Hope for motion sickness victims: Key neurons identified that sense unexpected movement

Main Category: Neurology / Neuroscience
Also Included In: Public Health
Article Date: 30 Jul 2013 - 1:00 PDT Current ratings for:
Hope for motion sickness victims: Key neurons identified that sense unexpected movement

It happens to all of us at least once each winter in Montreal. You're walking on the sidewalk and before you know it you are slipping on a patch of ice hidden under a dusting of snow. Sometimes you fall. Surprisingly often you manage to recover your balance and walk away unscathed. McGill researchers now understand what's going on in the brain when you manage to recover your balance in these situations. And it is not just a matter of good luck.

Prof. Kathleen Cullen and her PhD student Jess Brooks of the Dept of Physiology have been able to identify a distinct and surprisingly small cluster of cells deep within the brain that react within milliseconds to readjust our movements when something unexpected happens, whether it is slipping on ice or hitting a rock when skiing. What is astounding is that each individual neuron in this tiny region that is smaller than a pin's head displays the ability to predict and selectively respond to unexpected motion.

This finding both overturns current theories about how we learn to maintain our balance as we move through the world, and also has significant implications for understanding the neural basis of motion sickness.

Scientists have theorized for some time that we fine-tune our movements and maintain our balance, thanks to a neural library of expected motions that we gain through "sensory conflicts" and errors. "Sensory conflicts" occur when there is a mismatch between what we think will happen as we move through the world and the sometimes contradictory information that our senses provide to us about our movements.

This kind of "sensory conflict" may occur when our bodies detect motion that our eyes cannot see (such as during plane, ocean or car travel), or when our eyes perceive motion that our bodies cannot detect (such as during an IMAX film, when the camera swoops at high speed over the edge of steep cliffs and deep into gorges and valleys while our bodies remain sitting still). These "sensory conflicts" are also responsible for the feelings of vertigo and nausea that are associated with motion sickness.

But while the areas of the brain involved in estimating spatial orientation have been identified for some time, until now, no one has been able to either show that distinct neurons signaling "sensory conflicts" existed, nor demonstrate exactly how they work. "We've known for some time that the cerebellum is the part of the brain that takes in sensory information and then causes us to move or react in appropriate ways," says Prof. Cullen. "But what's really exciting is that for the first time we show very clearly how the cerebellum selectively encodes unexpected motion, to then send our body messages that help us maintain our balance. That it is such a very exact neural calculation is exciting and unexpected."

By demonstrating that these "sensory conflict" neurons both exist and function by making choices "on the fly" about which sensory information to respond to, Cullen and her team have made a significant advance in our understanding of how the brain works to keep our bodies in balance as we move about.

The research was done by recording brain activity in macaque monkeys who were engaged in performing specific tasks while at the same time being unexpectedly moved around by flight-simulator style equipment.

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.

To read the full paper in Current Biology click here.

The research was funded by the Fonds de Recherche du Québec Nature et Technologies and Canadian Institutes of Health Research as well as through a National Institutes of Health grant.

McGill University

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

MLA

University, McGill. "Hope for motion sickness victims: Key neurons identified that sense unexpected movement." Medical News Today. MediLexicon, Intl., 30 Jul. 2013. Web.
30 Jul. 2013. APA

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

'Hope for motion sickness victims: Key neurons identified that sense unexpected movement'

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

Novel mechanism identified in host-pathogen gastroenteritis interactions

Main Category: Infectious Diseases / Bacteria / Viruses
Also Included In: GastroIntestinal / Gastroenterology
Article Date: 30 Jul 2013 - 1:00 PDT Current ratings for:
Novel mechanism identified in host-pathogen gastroenteritis interactions

A seafood contaminant that thrives in brackish water during the summer works like a spy to infiltrate cells and quickly open communication channels to sicken the host, researchers at UT Southwestern Medical Center report.

Vibrio parahaemolyticus bacteria, which cause gastroenteritis, inject proteins called effectors into host cells. One of those effectors, VopQ, almost immediately starts to disrupt the important process of autophagy via a novel channel-forming mechanism, the scientists report in the investigation available online at the Proceedings of the National Academy of Sciences. Autophagy is the cellular housekeeping mechanism used to recycle nutrients in cells as well as to fight off pathogens. The term autophagy comes from the Greek words for self and eating. During the process, nutrients are recycled by the lysosome, an internal organelle, to produce metabolites that can be used by the cell.

"Our study identifies a bacterial effector that creates gated ion channels and reveals a novel mechanism that may regulate autophagy," said Dr. Kim Orth, professor of molecular biology and biochemistry. She is a corresponding author on the published study. The first author is Anju Sreelatha, a graduate student in Dr. Orth's laboratory.

"Disruptions of autophagic pathways are implicated in many human diseases, including neurodegenerative disease, liver disease, some cancers, and cardiomyopathy (heart muscle disease)," Ms. Sreelatha said.

She explained that ion channels are pores in the membranes of cells or of organelles within cells that allow regulated passage of small molecules or ions across membranes. Gated channels have a mechanism that opens and closes them, making these proteins potential targets for drug development.

"The identification of a channel that opens and closes and thereby affects autophagy may give us a handle by which to modulate this important process," she said, adding that the researchers found that VopQ's channel activity turned off autophagy.

"During infection, VopQ is injected into the host cell where the protein binds to a lysosomal membrane protein and forms small pores, all within minutes of infection. The resulting complex of proteins causes ions to leak and the lysosomes to de-acidify. Lacking acidification, lysosomes cannot degrade the unneeded cellular components and autophagy is disrupted," Ms. Sreelatha said.

Dr. Orth said "Bacterial pathogens have evolved a number of ways to target and manipulate host cell signaling; the ability of VopQ to form a gated ion channel and to inhibit autophagy represents a novel mechanism."

Further characterization of the mechanism by which VopQ sabotages cells to disrupt autophagy may lead to a better understanding of host-pathogen interactions as well as advance our understanding of the pathway, eventually leading to new treatments for diseases in which autophagy has gone awry, they noted.

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

Other UT Southwestern scientists involved were Dr. Hui Zheng, a postdoctoral researcher of cell biology, and Dr. Qiu-Xing Jiang, assistant professor of cell biology. Also participating were Terry Bennett and Dr. Vincent Starai of the University of Georgia.

Funding was provided by the National Institute of Allergy and Infectious Diseases; the Burroughs Wellcome Foundation; the Welch Foundation; the National Institute of General Medical Sciences; the Cancer Prevention and Research Institute of Texas; and by University of Georgia Startup Funds.

UT Southwestern Medical Center

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

MLA

UT Southwestern Medical Center. "Novel mechanism identified in host-pathogen gastroenteritis interactions." Medical News Today. MediLexicon, Intl., 30 Jul. 2013. Web.
30 Jul. 2013. APA

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

'Novel mechanism identified in host-pathogen gastroenteritis interactions'

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

Key brain circuits identified that control compulsive drinking in rats

Main Category: Alcohol / Addiction / Illegal Drugs
Article Date: 24 Jul 2013 - 1:00 PDT Current ratings for:
Key brain circuits identified that control compulsive drinking in rats

A research team led by scientists from the Ernest Gallo Clinic and Research Center at the University of California, San Francisco has identified circuitry in the brain that drives compulsive drinking in rats, and likely plays a similar role in humans.

The scientists found they could reduce compulsive drinking in rats by inhibiting key neural pathways that run between the prefrontal cortex, which is involved with higher functions such as critical thinking and risk assessment, and the nucleus accumbens, a critical area for reward and motivation.

The authors noted that there are already several FDA-approved medications that target activity in these pathways, thus potentially opening an accelerated track to new treatments for compulsive drinking.

The study describing their finding was published online recently in Nature Neuroscience.

The study was conducted on rats that regularly drank 20 percent alcohol. The rats drank both unmixed alcohol and alcohol mixed with extremely bitter quinine, said senior investigator F. Woodward Hopf, PhD, an assistant adjunct professor of neurology at UCSF.

Hopf explained that this alcohol-quinine solution, which he described as "like a vodka tonic without the sugar," is often used as a rodent model of compulsive drinking, or "drinking in the face of negative consequences." In rats, he said, the negative consequence is the bitter taste, while in humans who drink compulsively, "the negative consequences are profound: people continue to drink despite the potential loss of jobs, marriages, freedom, even their lives."

In the United States, alcoholism is estimated to cost $224 billion per year - almost $2 per drink - mostly from lost productivity and crime, and leads to 100,000 preventable deaths per year.

The drinking rats showed a notable increase in the NMDA receptor (NMDAR), which lead author Taban Seif, PhD, a Gallo Center researcher, called "a molecule that excites the brain." When the rats were injected with an NMDAR blocker, their consumption of quinine-laced alcohol dropped significantly, while regular alcohol use was unaffected. "In other words, only the compulsive drinking was affected," said Seif.

The team then focused its research on connections from two specific regions of the rats' prefrontal cortex where they had discovered the presence of unusual types of NMDARs: the medial prefrontal cortex, which mediates conflict during decision-making, and the insula, which is critical for self-awareness and feelings. "In a non-addict, these brain areas tell you when something is potentially harmful and bad, and to run away as fast as possible," said Hopf. "But if you're a compulsive drinker, it seems instead that they give you a comforting pat on the back, in effect telling you it's OK to have another drink, nothing to worry about."

Using a technique called optogenetics, the scientists inserted halorhodopsin, a light-sensitive protein, into these areas. They then used fiber-optic cables implanted in the rats' brains to send pulses of laser light that activated the halorhodopsin, which in turn inhibited the regions' connections to the nucleus accumbens. The researchers found that rats inhibited in this way drank significantly less quinine-laced alcohol, while their intake of regular alcohol solution remained unaffected.

"The fact that we reduced the rats' compulsive drinking using two different methods - an NMDAR blocker and direct inhibition of connections - tells us that we have probably identified the right areas," said Hopf.

The next logical step for the research team, said Hopf, would be to work with clinical researchers on an NMDAR blocker trial in human subjects.

"What is interesting is that we have a new drug which could perhaps treat compulsive aspects of drinking," said Hopf, "but only if you are in conflict about your drinking - if you care. Any therapy with NMDAR blockers would need a strong behavioral and cognitive component to make sure the patient stayed mentally engaged."

Seif and Hopf also plan further experimental studies focusing on how the insula drives behavior and connects to other areas of the brain.

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

Co-authors of the paper are Shao-Ju Chang, Jeffrey A Simms, Stuart L. Gibb, PhD, and Jahan Dadgar of the Gallo Center; Billy T. Chen, PhD, and Brandon K. Harvey of the National Institute on Drug Abuse; Dorit Ron, PhD, of the Gallo Center and UCSF; Robert O. Messing, MD, of the Gallo Center and UCSF at the time of the research and currently of the University of Texas at Austin; and Antonello Bonci, MD, of the Gallo Center, UCSF and the Johns Hopkins University, Baltimore, MD.

The study was supported by funds from the National Institute on Alcohol Abuse and Alcoholism, the National Institute on Drug Abuse and the State of California through UCSF.

University of California - San Francisco

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

MLA

University of California. "Key brain circuits identified that control compulsive drinking in rats." Medical News Today. MediLexicon, Intl., 24 Jul. 2013. Web.
24 Jul. 2013. APA

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

'Key brain circuits identified that control compulsive drinking in rats'

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

Key brain circuits identified that control compulsive drinking in rats

Main Category: Alcohol / Addiction / Illegal Drugs
Article Date: 24 Jul 2013 - 1:00 PDT Current ratings for:
Key brain circuits identified that control compulsive drinking in rats

A research team led by scientists from the Ernest Gallo Clinic and Research Center at the University of California, San Francisco has identified circuitry in the brain that drives compulsive drinking in rats, and likely plays a similar role in humans.

The scientists found they could reduce compulsive drinking in rats by inhibiting key neural pathways that run between the prefrontal cortex, which is involved with higher functions such as critical thinking and risk assessment, and the nucleus accumbens, a critical area for reward and motivation.

The authors noted that there are already several FDA-approved medications that target activity in these pathways, thus potentially opening an accelerated track to new treatments for compulsive drinking.

The study describing their finding was published online recently in Nature Neuroscience.

The study was conducted on rats that regularly drank 20 percent alcohol. The rats drank both unmixed alcohol and alcohol mixed with extremely bitter quinine, said senior investigator F. Woodward Hopf, PhD, an assistant adjunct professor of neurology at UCSF.

Hopf explained that this alcohol-quinine solution, which he described as "like a vodka tonic without the sugar," is often used as a rodent model of compulsive drinking, or "drinking in the face of negative consequences." In rats, he said, the negative consequence is the bitter taste, while in humans who drink compulsively, "the negative consequences are profound: people continue to drink despite the potential loss of jobs, marriages, freedom, even their lives."

In the United States, alcoholism is estimated to cost $224 billion per year - almost $2 per drink - mostly from lost productivity and crime, and leads to 100,000 preventable deaths per year.

The drinking rats showed a notable increase in the NMDA receptor (NMDAR), which lead author Taban Seif, PhD, a Gallo Center researcher, called "a molecule that excites the brain." When the rats were injected with an NMDAR blocker, their consumption of quinine-laced alcohol dropped significantly, while regular alcohol use was unaffected. "In other words, only the compulsive drinking was affected," said Seif.

The team then focused its research on connections from two specific regions of the rats' prefrontal cortex where they had discovered the presence of unusual types of NMDARs: the medial prefrontal cortex, which mediates conflict during decision-making, and the insula, which is critical for self-awareness and feelings. "In a non-addict, these brain areas tell you when something is potentially harmful and bad, and to run away as fast as possible," said Hopf. "But if you're a compulsive drinker, it seems instead that they give you a comforting pat on the back, in effect telling you it's OK to have another drink, nothing to worry about."

Using a technique called optogenetics, the scientists inserted halorhodopsin, a light-sensitive protein, into these areas. They then used fiber-optic cables implanted in the rats' brains to send pulses of laser light that activated the halorhodopsin, which in turn inhibited the regions' connections to the nucleus accumbens. The researchers found that rats inhibited in this way drank significantly less quinine-laced alcohol, while their intake of regular alcohol solution remained unaffected.

"The fact that we reduced the rats' compulsive drinking using two different methods - an NMDAR blocker and direct inhibition of connections - tells us that we have probably identified the right areas," said Hopf.

The next logical step for the research team, said Hopf, would be to work with clinical researchers on an NMDAR blocker trial in human subjects.

"What is interesting is that we have a new drug which could perhaps treat compulsive aspects of drinking," said Hopf, "but only if you are in conflict about your drinking - if you care. Any therapy with NMDAR blockers would need a strong behavioral and cognitive component to make sure the patient stayed mentally engaged."

Seif and Hopf also plan further experimental studies focusing on how the insula drives behavior and connects to other areas of the brain.

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

Co-authors of the paper are Shao-Ju Chang, Jeffrey A Simms, Stuart L. Gibb, PhD, and Jahan Dadgar of the Gallo Center; Billy T. Chen, PhD, and Brandon K. Harvey of the National Institute on Drug Abuse; Dorit Ron, PhD, of the Gallo Center and UCSF; Robert O. Messing, MD, of the Gallo Center and UCSF at the time of the research and currently of the University of Texas at Austin; and Antonello Bonci, MD, of the Gallo Center, UCSF and the Johns Hopkins University, Baltimore, MD.

The study was supported by funds from the National Institute on Alcohol Abuse and Alcoholism, the National Institute on Drug Abuse and the State of California through UCSF.

University of California - San Francisco

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

MLA

University of California. "Key brain circuits identified that control compulsive drinking in rats." Medical News Today. MediLexicon, Intl., 24 Jul. 2013. Web.
24 Jul. 2013. APA

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

'Key brain circuits identified that control compulsive drinking in rats'

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 functions identified for autoimmune disease 'risk' gene

Main Category: Immune System / Vaccines
Also Included In: Genetics
Article Date: 24 Jul 2013 - 0:00 PDT Current ratings for:
New functions identified for autoimmune disease 'risk' gene

Researchers at the University of Minnesota have identified infection-fighting and inflammation-suppressing functions for a gene associated with human autoimmune disease.

The discovery, centered on a gene known as PTPN22, could set into motion new treatment approaches for autoimmune diseases like lupus, rheumatoid arthritis and type 1 diabetes. The key to these advances may lie with a better understanding of how a variant of PTPN22, known as a "risk variant," impacts autoimmune disease development and the behavior of myeloid cells that act as the body's "first responders."

The study appears in the journal Immunity.

In launching their latest research project, University of Minnesota Center for Immunology researchers set out to determine how PTPN22 could regulate immune system function in health and disease.

"Almost a decade ago, researchers at the University of Minnesota and other institutions discovered that people carrying a variant form of the PTPN22 gene bear an increased risk of becoming sick with certain autoimmune diseases. However, we have lacked a deep understanding how the variant creates that increased risk," said Erik J. Peterson, M.D., one of the study's lead authors and a University of Minnesota Medical School associate professor in the Division of Rheumatic and Autoimmune Diseases. "We wanted to understand the molecular basis for PTPN22 association with disease."

Much of the work carried out in the latest study took place in Peterson's laboratory, which utilizes genetic, biochemical, and primary human sample-based approaches to investigate how "risk" genes predispose to development of autoimmune disease.

According to the study's authors, previous research showed that PTPN22 works in immune cells, but few studies had specifically examined PTPN22's function in infection-fighting cells called myeloid cells.

"Myeloid cells are among the body's 'first responders' to a challenge with a virus or bacterium," said Yaya Wang, Ph.D., one of the study's co-first authors and a research associate in the Center for Immunology. "Upon recognizing the presence of an infection, myeloid cells produce chemicals that increase inflammation and help fight the invading microbe. We were intrigued by the idea that PTPN22 and its disease-associated variant might have a role in myeloid cell functions."

Researchers found that both mouse and human myeloid cells carrying the PTPN22 "risk" variant show decreased production of molecules called type 1 Interferons. Type 1 Interferons are needed to boost immune responses to viruses and other infections. In mice lacking the PTPN22 gene, reduced type 1 Interferon production correlates with an impaired ability to fight infections.

But the PTPN22 gene does more than simply fight infection, the study showed.

"Unexpectedly, we also found that PTPN22 suppresses inflammation," said Wang. "Furthermore, we showed that the PTPN22 risk variant is defective in suppressing inflammatory arthritis."

"We anticipate that our findings will open new lines of investigation into how PTPN22 and other autoimmune disease 'risk' genes could work in infection-fighting and anti-inflammatory processes. Ultimately, we hope that the research will accelerate the drive toward better treatments and cures for autoimmune disorders," said Peterson.

More research is underway to determine the impact of the PTPN22 variant in the function of myeloid blood cells, particularly in patients suffering from lupus. Researchers are also comparing immune responses to influenza A vaccines between carriers and non-carriers of the PTPN22 variant. The goal is to understand the role of the disease-associated variant in mounting a normal response to immunizations against viruses.

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

This project was funded by grants from the National Institutes of Health (NIH), R01AR057781 (awarded to Peterson) and R01AI070544 (awarded to co-senior author Nunzio Bottini, M.D., Ph.D.), as well as from several other sources, including: the American College of Rheumatology Within Our Reach Campaign, the American Diabetes Association, the Alliance for Lupus Research, and the Lupus Foundation of Minnesota.

University of Minnesota Academic Health Center

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

MLA

University of Minnesota Academic Health Center. "New functions identified for autoimmune disease 'risk' gene." Medical News Today. MediLexicon, Intl., 24 Jul. 2013. Web.
24 Jul. 2013. APA

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

'New functions identified for autoimmune disease 'risk' gene'

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

Risk Factor For Autism Identified In A Subset Of Children

Main Category: Autism
Article Date: 11 Jul 2013 - 0:00 PDT Current ratings for:
Risk Factor For Autism Identified In A Subset Of Children

UC Davis MIND Institute researchers have identified the specific antibodies that target fetal brain proteins in the blood of a subset of women whose children are diagnosed with autism. The finding is the first to pinpoint a specific risk factor for a significant subset of autism cases, as well as a biomarker for drug development and early diagnosis. The researchers have named autism related to these antibodies "Maternal Autoantibody-Related," or MAR autism.

The study found that the mothers of children with autism were more than 21 times as likely to have the specific MAR antibodies in their systems that reacted with fetal brain proteins, or antigens, than were the mothers of children who did not have autism. In fact, specific combinations of MAR antibodies were not found in the blood of mothers whose children were typically developing.

The research, "Autism-specific maternal autoantibodies recognize critical proteins in developing brain," is published online in Translational Psychiatry, a Nature journal.

The study was led by principal investigator and immunologist Judy Van de Water, a researcher affiliated with the MIND Institute. Earlier studies by Van de Water and her colleagues found that women with certain antibodies in their bloodstreams are at greater risk of having a child with autism and that their children exhibited more severe language delays, irritability and self-injurious behaviors than did the autistic children of mothers whose blood did not have the antibodies.

"Now we will be able to better determine the role of each protein in brain development," said Van de Water, professor of internal medicine. "We hope that, one day, we can tell a mother more precisely what her antibody profile means for her child, then target interventions more effectively."

To identify the exact antigens targeted by the mothers' antibodies, Van de Water and her colleagues conducted the research in Northern California using blood samples from 246 mothers of children with autism and of a control group of 149 mothers of children without autism to examine their reactivity with the candidate antigens.

Seven antigens were significantly more reactive to the blood of mothers of children with autism than to that of the control mothers. The study found that the mothers with antibodies that reacted with any one of these antigens, either individually or in combination with other antigens, were more than three times as likely to have a child with autism spectrum disorder.

Several combinations of antibodies in the blood from mothers of children with autism were not found in the control mothers' blood. Nearly 23 percent of mothers of children with autism had certain combinations of autoantibodies against the target antigens, compared with less than 1 percent of mothers of children without the disorder.

The specific antigens identified in the study are lactate dehydrogenase A and B, cypin (guanine deaminase), stress-induced phosphoprotein 1, collapsing response mediator proteins 1 and 2, and Y-box binding protein. All are found throughout the body, but also are expressed at significant levels in the human fetal brain and have established roles in neurodevelopment. For example, cypin is an enzyme that plays an important role in normal neurite branching, a fundamental function in the developing brain, whereas the CRMP proteins are critical later in neuron development for axon outgrowth.

Maternal antibodies are known to cross the placenta during pregnancy and can be detected in a fetus as early as 13 weeks. By 30 weeks, maternal antibody levels in the fetus are about half that of the mother, and at birth, the concentration is even greater in the newborn than in the mother herself. The maternal antibodies stay in the baby's bloodstream for about 6 months after birth, after which the baby's own immune system takes over.

Once in the fetal bloodstream, the antibodies then may enter the brain and attack cells that have corresponding proteins that act as antigens. This antigen-antibody response is an important defense against foreign invaders, such as bacteria or viruses, but is not normally directed against oneself. When directed against one's own tissue, the antibodies are known as autoantibodies.

"It is important to note that women have no control over whether or not they develop these autoantibodies, much like any other autoimmune disorder," Van de Water said. "And, like other autoimmune disorders, we do not know what the initial trigger is that leads to their production."

Understanding which proteins and which pathways are implicated in MAR autism can help elucidate the causes of autism and possibly lead to new therapies, such as administering 'antibody blockers' to the mother during pregnancy to prevent damage to the developing fetal brain, Van de Water said.

These findings are leading to the development of a MAR diagnostic test for autism, which would be available to the mothers of young children who are showing signs of developmental delay. If the test were positive, the child would be a candidate for early behavioral intervention.

"These findings are incredibly important because they establish a cause for a significant portion of autism cases, thereby opening up new lines of inquiry into possible biological treatments," said MIND Institute Director Leonard Abbeduto. "In addition, the findings demonstrate that a diagnostic test is within reach. This test would be invaluable for women who are considering becoming pregnant and could lead to earlier and more accurate diagnosis of children with developmental challenges and help get them into behavioral interventions at younger ages."

A MAR diagnostic test also would assess a mother's risk of having a child with autism prior to conception, which is particularly important for women who already have a child with the disorder. UC Davis has patented this technology and licensed the exclusive worldwide rights to develop it for commercial purposes to Pediatric Bioscience, Inc.

"We know that early behavioral interventions for autism are critical," said Isaac Pessah, professor and chair of the Department of Molecular Biosciences in the UC Davis School of Veterinary Medicine and former director of the UC Davis Center for Children's Environmental Health. "Developing a predictive test for autism before symptoms become obvious could have an enormous impact on treating children with the condition."

Study participants were from the CHARGE (Childhood Autism Risks from Genetics and the Environment) study, an ongoing study that was launched in 2001 by the MIND Institute and the UC Davis Center for Children's Environmental Health, of which Van de Water now is director. Children with autism spectrum disorder, children with developmental delay and typically developing children between the ages of 2 and 5 years are studied with the goal of better understanding the causes of autism.

A related study is the MARBLES (Markers of Autism Risk in Babies - Learning Early Signs) study, also being conducted at the MIND Institute and the Center for Children's Environmental Health. This study follows pregnant women who already have a child with autism. Multiple factors related to genetics and the environment is under study in an effort to uncover predictors for having a child with autism.

Van de Water said knowing the specific protein targets of the maternal antibodies enables researchers to develop more precise animal models of autism.

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 study was funded by NIEHS grants P01 ES11269-01 and 1 R01-ES015359; United States Environmental Protection Agency Science to Achieve Results (STAR) program grant R829388; the UC Davis MIND Institute; and an Autism Speaks graduate fellowship.

Other authors include Daniel Braunschweig, Paula Krakowiak, Paul Duncanson, Robert Boyce, Robin Hansen, Paul Ashwood and Irva Hertz-Picciotto, all of UC Davis.

University of California - Davis Health System

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

MLA

University of California - Davis Health System. "Risk Factor For Autism Identified In A Subset Of Children." Medical News Today. MediLexicon, Intl., 11 Jul. 2013. Web.
11 Jul. 2013. APA

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

posted by kblanco on 11 Jul 2013 at 5:06 pm

Reactivity to these bands is also associated with Borrelia burgdorferi and to a lesser degree to Bartonella henselae, Bartonella quintana, Mycoplasma, Chlamydia pneumonia and Streptococcus pneumoniae .

Spelling out the viruses, bacteria and fungi would be helpful for treatment of pregnant moms....say it truthfully MIND.

| post followup | alert a moderator |

'Risk Factor For Autism Identified In A Subset Of Children'

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)

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

Risk Factor For Autism Identified In A Subset Of Children

Main Category: Autism
Article Date: 11 Jul 2013 - 0:00 PDT Current ratings for:
Risk Factor For Autism Identified In A Subset Of Children

UC Davis MIND Institute researchers have identified the specific antibodies that target fetal brain proteins in the blood of a subset of women whose children are diagnosed with autism. The finding is the first to pinpoint a specific risk factor for a significant subset of autism cases, as well as a biomarker for drug development and early diagnosis. The researchers have named autism related to these antibodies "Maternal Autoantibody-Related," or MAR autism.

The study found that the mothers of children with autism were more than 21 times as likely to have the specific MAR antibodies in their systems that reacted with fetal brain proteins, or antigens, than were the mothers of children who did not have autism. In fact, specific combinations of MAR antibodies were not found in the blood of mothers whose children were typically developing.

The research, "Autism-specific maternal autoantibodies recognize critical proteins in developing brain," is published online in Translational Psychiatry, a Nature journal.

The study was led by principal investigator and immunologist Judy Van de Water, a researcher affiliated with the MIND Institute. Earlier studies by Van de Water and her colleagues found that women with certain antibodies in their bloodstreams are at greater risk of having a child with autism and that their children exhibited more severe language delays, irritability and self-injurious behaviors than did the autistic children of mothers whose blood did not have the antibodies.

"Now we will be able to better determine the role of each protein in brain development," said Van de Water, professor of internal medicine. "We hope that, one day, we can tell a mother more precisely what her antibody profile means for her child, then target interventions more effectively."

To identify the exact antigens targeted by the mothers' antibodies, Van de Water and her colleagues conducted the research in Northern California using blood samples from 246 mothers of children with autism and of a control group of 149 mothers of children without autism to examine their reactivity with the candidate antigens.

Seven antigens were significantly more reactive to the blood of mothers of children with autism than to that of the control mothers. The study found that the mothers with antibodies that reacted with any one of these antigens, either individually or in combination with other antigens, were more than three times as likely to have a child with autism spectrum disorder.

Several combinations of antibodies in the blood from mothers of children with autism were not found in the control mothers' blood. Nearly 23 percent of mothers of children with autism had certain combinations of autoantibodies against the target antigens, compared with less than 1 percent of mothers of children without the disorder.

The specific antigens identified in the study are lactate dehydrogenase A and B, cypin (guanine deaminase), stress-induced phosphoprotein 1, collapsing response mediator proteins 1 and 2, and Y-box binding protein. All are found throughout the body, but also are expressed at significant levels in the human fetal brain and have established roles in neurodevelopment. For example, cypin is an enzyme that plays an important role in normal neurite branching, a fundamental function in the developing brain, whereas the CRMP proteins are critical later in neuron development for axon outgrowth.

Maternal antibodies are known to cross the placenta during pregnancy and can be detected in a fetus as early as 13 weeks. By 30 weeks, maternal antibody levels in the fetus are about half that of the mother, and at birth, the concentration is even greater in the newborn than in the mother herself. The maternal antibodies stay in the baby's bloodstream for about 6 months after birth, after which the baby's own immune system takes over.

Once in the fetal bloodstream, the antibodies then may enter the brain and attack cells that have corresponding proteins that act as antigens. This antigen-antibody response is an important defense against foreign invaders, such as bacteria or viruses, but is not normally directed against oneself. When directed against one's own tissue, the antibodies are known as autoantibodies.

"It is important to note that women have no control over whether or not they develop these autoantibodies, much like any other autoimmune disorder," Van de Water said. "And, like other autoimmune disorders, we do not know what the initial trigger is that leads to their production."

Understanding which proteins and which pathways are implicated in MAR autism can help elucidate the causes of autism and possibly lead to new therapies, such as administering 'antibody blockers' to the mother during pregnancy to prevent damage to the developing fetal brain, Van de Water said.

These findings are leading to the development of a MAR diagnostic test for autism, which would be available to the mothers of young children who are showing signs of developmental delay. If the test were positive, the child would be a candidate for early behavioral intervention.

"These findings are incredibly important because they establish a cause for a significant portion of autism cases, thereby opening up new lines of inquiry into possible biological treatments," said MIND Institute Director Leonard Abbeduto. "In addition, the findings demonstrate that a diagnostic test is within reach. This test would be invaluable for women who are considering becoming pregnant and could lead to earlier and more accurate diagnosis of children with developmental challenges and help get them into behavioral interventions at younger ages."

A MAR diagnostic test also would assess a mother's risk of having a child with autism prior to conception, which is particularly important for women who already have a child with the disorder. UC Davis has patented this technology and licensed the exclusive worldwide rights to develop it for commercial purposes to Pediatric Bioscience, Inc.

"We know that early behavioral interventions for autism are critical," said Isaac Pessah, professor and chair of the Department of Molecular Biosciences in the UC Davis School of Veterinary Medicine and former director of the UC Davis Center for Children's Environmental Health. "Developing a predictive test for autism before symptoms become obvious could have an enormous impact on treating children with the condition."

Study participants were from the CHARGE (Childhood Autism Risks from Genetics and the Environment) study, an ongoing study that was launched in 2001 by the MIND Institute and the UC Davis Center for Children's Environmental Health, of which Van de Water now is director. Children with autism spectrum disorder, children with developmental delay and typically developing children between the ages of 2 and 5 years are studied with the goal of better understanding the causes of autism.

A related study is the MARBLES (Markers of Autism Risk in Babies - Learning Early Signs) study, also being conducted at the MIND Institute and the Center for Children's Environmental Health. This study follows pregnant women who already have a child with autism. Multiple factors related to genetics and the environment is under study in an effort to uncover predictors for having a child with autism.

Van de Water said knowing the specific protein targets of the maternal antibodies enables researchers to develop more precise animal models of autism.

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 study was funded by NIEHS grants P01 ES11269-01 and 1 R01-ES015359; United States Environmental Protection Agency Science to Achieve Results (STAR) program grant R829388; the UC Davis MIND Institute; and an Autism Speaks graduate fellowship.

Other authors include Daniel Braunschweig, Paula Krakowiak, Paul Duncanson, Robert Boyce, Robin Hansen, Paul Ashwood and Irva Hertz-Picciotto, all of UC Davis.

University of California - Davis Health System

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

MLA

University of California - Davis Health System. "Risk Factor For Autism Identified In A Subset Of Children." Medical News Today. MediLexicon, Intl., 11 Jul. 2013. Web.
11 Jul. 2013. APA

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

posted by kblanco on 11 Jul 2013 at 5:06 pm

Reactivity to these bands is also associated with Borrelia burgdorferi and to a lesser degree to Bartonella henselae, Bartonella quintana, Mycoplasma, Chlamydia pneumonia and Streptococcus pneumoniae .

Spelling out the viruses, bacteria and fungi would be helpful for treatment of pregnant moms....say it truthfully MIND.

| post followup | alert a moderator |

'Risk Factor For Autism Identified In A Subset Of Children'

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)

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