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RESEARCH

* Gene Boosts Fear Response, May Be Anxiety-Linked

* Researchers Develop Mouse Model Of Rett Syndrome

* Researchers Produce Motor Neurons from Embryonic Stem Cells

* Tweaking Single Gene Makes Mice Brainier

AWARENESS

* Families, Experts Seek Answers To Autism - ASA Conference In Progress

* Boston Area Schools Awarded Autism Awareness Grants

ADVOCACY

* Special Ed Tax Could Spare Detroit Programs: Wayne County Proposal K

PUBLIC HEALTH

* Blair Insists MMR Jab Should Be Kept

TREATMENT

* Neuro-Immune Diagnosis and Treatment Gives Hope to Children With Autism

* Readers' Posts

REASEARCH

Gene Boosts Fear Response, May Be Anxiety-Linked

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Reuters Health - The genes we inherit from our parents are thought to influence how we act, but documenting a direct effect of genes on behavior has been difficult. Now, scientists have found that people who carry a particular genetic variation experience greater activity in a fear-related brain region when shown pictures of frightened or angry faces.

"This is the first study to show a genetic effect on a system in the brain related to human emotions," the study's lead author, Dr. Daniel R. Weinberger of the National Institute of Mental Health in Bethesda, Maryland, told Reuters Health.

He noted that scientists "have known for a long time that temperament is genetic and that it is present to some degree from very early in life." It has also been known that the amygdala--the brain region monitored in the study--is involved in emotions, especially danger-related fear and anxiety, he explained.

Anxiety varies widely from person to person, and some research has suggested that anxiety-related behavior may be influenced by a variation in a gene for a protein involved in moving the chemical serotonin around the brain. This serotonin transporter gene comes in long and short versions, and having at least one of the short versions, which leads to less efficient transporting of serotonin, has been tentatively linked to increased anxiety.

To test the connection between the short version of the serotonin transporter gene and anxiety, Weinberger and his colleagues screened 28 volunteers for the variations. Half of the participants had two copies of the long version-one inherited from each parent--while the others had at least one short copy.

The participants were presented with pictures of frightened or angry faces. They had to match the photos to other faces showing the same emotion. During the exercise, the researchers monitored the activity in the amygdala.

People with at least one short version of the gene exhibited greater activity in the amygdala than people with two long copies, the researchers report in the July 19th issue of the journal Science.

"This study shows that one of the factors related to the response of the amygdala to the environment, presumably how quick it is to see dangerousness, is related to the form of the gene that people inherit," Weinberger said.

"It is the first time we have been able to see how a gene contributes to aspects of human emotionality and temperament," he said.

Weinberger cautioned, however, "It is important to note that there is a lot more to fear and anxiety than this gene, but it appears to be one of the factors." Now that this factor has been identified, it may be easier to figure out the other influences, he said. The next step, according to Weinberger, is to explore other genes and environmental factors that interact with the gene and the amygdala's response to the environment.

SOURCE: Science 2002;297:400-403.

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Researchers Develop Mouse Model Of Rett Syndrome

Studies might improve understanding of leading cause of mental retardation in girls

By studying gene mutations in patients with the complex set of behavioral and neurological symptoms that accompany Rett syndrome, Howard Hughes Medical Institute investigator Huda Zoghbi and her colleagues at Baylor College of Medicine have designed a mouse model that faithfully recapitulates the disease down to its distinctive hand-wringing behavior.

The development of the mouse, reported in the July 18, 2002 issue of the journal Neuron, provides a springboard into the study of Rett syndrome, the leading cause of mental retardation in girls.

First recognized as a syndrome in the 1980s, the disorder affects one in 10,000-15,000 girls. It is particularly devastating for families with affected children because infants are seemingly normal at birth and achieve the usual developmental milestones for the first few months of life. Then, as the infant reaches toddlerhood, a sudden and dramatic decline in physical and mental capabilities takes hold, accompanied by onset of seizures, irregular breathing, awkward gait, and hand-wringing.

"I know of no other neurological disease that gives this distinctive stereotypic behavior -- this hand-wringing these girls do basically all the time they are awake," said Zoghbi. "With this mouse model we can now ask, 'Why is that?'"

Zoghbi has been studying Rett syndrome since the mid-1980s, when she first encountered patients with the disorder as a neurology fellow and decided to search for the gene responsible for the disorder. She reasoned that the gene must be on the X chromosome, the female sex chromosome, and it must also be essential because there had been no males reported to have the syndrome. (Since males have only one X chromosome, mutations that knock out the gene's function could be lethal at an embryonic stage.) In females, there are two copies of the X chromosome, but in each cell only one of the two X chromosomes is active. The scientists reasoned that if enough cells are "normal," they can compensate for the mutated gene.

After 14 years of searching, a scientist in Zoghbi's lab found that a gene called MECP2 was mutated in the Rett Syndrome patients they studied. Earlier research suggested that the MeCP2 protein was responsible for making sure that genes the cell has marked with a molecular tag, called a methyl group, are silenced. The MeCP2 protein latches on to these methyl groups and prevents them from being translated into protein.

How MeCP2's molecular role translates into a neurological disorder is still not clear. Ever since a diagnostic test for the gene mutation was developed, however, there has been a flood of new information about the prevalence of the disorder. This information reveals that mutations in the MECP2 gene can take a wide variety of forms.

"We now know of cases of classic autism and schizophrenia that are caused by mutations in this gene," said Zoghbi. "The clinical spectrum is so broad that we don't know the true prevalence of this mutation." She estimates that the mutation may be twice as common as is currently thought, with perhaps one in 10,000 children affected.

What is clear so far is that the MECP2 gene, which resides at the end of the long arm of the human and mouse X chromosome, plays a vital role in fine-tuning the developing nervous system during a crucial stage when infants are learning to sit up, walk, and begin language acquisition, said Zoghbi.

To understand the molecular details of what goes wrong, the scientists first needed to create a mouse model of the disorder. The first attempt at a mouse model, in which the MECP2 gene was deleted completely, resulted in severe disease and early death. Zoghbi and her colleagues sought to create a model that would more closely mimic the progression of the human disorder. So, they studied the various mutations that had been found in patients to design a mutant mouse that would produce a partially functional protein. The result was a mouse that mimics many of the aspects of the disease observed in humans.

Using the mouse model, the scientists will probe how the MeCP2 protein affects brain function at a crucial developmental stage. "The second part of the story is really in discovering what this protein is doing in the brain," said Zoghbi. "It may be that at a certain developmental stage, the brain suddenly requires the function of this protein. In humans, by birth a lot of the hardwiring has already happened. Infancy is a critical time as life experiences refine synaptic function and strengthen synapses. Experiences fine tune the brain. Perhaps more complex tasks require the input of this protein and its loss is now instrumental. Things fall apart and people regress. Perhaps key genes that are important at certain times are not put in place. We don't know the mechanism but having this mouse model will allow us to ask these questions."

Zoghbi is hopeful that studying the mouse model will also have implications for treatment of patients diagnosed with Rett Syndrome.

"As development progresses, what we encounter -- our experiences -- may also change how the brain responds. This may account for individual variation in disease severity," she said. "It may be that enrichment of the environment or exposure to certain stimuli may give affected children more milestones. I could envision that with interventional studies in mice, we may identify pathways that could lead to behavioral or pharmacological approaches that may provide at least symptomatic relief."

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Researchers Produce Motor Neurons from Embryonic Stem Cells

Beginning with cultured mouse embryonic stem cells, researchers have administered a precise mix of chemical signals to coax the cells to differentiate into functioning motor neurons.

The achievement was made possible by a decade of work in deciphering the signals that trigger differentiation of motor neurons, which are responsible for controlling the movement of muscles. The experiments represent an important step in applying that knowledge to grow functioning neurons from stem cells - undifferentiated cells that have the potential to become many different types of adult cells.

According to the researchers, the success of the experiments with mouse cells suggests that the same type of approach might be used to grow human motor neurons from stem cells. Such neurons could enable regeneration of nerve tissue lost to disease or trauma.

The experiments by researchers led by Howard Hughes Medical Institute investigator Thomas Jessell at Columbia University were reported in an article that was given immediate early publication status by the journal Cell and published online on July 17, 2002. The research was funded in part by Project A.L.S.

For more than 15 years, Jessell and his colleagues have been attempting to untangle the delicate connections of nerve cells in the developing spinal cord. Their studies have shown that the fledgling vertebrate nervous system is crackling with activity - genes are being turned on and off at a rapid pace, transforming immature cells into a billions-strong network of specialized neural cells. Ultimately, Jessell hopes that his research will provide a more thorough understanding of how the central nervous system (CNS) is constructed - this, he says, may suggest new ways to repair diseased or damaged components of the mature CNS.

According to Jessell, the attempt to generate motor neurons from stem cells relied on many years of research to identify the chemical cues in the developing embryo that coax "naive neuroprogenitor" cells to differentiate into spinal cord motor neurons. These chemical signals "direct" ES cells down a developmental pathway in successive stages -first into neurons and ultimately into ever more specialized spinal cord motor neurons. Two of the key signals, said Jessell, are retinoic acid, which converts mid-brain neural cells into spinal cord progenitors, and Sonic hedgehog, a protein that converts spinal cord progenitor cells into motor neurons.

"Until now, we have been trying to piece together these steps as individual bites," said Jessell. "But we hadn't shown that the normal signaling factors could be used conjointly to take a naive class of progenitors like ES cells, and by sequential exposure to these factors, recapitulate this developmental pathway."

First author Hynek Wichterle, a postdoctoral fellow in Jessell's laboratory, began by using retinoic acid and other chemical cues to induce ES cells to differentiate into mid-brain-type neurons and then into spinal cord neurons. The scientists could follow the steps of differentiation by looking for the expression of specific transcription factors that define the identity of cells as spinal cord progenitor cells.

"Retinoids will give you spinal cord identity, but that doesn't determine exactly which type of neuron emerges from these spinal cord progenitor cells," said Jessell. "And that's where Sonic hedgehog becomes important, because our work and that of others had shown that you need Sonic hedgehog signaling at exactly the right level of signal activation to generate motor neurons."

Thus, when the scientists exposed the cultured spinal cord neurons to appropriate levels of the Sonic hedgehog protein, the cells differentiated to become motor neurons. The dependence of this differentiation on a narrow concentration range of the Sonic hedgehog protein is significant, said Jessell, because in developing embryos the amount of Sonic hedgehog governs what type of neuron will be generated.

In additional experiments, the scientists used ES cells from transgenic mice whose motor neurons were tagged with a fluorescent marker. The fluorescent tagging enabled Jessell and his colleagues to monitor, isolate and purify the specific motor neurons they had induced - a technique that Jessell believes will be crucial to further attempts to define the signaling pathways involved in neuronal differentiation.

The researchers were also able to address an important question, namely, whether the motor neurons they had developed in culture could actually function in living animals. "We needed to demonstrate how well these in vitro-generated motor neurons did when they were put into a living embryo," Jessell said. "So, Hynek managed the very impressive technical feat of reintroducing these ES-cell-derived motor neurons back into the spinal cords of chick embryos at a stage when normal motor neurons are being generated." The scientists then tested in the chick embryos how well the introduced neurons survived, integrated themselves into the embryonic spinal cord and extended their long cable-like axons toward their normal targets in muscle.

"I think our results documented that these ES-cell-derived motor neurons do a pretty good job of mimicking their embryo-derived counterparts in all of those three tests," said Jessell. "In general, I was pleasantly surprised by how well neuralized ES cells recapitulate the developmental events that we have come to associate with motor neuron progenitors and motor neurons."

Jessell believes that these successes represent only the beginning of a promising line of research. "This is just the starting point for trying to take a rational approach to studying the ability of ES-cell-derived motor neurons to restore function, not just in an embryonic context, but in a more relevant adult context," he said.

Jessell and his colleagues hope to use ES-generated motor neurons in experiments to identify all the genes that govern the pathways of motor neuron differentiation. They are also developing collaborations with neurologists to explore in mouse models whether their motor neurons can regenerate spinal cords that have been damaged by trauma or neurodegenerative diseases, such as amyotrophic lateral sclerosis.

The researchers also plan to explore whether the signaling pathways of motor neuron differentiation mice resemble those in humans. "I think one can be cautiously optimistic that such parallels will exist," said Jessell. "While many scientists have shown that human ES cells can give rise to neurons, we don't know exactly which type of neurons they are. And, there's a much greater heterogeneity in the properties of human ES cells than in mouse ES cells; so it may be necessary to sift through a number of the available human ES cell lines before arriving at a cell which behaves as its mouse counterpart. But, in principle there is no reason why this type of approach might not be successful with human cells," he said.

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Tweaking Single Gene Makes Mice Brainier

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Scientists have succeeded in making brainier mice. Whether the animals were actually smarter remains unknown, but their cerebral cortex surface area was significantly larger than that of normal mice. The findings, published today in the journal Science, may help explain how human brains came to be disproportionately large compared to those of other species.

As the largest structure in the brain, the cerebral cortex harbors two-thirds of the brain's neurons in a thin layer. In humans the cortex folds in on itself in order to fit inside the skull, giving the brain a unique, wrinkled topography. To investigate what controls the surface area of the cerebral cortex, Anjen Chenn, now at Northwestern University School of Medicine, and Christopher A. Walsh of Beth Israel Deaconess Medical Center developed a line of transgenic mice. The animals carried a variant of a gene that makes a protein thought to play a role in regulating cell growth in the developing brain. "We found that in mice that overproduced the beta-catenin protein the mouse's cerebral cortex grew dramatically so that instead of a flat sheet, it folded in on itself and appeared 'wrinkled' much like it is in humans," Walsh explains. (The image to the right shows the brains of a control mouse (top) and a transgenic mouse (bottom).)

Specifically, beta-catenin was more abundant in precursor cells that become neurons. The researchers propose that the protein may act as a switch that tells the cells to keep dividing or to stop and become neurons. By causing more cell division, excess beta-catenin creates a larger cortex with a greater number of neurons. Further research is required to fully elucidate the role of beta-catenin, including studies of whether its production is aberrant in cases of mental retardation characterized by abnormally small brains. --Sarah Graham

+For the full article, go to:

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AWARENESS

Families, Experts Seek Answers To Autism - ASA Conference In Progress

When the video store doesn't have a movie or he doesn't like a math problem, Logan Reilly screams -- loud, long, extreme screams that draw stares in public.

Logan, 13, can't control the outbursts. They're caused by autism, a disability that affects the development of the brain in the areas of social interaction and communication skills.

"I've resigned myself that there isn't anything that will take it away," said his mother, Edys Reilly. "This is the way it is."

Nationwide, the number of children with autism has grown 10 percent to 17 percent a year during the past decade, according to the Centers for Disease Control and Prevention. From 500,000 to 1.5 million people are believed to have the condition, many of them children.

In Indiana, the number of children with autism registered in schools has grown from 116 in 1989 to 3,832 last year, according to the state Department of Education.

Some of the increase can be attributed to the broadening of diagnostic criteria. But experts say that alone can't account for what's becoming a major health crisis.

"We don't know the reasons for it, and we don't know the causes for it. But we do know it's growing at an alarming rate," said Robert L. Beck, executive director of the Autism Society of America.

Sharing ideas on how to tackle the epidemic will be the goal when about 1,750 people -- from parents to teachers to the world's leading experts on autism -- gather in Indianapolis today for the society's four-day annual conference.

"This is an opportunity for people to hear a diverse range of opinions," said Dr. Cathy Pratt, director of the Indiana Resource Center for Autism. "If we're to move forward as a community, we have to embrace those diverse opinions. We have to realize there may be multiple paths, multiple reasons, multiple causes."

Ten years ago, autism was thought to be a rare disorder affecting 1 in 10,000 people. It is now estimated to affect 1 in 250.

The disability can manifest itself in different ways. In some mild cases, such as Asperger's syndrome, the individual has social impairment but can have above-average intelligence; severe cases can include self-destructive behavior and an inability to communicate verbally.

Symptoms usually appear during a child's first three years. Children often lag in speech development, avoid social interaction and eye contact and, in some cases, throw tantrums for no apparent reason.

Researchers have found no cause and no cure. Many think the condition is genetic; others believe it is caused by childhood vaccines, though no link has been scientifically proven.

While the search for a cause continues, costs are mounting. Annually, about $20 billion is spent on health, education and other services for people with autism, Beck said.

Early intervention, such as speech and developmental therapies, can help reduce that cost and improve the quality of life for children with autism, he said.

Indiana hasn't increased funding for early intervention programs since the mid-1990s, Pratt said. And while the number of children with autism has risen, quality day care for children and adults is still scarce, she said.

But in some ways, Indiana is ahead of the nation. The state has provided money for teacher training, Pratt said, and it offers something many states don't: an autism waiver, funded through Medicaid, that pays for long-term care and therapy.

Still, the waiting list is about 1,800 families long.

"What's happened is that the increase has happened so quickly, it caught most every state off balance," Pratt said.

Amy and Steele Gudal of Carmel know how important those services are. Within months, they learned that their two daughters -- 6-year-old Gentry and 7-year-old Gabrielle -- had autism. "I was numb," Amy Gudal said. "That allowed me to just dive into the treatments and therapies."

Four years later, the Gudals want to help others. They hope to open a school for children with autism to provide one-on-one instruction.

In the meantime, Amy Gudal said, her daughters teach her more than she teaches them.

Tuesday morning, Gudal had a long list of things to do. But when Gentry wanted her to come lie in bed, Gudal dropped her list and headed for the top bunk.

"They're just who they are -- they love unconditionally," she said. "Instead of getting frustrated, you just have to stop and say, 'What can I learn from this?' "

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Boston Area Schools Awarded Autism Awareness Grants

reness_grants+.shtml

After her daughter was diagnosed with autism, Cathy Pitts learned quickly that it takes more than parents to raise an autistic child. "The educational support is just as important," said Pitts, of Brockton. "Teachers and administrators in schools have to be aware of what children with autism need."

That task will be made easier in two local school districts by federal autism-awareness grants announced last week. The Brockton and Old Rochester Regional school districts will each receive $75,000 to aid autism instruction and awareness.

Special education officials in both districts say they will use the money to hire an autism specialist and to develop professional training for teachers around Autism Spectrum Disorders, or ASD. According to the US Department of Health and Human Services, as many as one in 500 children has been diagnosed with some type of ASD, and the number is growing.

A developmental disability typically diagnosed within the first three years of a child's life, autism affects the normal development of the brain in the areas of social interaction and communication skills. In Massachusetts, there are 3,451 students with autism, according to the Department of Education.

Terri Hamm, director of special education for the Old Rochester Regional schools, said the 2,731-student district, which includes Marion, Mattapoisett, and Rochester, has seen a steady increase in the number of autistic students. She said the majority of the 26 students diagnosed with some type of ASD are placed in general education classes, requiring specialized teacher training, and special education support.

"It has been difficult on our staff because there are social issues, learning needs, and behavioral concerns," Hamm said. "We're thrilled the grant was funded because we're going to be able to develop social skills curriculum and help classroom teachers and special ed. teachers in all our schools improve instruction for kids with autism."

In the larger Brockton district, where about 70 students have been diagnosed with ASD, some schools have classrooms designated for autistic students, according to Joanne Malonson, director of special education services. But because of the wide spectrum of autism disorders, other students are placed in inclusion classrooms (a mix of general education students and students with disabilities) or in general education classes with support such as one-on-one assistance.

"Some of these kids are able to really achieve academically, but they're lacking in social skills, communication, adaptive daily living skills and the ability to manipulate life outside school community, like [to] order off a restaurant menu, handle money, or choose their own clothes," Malonson said. "They're not as successful in establishing relationships so we have to focus on a mix of academic and communication skills."

She said the autism grant, one of 26 approved by the state Department of Education last month, also will help the district provide more education on autism for parents. Pitts, the Brockton parent, said she hopes the autism specialist, who administrators hope to hire by the fall, will work to increase collaboration between educators and the parents of autistic students. She said her 12-year-old daughter, who attends Plouffe Elementary School, has benefited already from a one-on-one teaching assistant.

But as more children are diagnosed, schools will need to be even more prepared, Malonson said.

"Beyond early intervention, there hasn't been much done about what to do as these students get older," she said. "We need to develop more programs like vocational training to ensure their success."

c Copyright 2002 Globe Newspaper Company.

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ADVOCACY

Special Ed Tax Could Spare Detroit Area Programs: Wayne County Proposal K [Nickname it "Special K"?] 1.5 mills would help relieve tight budgets

Richard Ham-Kucharski constantly thinks about the future of his 4-year-old autistic son, Alex, which is why he has been working since May to get Proposal K passed.

The Wayne County Regional Educational Service Agency announced earlier this year that it would ask county voters to approve a 1.5-mill tax for special education, and parents like Ham-Kucharski with special needs children began educating others about the proposal.

"Special education students will not be the only ones to benefit," said Ham-Kucharski of Canton, who has worked with the University of Michigan to develop special education programs since 1998.

"This would put more money back into the school districts' general fund and it would prevent program cuts for regular education students."

Under Proposal K, Wayne County RESA hopes to raise about $59 million annually for special education programs. Local districts support the proposal because administrators say it will allow them to avoid cuts to programs such as music and art.

The 1.5-mill levy would raise taxes about $150 a year for owners of homes valued at $200,000.

The idea for Proposal K was considered a year ago after district superintendents agreed to support a millage, said Kathryn Mathey, executive director of special education services for Wayne RESA.

"Rising special education costs are taking more and more out of local districts' general education funds for state-mandated programs," said Mathey. "Many districts are forced to cut back on prevention programs, which causes more students to be referred to special education."

Detroit Public Schools has the most at stake: Of the 8,000 severely impaired students in Wayne County, half are Detroit residents, said Aleatha Kimbrough, executive director of student support programs for the school system.

Detroit schools will save millions of dollars if the millage passes, according to the district's finance office. Last school year, the district spent $14 million on programs for severely handicapped students. That figure is expected to rise to $17 million in 2002-03.

"This is critical for all the children in Detroit," Kimbrough said. "We need to support every revenue source we can for Detroit Public Schools. . . . If we don't have the millage, the district still has to pay for it. That means less money for children in general education."

Livonia Public Schools, the second-largest district in the county, is expected to save $1.5 million annually if the millage passes.

The proposal has the support of several organizations, including the Citizens Alliance to Uphold Special Education, known as CAUSE, and the Wayne County Citizens Committee.

Opponents feel the proposal comes at the wrong time.

"This is not the time to raise taxes, and I don't think the existing system needs to be fixed," said Roy Maybern of Dearborn Heights.

Wayne County voters will decide on Proposal K on Aug. 6.

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PUBLIC HEALTH

Blair Insists MMR Jab Should Be Kept

UK Prime Minister Tony Blair has insisted there is not a "scrap of evidence anywhere" to suggest the MMR vaccine should not be used.

He has also told the Commons the controversial triple vaccine should be retained in its present form to provide the necessary "coverage".

Tory former minister Sir Sydney Chapman invited the Prime Minister to distance himself from Mayor Ken Livingstone's advice to London parents not to use the vaccine.

He warned take-up in the capital had reached a "record low" - only 70% of parents in his constituency had sanctioned it for their children.

"The number of cases of measles in our capital city has quadrupled over the past year," Sir Sydney said.

"As these two events are not unconnected will you take this opportunity of publicly dissociating yourself from the remarks of the Mayor of London who is advising London parents not to give children the jab?"

Mr Blair said: "I don't agree obviously with what was said by the Mayor," adding: "What should be made very, very clear is this: there is not a shred of evidence anywhere that the MMR jab is anything but the right course to take.

"It is employed in 90 countries round the world, in America, Europe, everywhere. It is absolutely essential that we retain it and retain it indeed in its present form since that is the best way to get the coverage necessary to deal with these diseases."

Many parents have refused to let their children have the jab because of an alleged link to autism.

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TREATMENT

Neuro-Immune Diagnosis and Treatment Gives Hope to Children With Autism, Attention Deficit Disorder and Other Diseases

PRNewswire - Doctors and researchers on thecutting edge of medical research are bringing hope to many of the 500,000children in the U.S. diagnosed with autism and many of the more than2.5 million with attention deficit disorder (ADD), attentiondeficit/hyperactivity disorder (ADHD) or chronic fatigue syndrome (CFS).By treating these and other diseases as neuro-immune dysfunction syndromes(NIDS) and viewing them as medical rather than developmental disorders,Michael Goldberg, M.D., F.A.A.P, and his colleagues at the Neuro-Immune Dysfunction Syndromes Research Institute

(NIDS-RI) have seen dramaticimprovement and normalization in children previously deemed medicallyuntreatable.Autism is more prevalent today than it was in the early 1980s when one in10,000 children were afflicted.

Today, the National Institutes of Health(NIH) estimates that one in 250 children are diagnosed as autistic.

Treatingthese children costs more than $60,000 per child, per year, according toparents whose children have the disorder.

The number of children with ADD andADHD disorder also has increased dramatically in the past two decades, withestimates topping two million, according to the NIH. "Autism has migrated from a rare disorder to one that is now 10 to 20times more likely to be diagnosed.

It's scientifically impossible for anepidemic to be caused by developmental, genetic or 'brain damaged'conditions," said Dr. Goldberg.

"Without a doubt, this is a disease processmasquerading, or being misinterpreted, as a 'developmental' disorder.

We needto stop assuming that the symptoms are a result of birth or genetic defects orpsychological problems and start looking at the immune connection."According to Dr.

Goldberg, NIDS patients are genetically predisposed tohaving a dysregulated immune system.

The immune system malfunction can betriggered by a variety of factors. Diagnosis for NIDS is simple: an immune panel run through blood testingand a NeuroSPECT scan which measures blood flow to the brain.

orhttp://www.neuroimmunedr.com .

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Readers' Posts

A few weeks ago I asked everyone about the GF/CF diet and I thank you for the many helpful responses. Has anyone experienced bed wetting as a side affect? He doesn't normally do it & suddenly it is an issue. lhmirda@earthlink.net

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NIMH is pleased to announce that Dr. Audrey Thurm is joining the extramural staff of as a Program Specialist in the Division of Neuroscience and Basic Behavioral Science. She will be working mostly on issues related to autism that extend across the interagency, NIH, and NIMH levels. Major responsibilities include activities of the Interagency Autism Coordinating Committee, and will also have program responsibilities relevant to the new STAART Centers Program and the overall NIMH autism portfolio. Dr. Thurm has worked on studies of siblings of children diagnosed with autism spectrum disorders. Alison W. Bennett ab43b@nih.gov

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The Center For Developmental Excellence, LLC has moved! As of August 1, 2002, our new office will be located at 113 West White Horse Rd Kirkwood Plaza, Suite #5, Voorhees, NJ 08043. Our phone the same 856-778-1653. Many different therapies and services available for Autism and Developmental

Delays. eg. Sensory Integration/Occupational, Interactive Metronome, Yoga,

Music Therapy, Deep Pressure Massage, A DAN Doctor, The Listening Program and more.

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I am conducting a research study, funded by the borough of Barnet, into the effects of diet intervention and different behavioural intervention programmes, in the treatment of autism and related disorders. I would be very grateful if you could supply me with ANY relevant journal articles, a selection of the authors I am trying to find are: Reichelt, Knivsberg, Cade, Lucarelli, David Mascaral, Ted Kniker, E. Sponheim, Naturally, I would cover all copying and postage costs. Many thanks, Cheryl Ostryn [chezzie77@yahoo.com]

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Hello from Halifax, NS, Canada, I am looking for recent information on working with young children with autistic spectrum disorder as part of "interagency collaborative" efforts to provide a comprehensive continuum of services for children with asd and their families. I know you have a wider communications network and a wide search base than I would have through the university data search engines so I would appreciate any help that you could provide. Are there similar initiatives happening around the continent? Janice Keddy, Early Identification and Intervention Services Central Region of Nova Scotia jkeddy@Staff.Ednet.NS.Ca

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