. However, if the tumor were suppressing allergy, we would expect to see a bigger difference in risk near the time of diagnosis."

He hopes to further his research and analyze the serum samples for concentration of cytokines (chemical passengers that promote or suppress inflammation as part of the immune response) in order to see if these proteins play a part in the relationship between elevated IgE levels and reduced tumor risk.

Written by Sarah Glynn
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today

Visit our neurology / neuroscience section for the latest news on this subject. Association Between Prediagnostic IgE Levels and Risk of Glioma
Judith Schwartzbaum, Bo Ding, Tom Borge Johannesen, Liv T. N. Osnes, Linda Karavodin, Anders Ahlbom, Maria Feychting and Tom K. Grimsrud
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joi, 15 decembrie 2011

New Drug That Improves Memory And Prevents Brain Damage In Mice May Prevent Alzheimer's Disease Progression

Main Category: Alzheimer's / Dementia
Also Included In: Parkinson's Disease; Huntingtons Disease; Stroke
Article Date: 15 Dec 2011 - 7:00 PST

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A new drug candidate may be the first capable of halting the devastating mental decline of Alzheimer's disease, based on the findings of a study published in PLoS one.

When given to mice with Alzheimer's, the drug, known as J147, improved memory and prevented brain damage caused by the disease. The new compound, developed by scientists at the Salk Institute for Biological Studies, could be tested for treatment of the disease in humans in the near future.

"J147 enhances memory in both normal and Alzheimer's mice and also protects the brain from the loss of synaptic connections," says David Schubert, the head of Salk's Cellular Neurobiology Laboratory, whose team developed the new drug. "No drugs on the market for Alzheimer's have both of these properties."

Although it is yet unknown whether the compound will prove safe and effective in humans, the Salk researchers' say their results suggest the drug may hold potential for treatment of people with Alzheimer's.

As many as 5.4 million Americans suffer from Alzheimer's, according to the National Institutes of Health. More than 16 million will have the disease by 2050, according to Alzheimer's Association estimates, resulting in medical costs of over $1 trillion per year.

The disease causes a steady, irreversible decline in brain function, erasing a person's memory and ability to think clearly until they are unable to perform simple tasks such as eating and talking, and it is ultimately fatal. Alzheimer's is linked to aging and typically appears after age 60, although a small percentage of families carry a genetic risk for earlier onset. Among the top ten causes of death, Alzheimer's is the only one without a way to prevent, cure or slow disease progression.

Scientists are unclear what causes Alzheimer's, which appears to emerge from a complex mix of genetics, environment and lifestyle factors. So far, the drugs developed to treat the disease, such as Aricept, Razadyne and Exelon, only produce fleeting memory improvements and do nothing to slow the overall course of the disease.

To find a new type of drug, Schubert and his colleagues bucked the trend within the pharmaceutical industry of focusing exclusively on the biological pathways involved in the formation of amyloid plaques, the dense deposits of protein that characterize the disease. To date, Schubert says, all amyloid-based drugs have failed in clinical trials.

Instead, the Salk team developed methods for using living neurons grown in laboratory dishes to test whether or not new synthetic compounds were effective at protecting the brain cells against several pathologies associated with brain aging. Based on the test results from each chemical iteration of the lead compound, which was originally developed for treatment of stroke and traumatic brain injury, they were able to alter its chemical structure to make a much more potent Alzheimer's drug.

"Alzheimer's is a complex disease, but most drug development in the pharmaceutical world has focused on a single aspect of the disease - the amyloid pathway," says Marguerite Prior, a research associate in Schubert's lab, who led the project along with Qi Chen, a former Salk postdoctoral researcher. "In contrast, by testing these compounds in living cell cultures, we can determine what they do against a range of age-related problems and select the best candidate that addresses multiple aspects of the disease, not just one."

With a promising compound in hand, the researchers shifted to testing J147 as an oral medication in mice. Working with Amanda Roberts, a professor of molecular neurosciences at The Scripps Research Institute, they conducted a range of behavioral tests that showed that the drug improved memory in normal rodents.

The Salk researchers went on to show that it prevented cognitive decline in animals with Alzheimer's and that mice and rats treated with the drug produced more of a protein called brain-derived neurotrophic factor (BDNF), a molecule that protects neurons from toxic insults, helps new neurons grow and connect with other brain cells, and is involved in memory formation.

Because of the broad ability of J147 to protect nerve cells, the researchers believe that it may also be effective for treating other neurological disorders, such as Parkinson's disease, Huntington's disease and amyotrophic lateral sclerosis (ALS), as well as stroke.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our alzheimer's / dementia section for the latest news on this subject. The research was funded by the Fritz B. Burns Foundation, the National Institutes of Health, the Bundy Foundation and the Alzheimer's Association.
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Magnetic Stimulation Of Brain For Stroke Recovery

Editor's Choice
Main Category: Stroke
Also Included In: Neurology / Neuroscience
Article Date: 15 Dec 2011 - 8:00 PST

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In a fresh hope for those who have suffered a stroke, a new research has shown that magnetic stimulation of the nerve cells in the brain, can help speed the recovery.

Anyone who has had a friend or relative suffer a stroke knows what a shocking and debilitating affliction it can be. There are different types of stroke, but all essentially have the result of causing damage to the brain cells and blood circulation to the brain.

The study, published in Neurology, the medical journal of the American Academy of Neurology, explains the use of transcranial magnetic stimulation, a treatment that involves placing large electromagnetic coils against the scalp. It creates electrical currents that stimulate nerve cells.

Study author Giacomo Koch, MD, PhD, of the Santa Lucia Foundation in Rome, Italy said :

"The treatment is based on the theory that hemispatial neglect results when a stroke disrupts the balance between the two hemispheres of the brain.
A stroke on one side of the brain causes the other side to become overactive, and the circuits become overloaded."

The research so far has only involved 20 people, with a specific kind of stroke, known as hemispatial neglect. This is where the right side of the brain has been damaged and the person has little awareness on their left side. They may not even recognize the left side of a plate of food, or be able to see on their left side. (The brain works on opposite sides, so that generally speaking, the right side is responsible for the left side functions.)

10 patients were treated for two weeks, while the other 10 received a placebo treatment. Tests on those who did not receive the real treatment showed little improvement, while those who underwent the real magnetic stimulation had a 16% improvement at the end of the two weeks and a 22% improvement two weeks later. Dr. Koch also showed that over-activity in the damaged nerves of the brain had normalized in patients that had the real magnetic treatment.

Heidi M. Schambra, MD, of Columbia University Medical Center, who wrote an editorial on the study said :

"This study represents an important step forward in the effort to find ways to help people rehabilitate from hemispatial neglect after stroke ... Beyond its direct effect on people's visual-spatial abilities, hemispatial neglect also interferes with people's efforts to recover their cognitive abilities and movement."

It's not the first use of the power of magnetics as a therapy. It has shown success as an antidepressant, and there has been quite a fashion, especially amongst sportsmen, of wearing a small bracelet with a magnet, that is claimed to improve co-ordination and balance.

Other ideas include magnets in the bed to improve sleep, and even magnets in drinking water to enhance its qualities. Perhaps there is something to this "snakeoil" after all.

Written by Rupert Shepherd
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today

Visit our stroke section for the latest news on this subject. "Excitability out of balance: Treating hemineglect with transcranial magnetic brain stimulation"
Neurology WNL.0b013e318241f289; published ahead of print December 14, 2011
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marți, 13 decembrie 2011

Parkinsons' - Brain Volume Decrease And Cognitive Decline Linked

Editor's Choice
Academic Journal
Main Category: Parkinson's Disease
Also Included In: Neurology / Neuroscience
Article Date: 13 Dec 2011 - 9:00 PST

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According to a study published in the December issue of Archives of Neurology, one of the JAMA/Archives journals, individuals who suffer with Parkinson disease-related dementia seem to have increased brain atrophy in the parietal, hippocampal, temporal lobes, as well as decreased prefrontal cortex volume than individuals with Parkinson disease without dementia.

The researchers explain:

"Patients with Parkinson disease (PD) are at an increased risk of developing dementia (PDD), with cumulative prevalence rates of up to 80 percent.
Approximately 25 percent of non-demented PD patients meet neuropsychological criteria for mild cognitive impairment (PD-MCI), which converts to PDD in many cases, and even mild cognitive deficits in PD are associated with functional impairments and worse quality of life."

Daniel Weintraub, M.D., of the Perelman School of Medicine, University of Pennsylvania, Philadelphia, and colleagues, set out to evaluate the areas and patterns of brain atrophy in individuals with Parkinson disease with normal cognition (PD-NC), individuals with Parkinson disease with dementia-level cognitive deficits (PDD), as well as individuals with PD with mild cognitive impairment (PD-MCI).

The researchers enrolled 84 individual with Parkinson disease (61 PD-NC, 11 PDD, and 12 PD-MCI) and 23 healthy control individuals to participate in the study. All participants in the study underwent magnetic resonance imaging (MRI) of the brain. The team gathered data as part of the University of Pennsylvania Center of Excellence for Research on Neurodegenerative Diseases.

After the researchers adjusted for other factors, such as education level, sex, and age of the participant, they discovered no between-group differences in regional brain volumes for PD-NC participants compared with control group patients. The team found that among participants with Parkinson disease, there were cognitive group-level differences in medial temporal lobe and hippocampal volumes.

The hippocampal volumes among PD-MCI and PDD participants were smaller than PD-NC participants, although the team found no differences between participants in the PDD and PD-MCI groups. In addition, participants in the PDD group had medial temporal lobe atrophy compared with participants in the PD-NC group, but not those in the PD-MCI group. The researchers observed no between-group differences for other regions in the brain.

Patients in the PD-MCI group had a different pattern of brain atrophy than participants in the PD-NC group, although similar to that of PDD participants. The researchers characterized this pattern by atrophy in prefrontal cortex gray and white matter, hippocampal volume, parietal lobe white matter, and occipital lobe gray and white matter.

In Parkinson's disease patients without dementia, the team discovered an association between memory-encoding performance and hippocampal volume, "suggesting heterogeneity in the neural substrate of memory impairment."

The researchers conclude:

"With growing recognition of Parkinson disease with mild cognitive impairment as common and clinically significant, it will be important to develop consensus diagnostic criteria, validate assessment instruments for use in clinical care and research, and test treatments for their symptomatic and disease-modifying effects. Use of a pattern classification approach may allow identification of diffuse regions of cortical gray and white matter atrophy early in the course of cognitive decline."

Written by Grace Rattue
Copyright: Medical News Today
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Electrical Activity In The Brain Likened To An Orchestra

Main Category: Neurology / Neuroscience
Also Included In: Medical Devices / Diagnostics; Epilepsy; Parkinson's Disease
Article Date: 13 Dec 2011 - 2:00 PST

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Researchers at the Norwegian University of Life Sciences (UMB) have developed a new method for detailed analyses of electrical activity in the brain. The method, recently published in Neuron, can help doctors and researcher to better interpret brain cell signals.

In turn, this may lead to considerable steps forward in terms of interpreting for example EEG measurements, making diagnoses and treatment of various brain illnesses.

Researchers and doctors have been measuring and interpreting electrical activity generated by brain cells since 1875. Doctors have over the years acquired considerable practical skills in relating signal shapes to different brain illnesses such as epilepsy. However, doctors have so far had little knowledge on how these signals are formed in the network of nerve cells.

"Based on methods from physics, mathematics and informatics, as well as computational power from the Stallo supercomputer in Tromsø, we have developed detailed mathematical models revealing the connection between nerve cell activity and the electrical signal recorded by an electrode," says Professor Gaute Einevoll at the Department of Mathematical Sciences and Technology (IMT) at UMB.

Microphone in a crowd

The problem of interpreting electrical signals measured by electrodes in the brain is similar to that of interpreting sound signals measures by a microphone in a crowd of people. Just like people sometimes all talk at once, nerve cells are also sending signals "on top of each other".

The electrode records the sounds from the whole orchestra of nerve cells surrounding it and there are numerous contributors. One cubic millimetre can contain as many as 100,000 nerve cells.

Treble and bass

Similar to bass and treble in a soundtrack, high and low frequency electrical signals are distinguished in the brain.

"This project has focused on the bass - the low frequency signals called "local field potential" or simply LFP. We have found that if nerve cells are babbling randomly on top of each other and out of sync, the electrode's reach is narrow so that it can only receive signals from nerve cells less than about 0.3 millimetres away. However, when nerve cells are speaking simultaneously and in sync, the range can be much wider," Einevoll says.

Large treatment potential

Better understanding of the electrical brain signals may directly influence diagnosing and treatment of illnesses such as epilepsy.

"Electrodes are already being used to measure brain cell activity related to seizures in epilepsy patients, as well as planning surgical procedures. In the future, LFP signals measured by implanted electrodes could detect an impending epilepsy seizure and stop it by injecting a suitable electrical current," Einevoll says.

"A similar technique is being used on many Parkinson's patients, who have had electrodes surgically implanted to prevent trembling," researcher Klas Pettersen at UMB adds..

Einevoll and Pettersen also outline treatment of patients paralysed by spinal cord fracture as another potential area where the method can be used.

"When a patient is paralysed, nerve cells in the cerebral cortex continue to send out signals, but the signals do not reach the muscles, and the patient is thus unable to move arms or legs. By monitoring the right nerve cells and forwarding these signals to for example a robot arm, the patient may be able to steer by his or her thoughts alone," Einevoll says.

The Computational Neuroscience Group at UMB has already established contacts with clinical research groups in the USA and Europe for further research on using the approach in patient treatment.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our neurology / neuroscience section for the latest news on this subject. Gaute Einevoll recently published the article "Modeling the spatial reach of the LFP" in Neuron, together with his former research fellow Henrik Lindén, currently working at KTH Royal Institute of Technology in Stockholm, Sweden, and researchers Tom Tetzlaff and Klas H. Pettersen at UMB. German researchers Tobias Potjans, professor Sonja Grün and professor Markus Diesmann at Research Center Jülich have also contributed to the study.
The project is mainly financed by the Research Council of Norway's eScience programme and is an example of the increased importance of computational neuroscience in modern brain research.
Einevoll was recently appointed one of four new directors of Organization for Computational Neurosciences, and is also co-leader of the Norwegian national node of INCF (International Neuroinformatics Coordinating Facility).
Both organisations work to promote the use of methods from informatics, mathematics and physics in brain research.
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Brain Tumor Chemotherapy Resistance Prediction

Main Category: Cancer / Oncology
Also Included In: Neurology / Neuroscience; Radiology / Nuclear Medicine
Article Date: 13 Dec 2011 - 1:00 PST

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Glioblastoma multiforme (GBM) is the most common and lethal of all human brain tumors that originate in the brain.

For most patients, treatment involves surgery followed by both radiation therapy and chemotherapy with temozolomide. However, many GBMs are resistant to the effects of temozolomide.

A team of researchers led by Sameer Agnihotri, at the University of Toronto, Toronto, has now determined that the protein APNG can contribute to GBM resistance to the effects of temozolomide. Importantly, high levels of expression of APNG in the nucleus of ressected tumor cells correlated with poorer overall survival compared with patients lacking APNG expression. Agnihotri, and colleagues therefore suggest that monitoring APNG levels could provide insight into whether or not a patient with GBM will respond to temozolomide, although this awaits confirmation in predictive and prospective studies.

TITLE: Alkylpurine-DNA-N-glycosylase confers resistance to temozolomide in xenograft models of glioblastoma multiforme and is associated with poor survival in patients

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
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Erythropoietin May Pose A Risk To Blood Vessels In The Brain And Body

Main Category: Vascular
Also Included In: Neurology / Neuroscience; Sports Medicine / Fitness
Article Date: 13 Dec 2011 - 0:00 PST

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Erythropoietin or EPO might be considered a "performance enhancing" substance for athletes, but new research published online in /i>The FASEB Journal shows that these enhancements come at a high cost - increased risk of vascular problems in the brain. According to the study, short- or long-term use of EPO raises blood pressure by constricting arteries, which reduces the flow of blood to the brain. This finding also contradicts earlier evidence suggesting that EPO may be a viable early treatment for stroke victims.

"The new findings of this study urge to scrutinize present indications for EPO, and so help to better delineate positive versus adversary health effects of EPO for each patient," said Peter Rasmussen, Ph.D., a researcher involved in the work from the Zurich Center for Integrative Human Physiology at the University of Zurich in Switzerland. "Future research should aim at developing an EPO-based agent for treatment that does not have a negative effect on the blood vessels of the brain."

To make this discovery, Rasmussen and colleagues evaluated the effects of acute high doses of EPO for three days and chronic low doses of EPO for 13 weeks in two groups of healthy males. Responsiveness of brain vessels during rest and during bike-riding exercise, with and without hypoxia, was examined. Blood vessels were also analyzed using ultrasound measurements and by measuring how much oxygen reached the brain. They found that prolonged EPO administration increased hematocrit, while acute administration did not. They also found that both groups had increases in blood vessel constriction and higher blood pressure.

"EPO is used by doctors to increase red blood cells in sick people who can't make enough of them: it's called honest medicine. When EPO is used by healthy bikers and runners to boost their performance, it's called cheating. Now we know that folks who use EPO covertly are cheating not only the time-clock, but themselves," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "Not only is EPO likely unsafe in healthy athletes, but there are many other ways to build up stamina without drugs."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our vascular section for the latest news on this subject. Details: Peter Rasmussen, Yu-Sok Kim, Rikke Krogh-Madsen, Carsten Lundby, Niels V. Olsen, Niels H. Secher, and Johannes J. van Lieshout. Both acute and prolonged administration of EPO reduce cerebral and systemic vascular conductance in humans. FASEB J. December 9, 2011; doi:10.1096/fj.11-193508; http://www.fasebj.org/content/early/2011/12/08/fj.11-193508.abstract
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luni, 12 decembrie 2011

Depressed? Crossed Wires In The Brain

Main Category: Depression
Also Included In: Neurology / Neuroscience
Article Date: 12 Dec 2011 - 0:00 PST

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Major depressive disorder (MDD) is a severely debilitating illness characterized by sadness and an inability to cope. Not only does it affect a person's ability to concentrate and make decisions, it also alters their ability to experience pleasurable emotion, and instead prolongs negative thoughts and feelings. New research published in BioMed Central's open access journal Biology of Mood & Anxiety Disorders used functional magnetic resonance imaging (fMRI) to show aberrant connectivity in depressed brains.

Researchers from Stanford University compared the fMRI scans of women who were resting (but still awake). Half of the women were diagnosed with depression at the time of the scan and the other group consisted of women who did not currently have, nor had ever had, severe depression.

fMRI measures changes in blood flow and by overlaying images of depressed and unaffected brains, a number of differences came to light. The images showed that the depressed had decreased connectivity between several key regions of the brain responsible for emotional behaviour, learning, memory and decision making.

Daniella Furman explained, "In addition to decreased connectivity between emotion processing regions of the brain, we found that depression was linked to an increase in connectivity between the dorsal caudate and an area of the prefrontal cortex. Deep within the brain, the caudate is thought to be involved in learning, motivation, and emotion while the prefrontal cortex at the front of the head is involved in maintaining goals and likely regulating emotional behaviour. Together, these regions may act to filter out irrelevant thoughts or actions."

She continued, "Greater connectivity between the dorsal caudate and prefrontal cortex might reflect the inability of the depressed to update their working memory and, as a result, sustains negative thoughts. In fact we found evidence for a parallel increase in tendency to ruminate on bad thoughts."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
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vineri, 9 decembrie 2011

Biopsies Reveal Nature Of Brain Lesions Early In MS Progression, Countering Conventional Wisdom

Main Category: Multiple Sclerosis
Also Included In: Neurology / Neuroscience
Article Date: 09 Dec 2011 - 1:00 PST

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Working together, researchers at Cleveland Clinic and Mayo Clinic have for the first time examined early multiple sclerosis (MS) brain lesions in the cerebral cortex. These lesions are thought to be critical to MS progression and the researchers found that the lesions are distinctly different than previously speculated, giving clues to better disease management.

The long-accepted theory has been that MS begins in the myelin on the inner layers of the brain, also known as white matter. However, the findings of this collaborative study show the opposite -- that the disease likely can move from the outer (cortical) layers of the brain toward the white matter, offering new insight into the progression of MS.

"For patients, the key idea of this research is that we have discovered an entirely new concept of how MS may start," said Richard Ransohoff, M.D., Director of the Neuroinflammation Research Center of the Department of Neurosciences at Cleveland Clinic's Lerner Research Institute, who co-led the study. "This research shows that a non-inflammatory form of MS is much less likely, and the prevailing research path has been going in the right direction."

While the causes of MS remain undetermined, it is thought to be a disease in which the body's immune system attacks and destroys its own myelin, a fatty insulator of the crucial nerve fibers that are responsible for communication between different sections of the brain.

However, in autopsy tissues of MS patients, lesions in the cerebral cortex show demyelination without inflammation, raising a challenging issue: if cortical lesions form entirely without inflammation, then cortical demyelination would not be explainable by current theories of MS nor treatable by current MS therapies.

The present study, published in the New England Journal of Medicine, was a collaborative effort by Dr. Ransohoff, also a staff neurologist at the Mellen Center for Multiple Sclerosis Treatment and Research at Cleveland Clinic's Neurological Institute, and by Claudia Lucchinetti, M.D., of the Mayo Clinic's Department of Neurology.

The study involved examination of 563 brain biopsies resulting in the diagnosis of inflammatory demyelinating disease of the central nervous system, with 138 being determined to have sufficient cortex for study. Of these, 77 cases provided long-term follow-up data, with 58 cases (75 percent) going on to develop verified MS. The vast majority of biopsies were performed at community hospitals with the brain tissue being sent to the Mayo Clinic for neuropathological consultation services. Dr. Lucchinetti leads the National MS Society's MS Lesion project housed at the Mayo Clinic. This study was funded in part by that project as well as the National Institutes of Health.

MRI neuroimaging studies in early multiple sclerosis can't detect cortical lesions but have revealed cortical abnormalities, suggesting that the cortex may be damaged near the time of disease onset. The current research shows that the cortex harbors inflammatory lesions accounting for MRI indicators of damage.

"The next step in this research is to study the lesions to uncover new molecular targets for treatment. We also need to push forward to develop imaging techniques to view these cortical lesions," said Dr. Lucchinetti. "In that way, effects of treatment can more easily be measured."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our multiple sclerosis section for the latest news on this subject. Other authors on this study include: Natalia Moll, M.D., Ph.D., from the Neuroinflammation Research Center and Department of Neurosciences of Lerner Research Institute, Cleveland Clinic; Bogdan Popescu, M.D., Reem Bunyan, M.D., Shanu Roemer, M.D., Joseph Parisi, M.D., Bernd Scheithauer, M.D., Caterina Giannini, M.D., Stephen Weigand, M.S., Jay Mandrekar, Ph.D., all from Mayo Clinic; Hans Lassmann, M.D., from the Center for Brain Research, Medical University of Vienna, Austria; and Wolfgang Bruck, M.D., from the Department of Neuropathology, University Medical Center and Institute for MS Research in Gottingen, Germany.
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