Different brain organization identified in autistic children who excel at math

Main Category: Autism
Also Included In: Psychology / Psychiatry
Article Date: 20 Aug 2013 - 0:00 PDT Current ratings for:
Different brain organization identified in autistic children who excel at math

Children with autism and average IQs consistently demonstrated superior math skills compared with nonautistic children in the same IQ range, according to a study by researchers at the Stanford University School of Medicine and Lucile Packard Children's Hospital.

"There appears to be a unique pattern of brain organization that underlies superior problem-solving abilities in children with autism," said Vinod Menon, PhD, professor of psychiatry and behavioral sciences and a member of the Child Health Research Institute at Packard Children's.

The autistic children's enhanced math abilities were tied to patterns of activation in a particular area of their brains - an area normally associated with recognizing faces and visual objects.

Menon is senior author of the study, published online Aug. 17 in Biological Psychiatry. Postdoctoral scholar Teresa Iuculano, PhD, is the lead author.

Children with autism have difficulty with social interactions, especially interpreting nonverbal cues in face-to-face conversations. They often engage in repetitive behaviors and have a restricted range of interests.

But in addition to such deficits, children with autism sometimes exhibit exceptional skills or talents, known as savant abilities. For example, some can instantly recall the day of the week of any calendar date within a particular range of years - for example, that May 21, 1982, was a Friday. And some display superior mathematical skills.

"Remembering calendar dates is probably not going to help you with academic and professional success," Menon said. "But being able to solve numerical problems and developing good mathematical skills could make a big difference in the life of a child with autism."

The idea that people with autism could employ such skills in jobs, and get satisfaction from doing so, has been gaining ground in recent years.

The participants in the study were 36 children, ages 7 to 12. Half had been diagnosed with autism. The other half was the control group. Each group had 14 boys and four girls. (Autism disproportionately affects boys.) All participants had IQs in the normal range and showed normal verbal and reading skills on standardized tests administered as part of the recruitment process for the study. But on the standardized math tests that were administered, the children with autism outperformed children in the control group.

After the math test, researchers interviewed the children to assess which types of problem-solving strategies each had used: Simply remembering an answer they already knew; counting on their fingers or in their heads; or breaking the problem down into components - a comparatively sophisticated method called decomposition. The children with autism displayed greater use of decomposition strategies, suggesting that more analytic strategies, rather than rote memory, were the source of their enhanced abilities.

Then, the children worked on solving math problems while their brain activity was measured in an MRI scanner, in which they had to lie down and remain still. The brain scans of the autistic children revealed an unusual pattern of activity in the ventral temporal occipital cortex, an area specialized for processing visual objects, including faces.

"Our findings suggest that altered patterns of brain organization in areas typically devoted to face processing may underlie the ability of children with autism to develop specialized skills in numerical problem solving," Iuculano said.

Menon added that previous research "has focused almost exclusively on weaknesses in children with autism. Our study supports the idea that the atypical brain development in autism can lead, not just to deficits, but also to some remarkable cognitive strengths. We think this can be reassuring to parents."

The research team is now gathering data from a larger group of children with autism to learn more about individual differences in their mathematical abilities. Menon emphasized that not all children with autism have superior math abilities, and that understanding the neural basis of variations in problem-solving abilities is an important topic for future research.

"These findings not only empirically confirm that high-functioning children with autism have especially strong number-problem-solving abilities, but show that this cognitive strength in math is based on different patterns of functional brain organization," said Carl Feinstein, MD, director of the Center for Autism and Related Disorders at Packard Children's and professor of psychiatry and behavioral sciences at the School of Medicine. He was not involved in the study.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our autism section for the latest news on this subject.

Other Stanford co-authors are postdoctoral scholars Miriam Rosenberg-Lee, PhD, and Kaustubh Supekar, PhD; social science research assistants Charles Lynch and Amirah Khouzam; Jennifer Phillips, PhD, clinical associate professor of psychiatry and behavioral sciences and a clinical psychologist at Packard Children's; and Lucina Uddin, PhD, instructor in psychiatry and behavioral sciences.

The study was funded by grants from the Singer Foundation, the Stanford Institute for Neuro-Innovation & Translational Neurosciences, and the National Institutes of Health (grant MH084164).

Stanford University Medical Center

Please use one of the following formats to cite this article in your essay, paper or report:

MLA

Stanford University Medical Center. "Different brain organization identified in autistic children who excel at math." Medical News Today. MediLexicon, Intl., 20 Aug. 2013. Web.
20 Aug. 2013. APA

Please note: If no author information is provided, the source is cited instead.

'Different brain organization identified in autistic children who excel at math'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam). We reserve the right to amend opinions where we deem necessary.

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

Copper build up in brain 'could explain Alzheimer's dementia'

Featured Article
Academic Journal
Main Category: Alzheimer's / Dementia
Also Included In: Neurology / Neuroscience;  Water - Air Quality / Agriculture
Article Date: 20 Aug 2013 - 3:00 PDT Current ratings for:
Copper build up in brain 'could explain Alzheimer's dementia'

New research suggests copper that enters the body at levels encountered in the average modern diet may be leading, eventually, to Alzheimer's disease - by reducing the body's ability to clear away toxic proteins in the brain, and also by encouraging the clumping of those proteins.

Copper is an essential trace element in the diet. With iron, it helps make red blood cells, and it is also essential for the health of the immune system, blood vessels, nerves, and bones.

Copper enters the body via many sources, including drinking water carried in copper pipes, and from foods such as shellfish, nuts, red meat and many fruits and vegetables, and also via food supplements.

But now a study that used cells from both mice and humans, led by Rashid Deane, a research professor in the University of Rochester Medical Center (URMC) in the US, shows that copper can also build up in the brain and disrupt the body's ability to clear away amyloid beta proteins before they form the plaques that are the hallmark Alzheimer's disease.

Prof Deane says:

"It is clear that, over time, copper's cumulative effect is to impair the systems by which amyloid beta is removed from the brain."

He and his co-authors, all with URMC, write about their findings in Monday's online issue of the Proceedings of the National Academy of Sciences.

Normally, the body removes amyloid beta from the brain with the help of a protein called LRP1, short for lipoprotein receptor-related protein 1. This protein, which lines blood vessels in the brain, binds with amyloid beta and escorts it out of the brain.

For their study, the team gave mice trace levels of copper for three months.

They found the metal collected in the cells walls of the fine vessels that feed blood to the brain.

The cells the copper collected in are an important part of the brain's defence mechanism, the so-called blood/brain barrier, which controls the substances that can pass in and out of brain tissue.

By collecting copper in their membranes, the cells were just doing their job.

But the researchers found that with time, through the process of oxidation, the copper build up in the cell walls started to affect the ability of LRP1 to escort amyloid beta proteins out of the brain. They saw this happen in both mouse and human brain cells.

In a further experiment, they then examined the process in live mice bred to develop Alzheimer's disease. They found the cells responsible for maintaining the blood/brain barrier could not cope: they became leaky, probably with age and repeated damage from toxins.

Had they not been leaky, the cells would have trapped the copper in their cell walls, but in the Alzheimer's mice, the blood-borne metal was able to pass unhindered through the blood/brain barrier.

As it met with brain tissue, the leaked copper stimulated brain cells to increase their production of amyloid beta.

The copper also had a direct effect on the toxic protein itself: it encouraged it to clump together and form the characteristic plaques of Alzheimer's disease.

Once amyloid beta forms these large clumps inside brain cells, the body's natural ways of eliminating it are overwhelmed and cannot cope: scientists believe this is how Alzheimer's starts and progresses.

In a final experiment, the team also found that copper led to inflammation of brain tissue, which may also speed up the breakdown of the blood/brain barrier and the subsequent build up of Alzheimer's toxins.

The levels of copper the researchers used in their experiments were trace amounts, about one-tenth of that set by standards for water quality from the US Environmental Protection Agency.

Prof Deane says:

"These are very low levels of copper, equivalent to what people would consume in a normal diet."

But neither he nor his colleagues are suggesting people change their diets or intakes of copper on the basis of these findings, which they say should be interpreted with caution.

The body needs copper, it is an essential metal. The effects shown in this study are due to exposure over a long period, and the key is getting the balance between too much and too little.

"Right now we cannot say what the right level will be, but diet may ultimately play an important role in regulating this process," Prof. Deane says.

Help with finding for the study came from The Alzheimer's Association, the National Institute on Aging, and a pilot grant from the National Institute of Environmental Health Sciences.

This is not the first study to implicate copper in a neurodegenerative disease. In 2011, another group of US researchers reported how copper affected a protein associated with Parkinson's disease.

Written by Catharine Paddock PhD
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today Visit our alzheimer's / dementia section for the latest news on this subject.

Low levels of copper disrupt brain amyloid-ß homeostasis by altering its production and clearance Itender Singh, Abhay Sagare, Mireia Coma and others, PNAS. Published online 19 August 2013 (DOI: 10.1073/pnas.1302212110).

Please use one of the following formats to cite this article in your essay, paper or report:

MLA

Paddock, Catharine. "Copper build up in brain 'could explain Alzheimer's dementia'." Medical News Today. MediLexicon, Intl., 20 Aug. 2013. Web.
20 Aug. 2013. APA

Please note: If no author information is provided, the source is cited instead.

'Copper build up in brain 'could explain Alzheimer's dementia''

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam). We reserve the right to amend opinions where we deem necessary.

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

High-flying pilots at increased risk of brain lesions

Main Category: Neurology / Neuroscience
Also Included In: Public Health
Article Date: 20 Aug 2013 - 0:00 PDT Current ratings for:
High-flying pilots at increased risk of brain lesions

A new study suggests that pilots who fly at high altitudes may be at an increased risk for brain lesions. The study is published in the August 20, 2013, print issue of Neurology®, the medical journal of the American Academy of Neurology.

For the study, 102 U-2 United States Air Force pilots and 91 non-pilots between the ages of 26 and 50 underwent MRI brain scans. The scans measured the amount of white matter hyperintensities, or tiny brain lesions associated with memory decline in other neurological diseases. The groups were matched for age, education and health factors.

"Pilots who fly at altitudes above 18,000 feet are at risk for decompression sickness, a condition where gas or atmospheric pressure reaches lower levels than those within body tissues and forms bubbles," said study author Stephen McGuire, MD, with the University of Texas in San Antonio, the US Air Force School of Aerospace Medicine and a Fellow of the American Academy of Neurology. "The risk for decompression sickness among Air Force pilots has tripled from 2006, probably due to more frequent and longer periods of exposure for pilots. To date however, we have been unable to demonstrate any permanent clinical neurocognitive or memory decline."

Symptoms affecting the brain that sometimes accompany decompression sickness include slowed thought processes, confusion, unresponsiveness and permanent memory loss.

The study found that pilots had nearly four times the volume and three times the number of brain lesions as non-pilots. The results were the same whether or not the pilots had a history of symptoms of decompression sickness.

The research also found that while the lesions in non-pilots were mainly found in the frontal white matter, as occurs in normal aging, lesions in the pilots were evenly distributed throughout the brain.

"These results may be valuable in assessing risk for occupations that include high-altitude mountain climbing, deep sea diving and high-altitude flying," McGuire said.

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.

The study was supported by the United States Air Force Surgeon General.

To learn more about cognition, please visit http://www.aan.com/patients.

Study: http://neurology.org/lookup/doi/10.1212/WNL.0b013e3182a1ab12

American Academy of Neurology

Please use one of the following formats to cite this article in your essay, paper or report:

MLA

American Academy of Neurology. "High-flying pilots at increased risk of brain lesions." Medical News Today. MediLexicon, Intl., 20 Aug. 2013. Web.
20 Aug. 2013. APA

Please note: If no author information is provided, the source is cited instead.

'High-flying pilots at increased risk of brain lesions'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam). We reserve the right to amend opinions where we deem necessary.

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

Braintone has a therapeutic effect on ischemic brain damage

Main Category: Stroke
Also Included In: Neurology / Neuroscience
Article Date: 19 Aug 2013 - 0:00 PDT Current ratings for:
Braintone has a therapeutic effect on ischemic brain damage

Recently, the importance of the neurovascular unit, which is comprised of neurons, endothelial cells and astrocytes, has received great attention in the field of stroke, because stroke affects not only neurons, but also astrocytes and microvessels.

Within the neurovascular unit, endothelial cells are critical for maintaining normal hemodynamic and metabolic homeostasis. Vascular damage during ischemia often leads to the disruption of the blood-brain barrier and dysregulation of vascular tonus, eventually causing substantial cell death.

The Chinese herbs Rhodiolase, Notoginseng, Folium Ginkgo and Rhizoma Chuanxiong have been used for stroke ancillary treatment in China for years. Braintone contains four major active ingredients: Radix Rhodiolase Essence (a major constituent of Rhodiola rosea L.), Radix Notoginseng Essence, Folium Ginkgo Essence and Rhizoma Chuanxiong.

A recent study published in the Neural Regeneration Research (Vol. 8, No. 19, 2013) combined novel in vivo and in vitro experiments to show that Braintone dose-dependently increased the expression of hypoxia inducible factor 1a, heme oxygenase-1 and vascular endothelial growth factor in the ischemic cortex of rats with middle cerebral artery occlusion. Braintone-containing serum increased levels of hypoxia-inducible factor 1a mRNA and protein, and elevated vascular endothelial growth factor mRNA and heme oxygenase-1 protein expression in a dose-dependent manner in human umbilical vein endothelial cells after glucose-oxygen deprivation.

Collectively, these experimental findings suggest that Braintone has neuroprotective effects on ischemia-induced brain damage via the up-regulation of hypoxia-inducible factor 1a, heme oxygenase-1 and vascular endothelial growth factor expression in vascular endothelial cells.

Article: " Evidence for a therapeutic effect of Braintone on ischemic brain damage " by Yuanyuan Qin1, 2, Yu Luo1, Weiwei Gu1, Lei Yang1, Xikun Shen2, Zhenlun Gu1, Huiling Zhang1, Xiumei Gao3 (1 Department of Pharmacology and Laboratory of Cerebrovascular Pharmacology, College of Pharmaceutical Science, Suzhou Institute of Chinese Meteria Medica, Soochow University, Suzhou 215123, Jiangsu Province, China; 2 Department of Pharmacy, Suzhou Hospital of Traditional Chinese Medicine, Suzhou 215009, Jiangsu Province, China; 3 Department of Anesthesiology, Daxing Hospital, Capital University of Medical Sciences, Beijing 102600, China)

Qin YY, Luo Y, Gu WW, Yang L, Shen XK, Gu ZL, Zhang HL, Gao XM. Evidence for a therapeutic effect of Braintone on ischemic brain damage. Neural Regen Res. 2013;8(19):1743-1755. oi:10.3969/j.issn.1673-5374.2013.19.002

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our stroke section for the latest news on this subject. Please use one of the following formats to cite this article in your essay, paper or report:

MLA

Research, Neural Regeneration. "Braintone has a therapeutic effect on ischemic brain damage." Medical News Today. MediLexicon, Intl., 19 Aug. 2013. Web.
19 Aug. 2013. APA

Please note: If no author information is provided, the source is cited instead.

'Braintone has a therapeutic effect on ischemic brain damage'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam). We reserve the right to amend opinions where we deem necessary.

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

Oxytocin may make the brain take notice of faces in autism

Main Category: Autism
Also Included In: Endocrinology
Article Date: 19 Aug 2013 - 1:00 PDT Current ratings for:
Oxytocin may make the brain take notice of faces in autism

Difficulty in registering and responding to the facial expressions of other people is a hallmark of autism spectrum disorder (ASD). Relatedly, functional imaging studies have shown that individuals with ASD display altered brain activations when processing facial images.

The hormone oxytocin plays a vital role in the social interactions of both animals and humans. In fact, multiple studies conducted with healthy volunteers have provided evidence for beneficial effects of oxytocin in terms of increased trust, improved emotion recognition, and preference for social stimuli.

This combination of scientific work led German researchers to hypothesize about the influence of oxytocin in ASD. Dr. Gregor Domes, from the University of Freiburg and first author of the new study, explained: "In the present study, we were interested in the question of whether a single dose of oxytocin would change brain responses to social compared to non-social stimuli in individuals with autism spectrum disorder."

They found that oxytocin did show an effect on social processing in the individuals with ASD, "suggesting that oxytocin may help to treat a basic brain function that goes awry in autism spectrum disorders," commented Dr. John Krystal, Editor of Biological Psychiatry.

To conduct this study, they recruited fourteen individuals with ASD and fourteen control volunteers, all of whom completed a face- and house-matching task while undergoing imaging scans. Each participant completed this task and scanning procedure twice, once after receiving a nasal spray containing oxytocin and once after receiving a nasal spray containing placebo. The order of the sprays was randomized, and the tests were administered one week apart.

Using two sets of stimuli in the matching task, one of faces and one of houses, allowed the researchers to not only compare the effects of the oxytocin and placebo administrations, but also allowed them to discriminate findings between specific effects to only social stimuli and non-specific effects to more general brain processing.

What they found was intriguing. The data indicate that oxytocin specifically increases responses of the amygdala to social stimuli in individuals with ASD. The amygdala, the authors explain, "has been associated with processing of emotional stimuli, threat-related stimuli, face processing, and vigilance for salient stimuli".

This finding suggests oxytocin might promote the salience of social stimuli in ASD. Increased salience of social stimuli might support behavioral training of social skills in ASD.

These data support the idea that oxytocin may be a promising approach in the treatment of ASD and could stimulate further research, even clinical trials, on the exploration of oxytocin as an add-on treatment for individuals with autism spectrum disorder.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our autism section for the latest news on this subject.

The article is "Effects of Intranasal Oxytocin on the Neural Basis of Face Processing in Autism Spectrum Disorder" by Gregor Domes, Markus Heinrichs, Ekkehardt Kumbier, Annette Grossmann, Karlheinz Hauenstein, and Sabine C. Herpertz (doi: 10.1016/j.biopsych.2013.02.007). The article appears in Biological Psychiatry, Volume 74, Issue 3 (August 1, 2013), published by Elsevier.

Elsevier

Please use one of the following formats to cite this article in your essay, paper or report:

MLA

Elsevier. "Oxytocin may make the brain take notice of faces in autism." Medical News Today. MediLexicon, Intl., 19 Aug. 2013. Web.
19 Aug. 2013. APA

Please note: If no author information is provided, the source is cited instead.

'Oxytocin may make the brain take notice of faces in autism'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam). We reserve the right to amend opinions where we deem necessary.

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

New brain drugs could follow 'rocking receptor' discovery

Editor's Choice
Main Category: Neurology / Neuroscience
Also Included In: Alzheimer's / Dementia;  Schizophrenia;  Pharma Industry / Biotech Industry
Article Date: 17 Aug 2013 - 0:00 PDT Current ratings for:
New brain drugs could follow 'rocking receptor' discovery

John Hopkins biophysicists have identified a "rocking" motion in a protein ensemble, a "back and forth" movement critical in the normal functioning of brain signaling molecules. The work could lead to advancements in neurological treatments.

The newly discovered "rocking receptor" is thought to be critical to the communication between nerve cells in the brain and spinal cord; the back-and-forth motion responsible for fully activating a protein.

The discovery may reveal multiple drug targets within the protein ensemble that could lead to treatments for neurological disorders such as epilepsy, schizophrenia, Parkinson's and Alzheimer's disease.

The researchers - led by Albert Lau, PhD, assistant professor of biophysics and biophysical chemistry at the Johns Hopkins University School of Medicine - believe the research may prove to be a critical.

Dr Lau says of the "rocking motion" discovery:

"We believe that our study is the first to show the molecular architecture and behaviour of a prominent neural receptor protein ensemble in a state of partial activation."

Using a combination of methods, the team were able to tease apart the process of zero and full activation in cells to reveal the critical protein ensemble motion. Their methods included:

Computer modellingBiophysical "imaging"Biochemical analysisElectrical monitoring.

The results of the study have been published in the journal Neuron.

The full activation of certain receptors required in synaptic transmission may be far more complex than previously understood, the researchers say.

Dr Lau explains that glutamate receptors reside within the outer envelope of every nerve cell in the brain and spinal cord. These receptors are responsible for changing chemical information into electrical information.

If these receptors are disabled, communication between nerve cells in the brain is sharply reduced, resulting in thought and normal brain function being severely compromised.

Malfunctioning receptors, Dr Lau says, have been linked with numerous neurological disorders and are therefore potential targets for drug therapies.

Lau continued to explain that each glutamate receptor is a united group of four protein segments that has a pocket for clamping down on glutamate like a Venus fly trap snaring a bug. Below the glutamate-binding segments are four other segments embedded in the cell's outer envelope to form a channel for charged particles to flow through. When no glutamates are bound to the receptor, the channel is closed; full activation of the receptor and full opening of the channel occur when four glutamates are bound, each to a difference pocket.

It was previously thought that the level of receptor activation simply corresponded to the degree to which each glutamate-binding segment changed shape during the glutamate-binding process. However, the John Hopkins team were able to show that the four glutamate-binding segments, in addition to clamping down on glutamate, also rock back and forth in pairs when fewer than four glutamates are bound.

"It isn't clear yet how this rocking motion affects receptor function, but we now know that activation depends on more than how much each glutamate-binding segment clamps down," Albert Lau, Ph.D., assistant professor of biophysics and biophysical chemistry and research lead.

Development of drugs for neurological disorders have previously targeted the receptor focused on the four glutamate-binding pockets, rather than the motion involved within the successful execution of the process.

He adds:

"Our discovery of this molecular motion could aid the development of drugs by revealing additional drug-binding sites on the receptor."

Written by Sally Burr

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.

A Conformational Intermediate in Glutamate Receptor Activation Albert Y. Lau, et al., Neuron, published online 7 August 2013.

Please use one of the following formats to cite this article in your essay, paper or report:

MLA

Burr, Sally. "New brain drugs could follow 'rocking receptor' discovery." Medical News Today. MediLexicon, Intl., 17 Aug. 2013. Web.
17 Aug. 2013. APA

Please note: If no author information is provided, the source is cited instead.

'New brain drugs could follow 'rocking receptor' discovery'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam). We reserve the right to amend opinions where we deem necessary.

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

Brain functioning in HIV-infected adults improved by Exercise

Main Category: HIV / AIDS
Also Included In: Obesity / Weight Loss / Fitness;  Neurology / Neuroscience
Article Date: 15 Aug 2013 - 1:00 PDT Current ratings for:
Brain functioning in HIV-infected adults improved by Exercise

Regular exercise is not only good for health, but can give people living with HIV a significant mental boost. This is according to a study by Dr. David J. Moore and colleagues at the University of California, San Diego (UCSD), published in Springer's Journal of NeuroVirology.

The study found that HIV-infected adults who exercise suffered significantly less neurocognitive impairment compared to patients who do not exercise.

Moore and his team, including UCSD medical student Catherine Dufour, found that HIV-infected adults who exercise were approximately half as likely to show signs of neurocognitive impairment as compared to those who do not. They also had better working memory and could process information faster than patients who follow a sedentary lifestyle.

Despite recent advances in antiretroviral treatment, impaired brain functioning is a reality faced by nearly half of all people living with HIV. This ranges from asymptomatic neurocognitive impairment, to more pronounced deficits that interfere with daily functioning, such as problems with financial management, driving and taking medication regularly.

The major benefit of exercise to the brain seems to be the reduction of neurocognitive risk factors, such as high blood pressure and abnormally high levels of lipids in the blood. Metabolic syndrome associated with the use of antiretroviral treatment is also linked to an increase in cerebrovascular risk factors, such as diabetes, hypertension and obesity.

In the study, 335 community-dwelling HIV-infected people were asked how much exercise they undertook during the previous 72 hours, and persons were classified into those who engaged in significant exercise (e.g., activities that make the heart beat rapidly) and those who did not. Seven cognitive areas commonly affected by HIV were tested, including verbal fluency, working memory, speed of information processing, learning, recall, executive function and motor function.

The study extends prior findings about the link between exercise and cognition among HIV-infected people by showing that this association is also true in a diverse and large group of people living with the disease. Compounding factors were taken into account, such as demographics, HIV disease characteristics, substance use, past and current depression, mental health status and physical functioning.

"Exercise as a modifiable lifestyle behavior may reduce or potentially prevent neurocognitive impairment in HIV-infected persons," says Moore. "Physical exercise, together with other modifiable lifestyle factors such as education, social engagement, cognitive stimulation and diet could be fruitful interventions to support people living with HIV."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our hiv / aids section for the latest news on this subject.

Physical exercise is associated with less neurocognitive impairment among HIV-infected adults

Dufour, C.A. et al (2013). Journal of NeuroVirology DOI 10.1007/s13365-013-0184-8.

212-620-8063 Springer Science+Business Media

Please use one of the following formats to cite this article in your essay, paper or report:

MLA

Media, Springer Science+Business. "Brain functioning in HIV-infected adults improved by Exercise." Medical News Today. MediLexicon, Intl., 15 Aug. 2013. Web.
15 Aug. 2013. APA

Please note: If no author information is provided, the source is cited instead.

'Brain functioning in HIV-infected adults improved by Exercise'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam). We reserve the right to amend opinions where we deem necessary.

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

Brain injuries: measuring consciousness by 'perturbing the brain'

Featured Article
Main Category: Neurology / Neuroscience
Also Included In: Medical Devices / Diagnostics
Article Date: 15 Aug 2013 - 8:00 PDT Current ratings for:
Brain injuries: measuring consciousness by 'perturbing the brain'

Assessing consciousness in patients with severe brain trauma is a difficult challenge for doctors, as the injury effectively takes away any ability to blink, squeeze a hand or otherwise respond. But scientists have found a way to measure the brain's response to a magnetic pulse, helping them determine a person's level of awareness.

The researchers in Italy, led by Marcello Massimini, set out to find a reliable, objective way to distinguish an unconscious brain from a conscious one. Though many existing methods use brain imaging or electrical activity of neurons, Massimini says "that's not enough."

He notes that sometimes an unconscious brain can appear integrated, meaning groups of cells from different regions can activate to make a connected pattern.

Stimulating a sleeping person's brain, he says, can produce a wave of activity that "propagates like a ripple in water," even though the person is not conscious.

On the other side of the fence, the researchers say that around 40% of patients who are initially judged to be unresponsive are found later to possess a level of consciousness.

To measure consciousness, Massimini and his colleagues created the perturbational complexity index (PCI), which involves holding a magnetic coil to the skull and measuring the response. This transcranial magnetic stimulation (TMS) generates a pulse that sparks a response through the underlying neurons and propagates throughout the brain.

EEG readings were analyzed after pulsing unconscious brains with the magnetic coil.

By recording the brain's response by electroencephalography (EEG), the researchers then turned the information into a score between 0 and 1. The so-called information-rich responses - those distributed across the brain that are still individualized - receive higher scores, denoting a higher level of consciousness.

The researchers calibrated their system by using healthy patients in three different states: awake, deep sleep and under anesthesia, which served as a reference for unconsciousness.

For the healthy patients, they measured the highest unconscious score at 0.31 and the lowest conscious score at 0.44.

When they tested 20 people with brain damage who were believed to be in a state of partial wakefulness but who showed no signs of awareness, they observed low scores between 0.19 and 0.31.

Additionally, when Massimini and his team tested on two patients who had normal cognitive abilities (for example, they could shift their eyes) but were unable to move, they received PCI scores of 0.51 and 0.62, which rated at the same level as the healthy patients.

The researchers say that the index they have effectively created provides a scale of consciousness and unconsciousness that could be used as an "objective" test "at the bedside."

In an interview with Bloomberg, Marcello Massimini said:

"It will be very important to perform measurements right in the ICU in the acute phase to have an objective marker of what's happening and to track improvements occurring spontaneously or brought about by treatment.

If you have a number, you can start working towards an evidence-based treatment."

A team from Belgium recently discovered a simple method for testing coma patients involving resistance to eye-opening, but the index from Massimini and his colleagues could provide a measurable indicator for diagnosing levels of consciousness. Written by Marie Ellis
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.

A Magnetic Trick to Define Consciousness Kelly Servick, Science, published online 14 August 2013.

A Theoretically Based Index of Consciousness Independent of Sensory Processing and Behavior Marcello Massimini, et al., Science Translational Medicine, published online 14 August 2013.

Please use one of the following formats to cite this article in your essay, paper or report:

MLA

Ellis, Marie. "Brain injuries: measuring consciousness by 'perturbing the brain'." Medical News Today. MediLexicon, Intl., 15 Aug. 2013. Web.
15 Aug. 2013. APA

Please note: If no author information is provided, the source is cited instead.

posted by Mark on 15 Aug 2013 at 11:12 am

This is an interesting study and approach. A few questions come to mind:

1) when sending such a ping request to the brain in a conscious person, does the person feel such a magnetic pulse?

2) Did the researchers test said device on themselves first before attaching it to patients?

3) if such stimulus reports the person is not conscious, they could be sleeping, or truly in a coma state...would this test be used to determine whether a person lives or dies?

If question 3 becomes a fact, and it could potentially be used to determine whether to keep someone on life supporting equipment or not, then I would have to say I have some objections to said test. As much as we think we know about the brain, we still don't know enough, and the decisions of life and death are taken up by persons assuming certain facts.

We don't know enough about the conscious or unconscious states, and for all we know, a coma could be an altered sense of reality, in a dream like world, but for that person they are alive, and breathing, in their mind, but perhaps this test says they're conscious.

| post followup | alert a moderator |

posted by Kevin K on 15 Aug 2013 at 8:25 am

How can you be awake and unconscious at the same time?

"...20 people with brain damage who were believed to be awake but completely unconscious..."

Editor's note: Thank for your comment, Kevin. Marcello Massimini, (lead author of the study) reported, "those who were believed to be in a vegetative state - awake but completely unconscious - got very low scores (between 0.19 to 0.31)."

| post followup | alert a moderator |

'Brain injuries: measuring consciousness by 'perturbing the brain''

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam). We reserve the right to amend opinions where we deem necessary.

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

'Molecular flashlight' developed that illuminates brain tumors in mice

Main Category: Neurology / Neuroscience
Also Included In: Cancer / Oncology;  Pediatrics / Children's Health
Article Date: 14 Aug 2013 - 0:00 PDT Current ratings for:
'Molecular flashlight' developed that illuminates brain tumors in mice

In a breakthrough that could have wide-ranging applications in molecular medicine, Stanford University researchers have created a bioengineered peptide that enables imaging of medulloblastomas, among the most devastating of malignant childhood brain tumors, in lab mice.

The researchers altered the amino acid sequence of a cystine knot peptide - or knottin - derived from the seeds of the squirting cucumber, a plant native to Europe, North Africa and parts of Asia. Peptides are short chains of amino acids that are integral to cellular processes; knottin peptides are notable for their stability and resistance to breakdown.

The team used their invention as a "molecular flashlight" to distinguish tumors from surrounding healthy tissue. After injecting their bioengineered knottin into the bloodstreams of mice with medulloblastomas, the researchers found that the peptide stuck tightly to the tumors and could be detected using a high-sensitivity digital camera.

The findings are described in a study published online in the Proceedings of the National Academy of Sciences.

"Researchers have been interested in this class of peptides for some time," said Jennifer Cochran, PhD, an associate professor of bioengineering and a senior author of the study. "They're extremely stable. For example, you can boil some of these peptides or expose them to harsh chemicals, and they'll remain intact."

That makes them potentially valuable in molecular medicine. Knottins could be used to deliver drugs to specific sites in the body or, as Cochran and her colleagues have demonstrated, as a means of illuminating tumors.

For treatment purposes, it's critical to obtain accurate images of medulloblastomas. In conjunction with chemotherapy and radiation therapy, the tumors are often treated by surgical resection, and it can be difficult to remove them while leaving healthy tissue intact because their margins are often indistinct.

"With brain tumors, you really need to get the entire tumor and leave as much unaffected tissue as possible," Cochran said. "These tumors can come back very aggressively if not completely removed, and their location makes cognitive impairment a possibility if healthy tissue is taken."

The researchers' molecular flashlight works by recognizing a biomarker on human tumors. The bioengineered knottin is conjugated to a near-infrared imaging dye. When injected into the bloodstreams of a strain of mice that develop tumors similar to human medullublastomas, the peptide attaches to the brain tumors' integrin receptors - sticky molecules that aid in adhesion to other cells.

But while the knottins stuck like glue to tumors, they were rapidly expelled from healthy tissue. "So the mouse brain tumors are readily apparent," Cochran said. "They differentiate beautifully from the surrounding brain tissue."

The new peptide represents a major advance in tumor-imaging technology, said Melanie Hayden, MD, a neurosurgeon at the Stanford Brain Tumor Center and a lead author of the paper. The most common extant technique employs a high-contrast dye that is injected intravenously shortly before or during an operation. Tumors absorb some of the dye, and can be identified on a magnetic resonance imaging scan.

"But that has limitations," Hayden said. "When you're using dye and an MRI scan, you're basically working off a snapshot. And the brain can sometimes shift during an operation, so there's always the possibility you may not be precisely where you want to be. The great advantage of this new approach is that you're illuminating the tumor in real time - you're seeing it directly under your scope instead of relying on an image that was taken earlier." An important next step will be to translate these results from mice to human patients.

Though the team's research focused on medulloblastomas, Hayden said it's likely the new knottins could prove useful in addressing other cancers.

"We know that integrins exist on many types of tumors," she said. "The blood vessels that tumors develop to sustain themselves also contain integrins. So this has the potential for providing very detailed, real-time imaging for a wide variety of tumors."

And imaging may not be the only application for the team's engineered peptide.

"We're very interested in related opportunities," Cochran said. "We envision options we didn't have before for getting molecules into the brain." In other words, by substituting drugs for dye, the knottins might allow the delivery of therapeutic compounds directly to cranial tumors - something that has proved extremely difficult to date because of the blood/brain barrier, the mechanism that makes it difficult for pathogens, as well as medicines, to traverse from the bloodstream to the brain.

"We're looking into it now," Cochran said.

A little serendipity was involved in the peptide's development, said Sarah Moore, a recently graduated bioengineering PhD student and another lead author of the study. Indeed, the propinquity of Cochran's laboratory to co-author Matthew Scott's lab at Stanford's James H. Clark Center catalyzed the project. "Our labs are next to each other," Moore said. "We had the peptide, and Matt had ideal models of pediatric brain tumors - mice that develop tumors in a similar manner to human medulloblastomas. Our partnership grew out of that."

Scott, PhD, professor of bioengineering and of developmental biology, credits the design of the Clark Center as a contributor to the project. The building is home to Stanford's Bioengineering Department, a collaboration between the School of Engineering and the School of Medicine, and Stanford Bio-X, an initiative that encourages communication among researchers in diverse scientific disciplines.

"So in a very real sense, our project wasn't an accident," Scott said. "In fact, it's exactly the kind of work the Clark Center was meant to foster. The lab spaces are wide and open, with very few walls and lots of glass. We have a restaurant that only has large tables - no tables for two, so people have to sit together. Everything is designed to increase the odds that people will meet and talk. It's a form of social engineering that really works."

Scott said he is gratified by the collaboration that led to the team's breakthrough, and observed that the peptide has proved a direct boon to his own work. About 15 percent of Scott's mice develop the tumors requisite for medulloblastoma research. The problem, he said, is that the cancers are cryptic in their early stages.

"By the time you know the mice have them, many of the things you want to study - the genesis and development of the tumors - are past," Scott said. "We needed ways to detect these tumors early, and we needed methods for following the steps of tumor genesis."

Ultimately, Scott concluded, the development of the new peptide can be attributed to Stanford's long-established traditions of openness and relentless inquiry.

"You find not just a willingness, but an eagerness to exchange ideas and information here," Scott said. "It transcends any competitive instinct, any impulse toward proprietary thinking. It is what makes Stanford - well, Stanford."

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.

Other Stanford co-authors were postdoctoral scholar Jamie Bergen, PhD; medical student Yourong Sophie Su; and life science research assistant Helen Rayburn.

Stanford University Medical Center

Please use one of the following formats to cite this article in your essay, paper or report:

MLA

Stanford University Medical Center. "'Molecular flashlight' developed that illuminates brain tumors in mice." Medical News Today. MediLexicon, Intl., 14 Aug. 2013. Web.
14 Aug. 2013. APA

Please note: If no author information is provided, the source is cited instead.

''Molecular flashlight' developed that illuminates brain tumors in mice'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam). We reserve the right to amend opinions where we deem necessary.

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

'Molecular flashlight' developed that illuminates brain tumors in mice

Main Category: Neurology / Neuroscience
Also Included In: Cancer / Oncology;  Pediatrics / Children's Health
Article Date: 14 Aug 2013 - 0:00 PDT Current ratings for:
'Molecular flashlight' developed that illuminates brain tumors in mice

In a breakthrough that could have wide-ranging applications in molecular medicine, Stanford University researchers have created a bioengineered peptide that enables imaging of medulloblastomas, among the most devastating of malignant childhood brain tumors, in lab mice.

The researchers altered the amino acid sequence of a cystine knot peptide - or knottin - derived from the seeds of the squirting cucumber, a plant native to Europe, North Africa and parts of Asia. Peptides are short chains of amino acids that are integral to cellular processes; knottin peptides are notable for their stability and resistance to breakdown.

The team used their invention as a "molecular flashlight" to distinguish tumors from surrounding healthy tissue. After injecting their bioengineered knottin into the bloodstreams of mice with medulloblastomas, the researchers found that the peptide stuck tightly to the tumors and could be detected using a high-sensitivity digital camera.

The findings are described in a study published online in the Proceedings of the National Academy of Sciences.

"Researchers have been interested in this class of peptides for some time," said Jennifer Cochran, PhD, an associate professor of bioengineering and a senior author of the study. "They're extremely stable. For example, you can boil some of these peptides or expose them to harsh chemicals, and they'll remain intact."

That makes them potentially valuable in molecular medicine. Knottins could be used to deliver drugs to specific sites in the body or, as Cochran and her colleagues have demonstrated, as a means of illuminating tumors.

For treatment purposes, it's critical to obtain accurate images of medulloblastomas. In conjunction with chemotherapy and radiation therapy, the tumors are often treated by surgical resection, and it can be difficult to remove them while leaving healthy tissue intact because their margins are often indistinct.

"With brain tumors, you really need to get the entire tumor and leave as much unaffected tissue as possible," Cochran said. "These tumors can come back very aggressively if not completely removed, and their location makes cognitive impairment a possibility if healthy tissue is taken."

The researchers' molecular flashlight works by recognizing a biomarker on human tumors. The bioengineered knottin is conjugated to a near-infrared imaging dye. When injected into the bloodstreams of a strain of mice that develop tumors similar to human medullublastomas, the peptide attaches to the brain tumors' integrin receptors - sticky molecules that aid in adhesion to other cells.

But while the knottins stuck like glue to tumors, they were rapidly expelled from healthy tissue. "So the mouse brain tumors are readily apparent," Cochran said. "They differentiate beautifully from the surrounding brain tissue."

The new peptide represents a major advance in tumor-imaging technology, said Melanie Hayden, MD, a neurosurgeon at the Stanford Brain Tumor Center and a lead author of the paper. The most common extant technique employs a high-contrast dye that is injected intravenously shortly before or during an operation. Tumors absorb some of the dye, and can be identified on a magnetic resonance imaging scan.

"But that has limitations," Hayden said. "When you're using dye and an MRI scan, you're basically working off a snapshot. And the brain can sometimes shift during an operation, so there's always the possibility you may not be precisely where you want to be. The great advantage of this new approach is that you're illuminating the tumor in real time - you're seeing it directly under your scope instead of relying on an image that was taken earlier." An important next step will be to translate these results from mice to human patients.

Though the team's research focused on medulloblastomas, Hayden said it's likely the new knottins could prove useful in addressing other cancers.

"We know that integrins exist on many types of tumors," she said. "The blood vessels that tumors develop to sustain themselves also contain integrins. So this has the potential for providing very detailed, real-time imaging for a wide variety of tumors."

And imaging may not be the only application for the team's engineered peptide.

"We're very interested in related opportunities," Cochran said. "We envision options we didn't have before for getting molecules into the brain." In other words, by substituting drugs for dye, the knottins might allow the delivery of therapeutic compounds directly to cranial tumors - something that has proved extremely difficult to date because of the blood/brain barrier, the mechanism that makes it difficult for pathogens, as well as medicines, to traverse from the bloodstream to the brain.

"We're looking into it now," Cochran said.

A little serendipity was involved in the peptide's development, said Sarah Moore, a recently graduated bioengineering PhD student and another lead author of the study. Indeed, the propinquity of Cochran's laboratory to co-author Matthew Scott's lab at Stanford's James H. Clark Center catalyzed the project. "Our labs are next to each other," Moore said. "We had the peptide, and Matt had ideal models of pediatric brain tumors - mice that develop tumors in a similar manner to human medulloblastomas. Our partnership grew out of that."

Scott, PhD, professor of bioengineering and of developmental biology, credits the design of the Clark Center as a contributor to the project. The building is home to Stanford's Bioengineering Department, a collaboration between the School of Engineering and the School of Medicine, and Stanford Bio-X, an initiative that encourages communication among researchers in diverse scientific disciplines.

"So in a very real sense, our project wasn't an accident," Scott said. "In fact, it's exactly the kind of work the Clark Center was meant to foster. The lab spaces are wide and open, with very few walls and lots of glass. We have a restaurant that only has large tables - no tables for two, so people have to sit together. Everything is designed to increase the odds that people will meet and talk. It's a form of social engineering that really works."

Scott said he is gratified by the collaboration that led to the team's breakthrough, and observed that the peptide has proved a direct boon to his own work. About 15 percent of Scott's mice develop the tumors requisite for medulloblastoma research. The problem, he said, is that the cancers are cryptic in their early stages.

"By the time you know the mice have them, many of the things you want to study - the genesis and development of the tumors - are past," Scott said. "We needed ways to detect these tumors early, and we needed methods for following the steps of tumor genesis."

Ultimately, Scott concluded, the development of the new peptide can be attributed to Stanford's long-established traditions of openness and relentless inquiry.

"You find not just a willingness, but an eagerness to exchange ideas and information here," Scott said. "It transcends any competitive instinct, any impulse toward proprietary thinking. It is what makes Stanford - well, Stanford."

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.

Other Stanford co-authors were postdoctoral scholar Jamie Bergen, PhD; medical student Yourong Sophie Su; and life science research assistant Helen Rayburn.

Stanford University Medical Center

Please use one of the following formats to cite this article in your essay, paper or report:

MLA

Stanford University Medical Center. "'Molecular flashlight' developed that illuminates brain tumors in mice." Medical News Today. MediLexicon, Intl., 14 Aug. 2013. Web.
14 Aug. 2013. APA

Please note: If no author information is provided, the source is cited instead.

''Molecular flashlight' developed that illuminates brain tumors in mice'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam). We reserve the right to amend opinions where we deem necessary.

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

Near-death experiences are 'electrical brain surges'

Featured Article
Academic Journal
Main Category: Neurology / Neuroscience
Also Included In: Cardiovascular / Cardiology
Article Date: 14 Aug 2013 - 0:00 PDT Current ratings for:
Near-death experiences are 'electrical brain surges'

Many people worldwide have reported 'near-death experiences' - particularly following a heart attack. But what causes the visions and perceptions that these survivors report after their brush with death? Scientists from the University of Michigan believe they have found the answer.

A near-death experience (NDE) is defined as a psychological event that occurs when a person is close to death.

Reported circumstances of a NDE, from the educational nonprofit the International Association for Near-Death Studies, include vivid perceptions of movement, light, darkness, encounters with deceased loved ones, encounters with spiritual presences or entities, and some people talk of an "out-of-body experience."

According to the researchers in the Michigan study, around 20% of cardiac arrest survivors have reported a NDE. However, they add that although these experiences have been described as "realer than real," it has been unclear as to whether the brain is able to produce these senses during clinical death.

Jimo Borjigin, who holds associate professorships in molecular and integrative psychology, and in neurology at the University of Michigan Medical School, says:

"We reasoned that if near-death experience stems from brain activity, neural correlates of consciousness should be identifiable in humans or animals even after the cessation of cerebral blood flow."

The researchers analyzed the recordings of brain activity, electroencephalograms (EEGs), of nine anesthetized rats as they were in the midst of induced cardiac arrest.

Researchers found that during near-death experiences, there is an electrical surge of brain activity

The study, published in the journal Proceedings of the National Academy of Sciences, revealed that following clinical death - when the heart stops beating and blood stops flowing to the brain, the rats showed brain activity patterns similar to "conscious perception."

Within the first 30 seconds of a cardiac arrest, all rats showed a widespread electrical surge of transient brain activity, which had characteristics similar to a fully active brain.

Additionally, when the rats were undergoing asphyxiation - death from lack of oxygen, they showed almost identical brain patterns.

George Mashour, assistant professor of anesthesiology and neurosurgery at the University of Michigan, explains:

"We were surprised by the high levels of activity. In fact, at near-death, many known electrical signatures of consciousness exceeded levels found in the waking state, suggesting that the brain is capable of well-organized electrical activity during the early stage of clinical death."

Borjigin adds: "This study tells us that reduction of oxygen, or both oxygen and glucose, during cardiac arrest can stimulate brain activity that is characteristic of conscious processing."

The study authors say that previously, it was assumed the brain was inactive during cardiac arrest, but this is the first time the neurophysiological state of the brain has been systemically investigated.

The researchers say their findings provide the first scientific framework for the near-death experiences reported by many cardiac arrest survivors.

"This study, performed in animals, is the first dealing with what happens to the neurophysiological state of the dying brain," Borjigin says.

"It will form the foundation for future human studies investigating mental experiences occurring in the dying brain, including seeing light during cardiac arrest."

There have been previous reports from neurologists looking into near death experiences. Researchers from the University of Kentucky wrote in 2006 that when a person is experiencing clinical death, the same parts of the brain are activated as when a person is having a dream.

Written by Honor Whiteman

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. Surge of neurophysiological coherence and connectivity in the dying brain, Proceedings of the National Academy of Sciences, published online August 12, 2013. Please use one of the following formats to cite this article in your essay, paper or report:

MLA

Whiteman, Honor. "Near-death experiences are 'electrical brain surges'." Medical News Today. MediLexicon, Intl., 14 Aug. 2013. Web.
14 Aug. 2013. APA

Please note: If no author information is provided, the source is cited instead.

posted by Janet Webber on 14 Aug 2013 at 2:44 pm

I have had a near death experience when I "broke down" into a state of being outside of my body. My mind was aware that it was an eternal, empty, black, void of complete and utter nothingness and it felt like a horrific scream. It lasted only seconds but I could fathom exactly what forever felt like. To this day I am scared of Hell, that place where my soul went, that is infinitely horrifying and real.

| post followup | alert a moderator |

'Near-death experiences are 'electrical brain surges''

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam). We reserve the right to amend opinions where we deem necessary.

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

Odor memory: The nose and the brain make quite a team... in disconnection

Main Category: Neurology / Neuroscience
Article Date: 14 Aug 2013 - 1:00 PDT Current ratings for:
Odor memory: The nose and the brain make quite a team... in disconnection

Alan Carleton's team from the Neuroscience Department at the University of Geneva (UNIGE) Faculty of Medicine has just shown that the representation of an odor evolves after the first breath, and that an olfactory retentivity persists at the central level. The phenomenon is comparable to what occurs in other sensory systems, such as vision or hearing. These movements undoubtedly enable the identification of new odors in complex environments or participate in the process of odor memorization. This research is the subject of a publication in the latest online edition of the journal PNAS (Proceedings of the National Academy of Sciences of the United States of America).

Rodents can identify odors in a single breath, which is why research on sense of smell in mammals focuses on that first inhalation. Yet we must remember that from a neurological standpoint, sensory representations change during and after the stimuli. To understand the evolution of these mental representations, an international team of researchers led by Professor Alan Carleton at the University of Geneva (UNIGE) Faculty of Medicine conducted the following experiment: by observing the brain of an alert mouse, the neuroscientists recorded the electrical activity emitted by the olfactory bulb of animals inhaling odors.

They were surprised to find that in mitral cells, some representations evolved during the first inhalations, and others persisted and remained stable well after the odor ceased. The cohort subjected to these analyses revealed that the post-odor responses contained an odor retentivity - a specific piece of information about the nature of odor and its concentration.

Will odor memory soon be understood?

Using cerebral imaging, researchers discovered that the majority of sensory activity is visible only during the presentation of odors, which implies that retentivity is essentially internal to the brain. Therefore, odor retentivity would not be dependent upon odorous physicochemical properties. Finally, to artificially induce retentivity, the team photostimulated mitral cells using channelrhodopsin, then recorded the persistent activity maintained at the central level. The strength and persistence of the retentivity were found to be dependent on the duration of the stimulation, both artificial and natural.

In summary, the neuroscientists were able to show that the representation of an odor changes after the first breath, and that an olfactory retentivity persists at the central level, a phenomenon comparable to what occurs in other sensory systems, such as vision and hearing. These movements undoubtedly enable the identification of new odors in complex environments or participate in the process of odor memorization.

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.

The journal PNAS has just published these findings in its latest online edition.

Odor representations in the olfactory bulb evolve after the first breath and persist as an odor afterimage

Published online before print August 5, 2013, doi: 10.1073/pnas.1303873110. PNAS August 5, 2013

Université de Genève

Please use one of the following formats to cite this article in your essay, paper or report:

MLA

de Genève, Université. "Odor memory: The nose and the brain make quite a team... in disconnection." Medical News Today. MediLexicon, Intl., 14 Aug. 2013. Web.
14 Aug. 2013. APA

Please note: If no author information is provided, the source is cited instead.

'Odor memory: The nose and the brain make quite a team... in disconnection'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam). We reserve the right to amend opinions where we deem necessary.

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

Scientists decode mechanisms of cell orientation in the brain

Main Category: Neurology / Neuroscience
Also Included In: Biology / Biochemistry
Article Date: 02 Aug 2013 - 1:00 PDT Current ratings for:
Scientists decode mechanisms of cell orientation in the brain

When the central nervous system is injured, oligodendrocyte precursor cells (OPC) migrate to the lesion and synthesize new myelin sheaths on demyelinated axons. Scientists at the Institute of Molecular Cell Biology at Johannes Gutenberg University Mainz (JGU) have now discovered that a distinct protein regulates the direction and movement of OPC toward the wound. The transmembrane protein NG2, which is expressed at the surface of OPCs and down-regulated as they mature to myelinating oligodendrocytes, plays an important role in the reaction of OPC to wounding. The results of this study have recently been published in the renowned Journal of Neuroscience.

The myelin sheath functions to electrically isolate axons of many nerve fibers and is synthesized by oligodendrocytes which mature from the OPC. In the case of injury, neural cells send out signaling molecules which attract the OPC. The NG2 protein helps OPCs to react to some of these and move in a directed and orientated fashion. "We were able to prove in cell biological experiments that NG2 orientates OPC toward the lesion and ensures targeted OPC migration toward the wound through the regulation of cell polarity", explained Dr. Fabien Binamé, lead author of the study. Supported by funding of the German Research Foundation (DFG), Dr. Fabien Binamé is currently carrying out his research at the Institute of Molecular Cell Biology headed by Professor Jacqueline Trotter.

"The function and mode of operation of NG2 is not yet fully understood", added co-author Dominik Sakry, who was also involved in the study. "But it looks as if the NG2-associated regulatory mechanism becomes apparent only in cases of injury of the nervous system."

Diseases such as Multiple Sclerosis or brain tumors go hand in hand with damage of nerve tissue. "The results of our study on NG2-mediated basic mechanisms of cell orientation and migration could aid in understanding the repair of damaged demyelinated tissue, or be important for treatment of highly active migratory brain tumors which often express high levels of NG2", said Professor Jacqueline Trotter, head of the JGU Institute of Molecular Cell Biology.

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. Please use one of the following formats to cite this article in your essay, paper or report:

MLA

Johannes Gutenberg Universitaet Mainz. "Scientists decode mechanisms of cell orientation in the brain." Medical News Today. MediLexicon, Intl., 2 Aug. 2013. Web.
3 Aug. 2013. APA

Please note: If no author information is provided, the source is cited instead.

'Scientists decode mechanisms of cell orientation in the brain'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam). We reserve the right to amend opinions where we deem necessary.

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

Speedier scans reveal new distinctions in resting and active brain

Main Category: Neurology / Neuroscience
Article Date: 05 Aug 2013 - 0:00 PDT Current ratings for:
Speedier scans reveal new distinctions in resting and active brain

A boost in the speed of brain scans is unveiling new insights into how brain regions work with each other in cooperative groups called networks.

Scientists at Washington University School of Medicine in St. Louis and the Institute of Technology and Advanced Biomedical Imaging at the University of Chieti, Italy, used the quicker scans to track brain activity in volunteers at rest and while they watched a movie.

"Brain activity occurs in waves that repeat as slowly as once every 10 seconds or as rapidly as once every 50 milliseconds," said senior researcher Maurizio Corbetta, MD, the Norman J. Stupp Professor of Neurology. "This is our first look at these networks where we could sample activity every 50 milliseconds, as well as track slower activity fluctuations that are more similar to those observed with functional magnetic resonance imaging (fMRI). This analysis performed at rest and while watching a movie provides some interesting and novel insights into how these networks are configured in resting and active brains."

Understanding how brain networks function is important for better diagnosis and treatment of brain injuries, according to Corbetta.

The study appears online in Neuron.

Researchers know of several resting-state brain networks, which are groups of different brain regions whose activity levels rise and fall in sync when the brain is at rest. Scientists used fMRI to locate and characterize these networks, but the relative slowness of this approach limited their observations to activity that changes every 10 seconds or so. A surprising result from fMRI was that the spatial pattern of activity (or topography) of these brain networks is similar at rest and during tasks.

In contrast, a faster technology called magnetoencephalography (MEG) can detect activity at the millisecond level, letting scientists examine waves of activity in frequencies from slow (0.1-4 cycles per second) to fast (greater than 50 cycles per second).

"Interestingly, even when we looked at much higher temporal resolution, brain networks appear to fluctuate on a relatively slow time scale," said first author Viviana Betti, PhD, a postdoctoral researcher at Chieti. "However, when the subjects went from resting to watching a movie, the networks appeared to shift the frequency channels in which they operate, suggesting that the brain uses different frequencies for rest and task, much like a radio."

In the study, the scientists asked one group of volunteers to either rest or watch the movie during brain scans. A second group was asked to watch the movie and look for event boundaries, moments when the plot or characters or other elements of the story changed. They pushed a button when they noticed these changes.

As in previous studies, most subjects recognized similar event boundaries in the movie. The MEG scans showed that the communication between regions in the visual cortex was altered near the movie boundaries, especially in networks in the visual cortex.

"This gives us a hint of how cognitive activity dynamically changes the resting-state networks," Corbetta said. "Activity locks and unlocks in these networks depending on how the task unfolds. Future studies will need to track resting-state networks in different tasks to see how correlated activity is dynamically coordinated across the brain."

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.

This research was funded by the European Community’s Seventh Framework Programme Grant Agreement HEALTH-F2-2008-200728 (BrainSynch) and by the Human Connectome Project (1U54MH091657-01). V.B. was additionally supported by a fellowship from the University of Chieti. M.C. was supported by R01 MH096482-01 (NIMH) and 5R01HD061117-08 (NICHD). Betti V, Della Penna S, de Pasquale F, Mantini D, Marzetti L, Romani GL, Corbetta M. Natural Scenes Viewing Alters the Dynamics of Functional Connectivity in the Human Brain. Neuron, published online.

Washington University School of Medicine

Please use one of the following formats to cite this article in your essay, paper or report:

MLA

Washington University School of Medicine. "Speedier scans reveal new distinctions in resting and active brain." Medical News Today. MediLexicon, Intl., 5 Aug. 2013. Web.
5 Aug. 2013. APA

Please note: If no author information is provided, the source is cited instead.

'Speedier scans reveal new distinctions in resting and active brain'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam). We reserve the right to amend opinions where we deem necessary.

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

The flexible tail of the prion protein poisons brain cells

Main Category: CJD / vCJD / Mad Cow Disease
Also Included In: Neurology / Neuroscience;  Biology / Biochemistry
Article Date: 03 Aug 2013 - 0:00 PDT Current ratings for:
The flexible tail of the prion protein poisons brain cells

Prion proteins are the infectious pathogens that cause Mad Cow Disease and Creutzfeldt-Jakob disease. They occur when a normal prion protein becomes deformed and clumped. The naturally occurring prion protein is harmless and can be found in most organisms. In humans, it is found in our brain cell membrane. By contrast, the abnormally deformed prion protein is poisonous for the brain cells. Adriano Aguzzi, Professor of Neuropathology at the University of Zurich and University Hospital Zurich, has spent many years exploring why this deformation is poisonous. Aguzzi's team has now discovered that the prion protein has a kind of «switch» that controls its toxicity. This switch covers a tiny area on the surface of the protein. If another molecule, for example an antibody, touches this switch, a lethal mechanism is triggered that can lead to very fast cell death.

Flexible tail induces cell death

In the current edition of «Nature», the scientists demonstrate that the prion protein molecule comprises two functionally distinct parts: a globular domain, which is tethered to the cell membrane, and a long and unstructured tail. Under normal conditions, this tail is very important in order to maintain the functioning of nerve cells. By contrast, in the case of a prion infection the pathogenic prion protein interacts with the globular part and the tail causes cell death - this is the hypothesis put forward by the researchers.

Aguzzi and his team tested this by generating mimetic antibodies in tissue sections from the cerebellum of mice which have a similar toxicity to that of a prion infection. The researchers found that these antibodies tripped the switch of the prion protein. «Prion proteins with a trimmed version of the flexible tail can, however, no longer damage the brain cells, even if their switch has been recognized by antibodies», explains Adriano Aguzzi. "This flexible tail is responsible for causing cell death." If the tail is bound and made inaccessible using a further antibody, activation of the switch can likewise no longer trigger cell death.

"Our discovery has far-reaching consequences for understanding prion diseases", says Aguzzi. The findings reveal that only those antibodies that target the prion protein tail are suitable for use as potential drugs. By contrast, antibodies that trip the switch of the prion are very harmful and dangerous.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our cjd / vcjd / mad cow disease section for the latest news on this subject. Please use one of the following formats to cite this article in your essay, paper or report:

MLA

University of Zurich. "The flexible tail of the prion protein poisons brain cells." Medical News Today. MediLexicon, Intl., 3 Aug. 2013. Web.
3 Aug. 2013. APA

Please note: If no author information is provided, the source is cited instead.

'The flexible tail of the prion protein poisons brain cells'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam). We reserve the right to amend opinions where we deem necessary.

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here

The human brain spatial map

Main Category: Neurology / Neuroscience
Article Date: 04 Aug 2013 - 10:00 PDT Current ratings for:
The human brain spatial map

Grid-like activity can be seen in the human brain in response to exploring a virtual environment, reports a study published online this week in the journal Nature Neuroscience. These findings imply that our internal navigation system is active even in the absence of movement in physical space.

Previous studies suggest that the sense of place is supported by neurons called place cells, which are active when an animal is in a specific region in an environment, and grid cells that display a spatial pattern of activity that resembles a grid on a map. Though place cells had previously been found in humans, grid cells had been observed only in rodents, bats and monkeys.

Joshua Jacobs and colleagues report evidence for grid-like activity in the human brain, providing the most direct evidence for the existence of grid cells, and suggesting that humans use a coordinate system for navigation similar to that used by other mammalian species. The scientists recorded neuronal activity with electrodes intra-cranially implanted in the brain of patients undergoing treatment for drug-resistant epilepsy. They asked the patients to find objects in a computer-generated virtual environment using a joystick and looked for grid-like features in the recorded activity. In addition to place cell activity in the hippocampus, Jacobs and colleagues found that neurons in the entorhinal and cingulate cortices were active at multiple locations in the environment, forming a lattice covering the entire virtual space. This grid-like pattern strongly resembles the characteristic pattern of activity of grid cells found in animals exploring their physical environment.

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.

The human brain spatial map

Nature Neuroscience - DOI: 10.1038/nn.3466

Nature

Please use one of the following formats to cite this article in your essay, paper or report:

MLA

Nature. "The human brain spatial map." Medical News Today. MediLexicon, Intl., 4 Aug. 2013. Web.
5 Aug. 2013. APA

Please note: If no author information is provided, the source is cited instead.

'The human brain spatial map'

Please note that we publish your name, but we do not publish your email address. It is only used to let you know when your message is published. We do not use it for any other purpose. Please see our privacy policy for more information.

If you write about specific medications or operations, please do not name health care professionals by name.

All opinions are moderated before being included (to stop spam). We reserve the right to amend opinions where we deem necessary.

Contact Our News Editors

For any corrections of factual information, or to contact the editors please use our feedback form.

Please send any medical news or health news press releases to:

Note: Any medical information published on this website is not intended as a substitute for informed medical advice and you should not take any action before consulting with a health care professional. For more information, please read our terms and conditions.

View the original article here