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The Maternal Anti-Fetal Brain Antibody Story – where are we now?

April 19, 2010 17 comments

We have asked several scientists who gave presentations at the April 10-11 DAN! conference in Baltimore to share their research and perspectives from the meeting with you here on the blog.  The following piece is from Judy Van de Water, Ph.D. Professor of Rheumatology, Allergy and Clinical Immunology, Department of Internal Medicine and The M.I.N.D. Institute (Medical Investigation of Neurodevelopmental Disorders) at the University of California, Davis. Dr. Van de Water’s laboratory research programs include the identification of the various mechanisms associated with autoimmune and other immune-mediated disorders. Dr. Van de Water is currently part of the NIEHS funded Center for Children’s Environmental Health as the principal investigator of the Immunological Susceptibility in Autism project.  She is also part of a project funded by NIMH in collaboration with an epidemiologist at Kaiser Permanente to examine the plasma of mothers whose children have autism for early biomarkers.

I am extremely fortunate to have been involved in a research project that has provided such rich and satisfying results at this point in my career. We have spent the past few years working on the identification and characterization of antibodies in the blood of mothers that recognized fetal brain proteins. We have found that these specific antibodies are associated with autism in about 13-15% of cases. It has been a bumpy path at times, but the hard work and diligence of the individuals in my laboratory that actually do all of the work, has been worth it.



What are autoantibodies?

The immune system is charged with identifying and destroying unwanted assailants. It is made up of a complex network of specialized cells and molecules that patrol the body seeking out intruders. In order to defend us, the immune system must be able to distinguish between self-tissues and foreign invaders. In healthy individuals, the immune system will mount responses to unfamiliar objects only, and ignore the body itself.

Sometimes this identification system breaks down, and the immune system mistakenly targets the body’s own tissues. This phenomenon is known as autoimmunity, and is observed in diseases like lupus, rheumatoid arthritis, myasthenia gravis, and multiple sclerosis.

A major weapon used by the immune system to protect the body is a group of proteins called antibodies. Produced by highly specialized white blood cells, antibodies work by attacking unwanted invaders, and letting other immune cells know that there is an intruder that needs to be destroyed.

Self-directed antibodies are called ‘autoantibodies’, and are a major contributor to the destruction observed in autoimmune disorders. In autoimmune disorders, antibodies may be directed against various building blocks of the body like DNA or neurons.

From the Beginning…

The first suggestion that maternal antibodies might be involved in autism came from early studies showing that antibodies from mothers of children with an autism spectrum disorder reacted to proteins on lymphocytes (a type of white blood cell) from their affected children. Given that antigens expressed on lymphocytes are also found on cells of the central nervous system, the authors proposed that aberrant maternal immunity might be associated with the development of some cases of autism [1]. More evidence of a link between maternal immunity and autism came from the study of one mother whose antibodies reacted to adult rat cerebellar Purkinje cells. Furthermore, when these antibodies were injected into pregnant mice, the offspring exhibited some behavioral abnormalities [2]. It was subsequently shown that plasma from several women whose children had autism contained antibodies that recognized proteins in fetal rat brain [3].

Most recently, we identified a highly specific pattern of autoantibody reactivity to fetal human brain proteins in the serum of mothers who have a child with autism [4]. This work by my graduate student, Dan, was awarded the very prestigious honor of being named among the Top 10 Research Achievements of 2008 by Autism Speaks, and a mention again in 2009. Our colleagues, Harvey Singer and Andrew Zimmerman at Johns Hopkins University and the Kennedy Krieger Institute [5] also reported similar findings, which helped to confirm our work. In addition we demonstrated that similar antibodies exist in pregnant women whose children were subsequently diagnosed with autism in a study with our colleague Lisa Croen at Kaiser Permanente [6]. It is important to note that in this case the samples were collected during pregnancy, while in the other cases the samples were collected after the child was born and diagnosed. This may lead to the possibility of diagnosing autism at a much earlier age than is currently possible.

Compelling data linking these maternal antibodies to a potential role in autism come from antibody transfer studies in primates. Briefly, antibodies (purified from women with multiple children with autism) were injected into pregnant rhesus monkeys, and the pregnancies were allowed to continue to term. The resultant offspring showed dramatically altered behaviors including hyperactivity, repetitive behavior patterns, and impaired social interactions, not unlike symptoms seen in children with autism. A similar study has now been published using a mouse model, with analogous results: offspring that were exposed in utero to antibodies taken from mothers of children with autism had a number of behaviors consistent with those seen in children with autism [7]. Collectively, these studies suggest that in at least some cases of autism, circulating maternal antibodies directed against certain fetal brain proteins might cross the placenta and bind to targets in the developing fetal brain. These antibodies may interfere with fetal neurodevelopment, potentially leading to neurodevelopmental disorders such as autism.

How can these brain-reactive antibodies affect the developing fetus?

During pregnancy, antibodies are passed from the mother to the developing fetus. These antibodies have a protective role, serving as a temporary immune system until the child’s own system matures during the first year of life.

If autoantibodies are present in maternal circulation, the fetus will receive them as well. Autoantibodies passed from the mother are capable of reacting with targets in the body of the developing fetus (see diagram). In some autoimmune disorders, including lupus, rhematoid arthritis, myasthenia gravis and Grave’s disease, autoantibodies produced by the mother can have a damaging or altering effect on the developing fetus.

So, where are we now?

The above observations suggest that detection of antibodies directed against fetal brain proteins may in the future serve as valuable biomarkers to identify women who have an increased risk of having a child with autism. It is anticipated that the presence of these antibodies would identify those women who are at particularly high risk for having a subsequent child with autism.  Therefore, the primary goal of our current work is the identification of the proteins that the maternal antibodies recognize. Therein lies a more difficult task.  I recently presented an update of this work in a science session at the DAN! meeting in Baltimore.  It was a wonderful experience, with a full audience and lots of great questions following the presentations. Many of the researchers in the field feel that bringing the most recent science to the DAN! community is important, and we value our interaction with the families and practitioners at the conference. During my session at the April 2010 meeting, I presented our more recent studies through which we are working to identify the proteins recognized by the maternal antibodies. While we have identified two of the proteins, the third remains frustratingly elusive. However, we are confident that we will eventually get it, thus allowing us to design a better test for these antibodies. Unfortunately, we do not yet know what causes these antibodies to be made. We are working on what triggers the immune system of some women to produce these antibodies to brain proteins. Another thing to keep in mind is that the antibodies are associated with only 13-15% cases, and there are lots of other causes of autism.  Finally, we hope that through the identification of the targets for these antibodies, we can someday provide a therapeutic to those individuals who have the antibodies, and wish to have more children while potentially reducing the risk that their next child will also be on the spectrum.

1.         Warren, R.P., et al., Detection of maternal antibodies in infantile autism. Journal for the American Academy of Child & Adolescent Psychiatry, 1990. 29(6): p. 873-7.

2.         Dalton, P., et al., Maternal neuronal antibodies associated with autism and a language disorder. Ann Neurol, 2003. 53(4): p. 533-7.

3.         Zimmerman, A.W., et al., Maternal antibrain antibodies in autism. Brain Behav Immun, 2007. 21: p. 351-357.

4.         Braunschweig, D., et al., Maternal serum antibodies to fetal brain in autism. Neruotoxicology, 2008. 29: p. 226-231.

5.         Singer, H.S., et al., Antibodies against fetal brain in sera of mothers with autistic children. J Neuroimmunol, 2008. 194(1-2): p. 165-72.

6.         Croen, L.A., et al., Maternal mid-pregnancy autoantibodies to fetal brain protein: the early markers for autism study. Biol Psychiatry, 2008. 64(7): p. 583-8.

7.         Singer, H.S., et al., Prenatal exposure to antibodies from mothers of children with autism produces neurobehavioral alterations: A pregnant dam mouse model. J Neuroimmunol, 2009. 211(1-2): p. 39-48.

UPDATE:

I want to thank everyone for their interest in our work and for their responses and questions regarding the research presented in the AS blog.  I thought that I would take this opportunity to clear up a few things and answer some general questions.  First, and foremost, we do not know at this time what causes someone to start making antibodies to fetal brain proteins.  While we know from research on other autoimmune diseases that some individuals are more susceptible to breaking tolerance to self-proteins, we don’t know the cause for most autoimmune disorders. 

We are investigating one gene that we think may contribute to the susceptibility to make these antibodies, but the work is still too early to report.  However, there is not likely to be just one cause, just like there are multiple ways that a child can develop autism.  I would also like to stress that while it is true that the tendency towards getting an autoimmune disease can be inherited, we still cannot predict who will ultimately become affected. What we now know about autoimmune disorders in general is that there is likely a genetic susceptibility combined with an environmental ‘hit’ of some kind, which can include infectious agents, certain medications, and/or toxicants, that pushes the immune system past its regulatory mechanisms thereby resulting in loss of tolerance to self.  The majority of the time, this occurs long before an individual shows signs of an autoimmune disorder, making it very difficult to determine the inciting factor.  So while we know that in a subset of cases maternal antibodies to fetal brain proteins may play a role in changing neurodevelopment, we may never know what the trigger is that causes the generation of these antibodies.  But, we will keep working on it!!

Finally, for all of you who are interested in participating in our research, please contact me and I will get your contact information. 

Thank you all again for your generous support of our work, and for sharing your stories with me. I learn so much from each of you.

Wrights Attend DAN! Conference

April 15, 2010 6 comments

From left, Bob Wright, Stephen Walker, Ph.D., assistant professor at Wake Forest Institute for Regenerative Medicine, Arthur Krigsman, M.D., assistant professor of Pediatrics at NYU School of Medicine, Katie Wright, Suzanne Wright, Andrew Levinson, M.D.

Read posts about the DAN! conference from Pat Kemp of Autism Speaks, Dr. Alessio Fasano, M.D., Dr. Simon G. Gregory, Ph.D., and Dr. Judy Van de Water, Ph.D.

Many journeys to the same location – methods that 21st century scientists are using to identify genes that cause autism

April 15, 2010 11 comments

We have asked several scientists who gave presentations at the April 10-11 DAN! conference in Baltimore to share their research and perspectives from the meeting with you here on the blog.  The following piece is from Dr. Simon G. Gregory, Ph.D. Dr. Gregory is an Associate Professor in the Center for Human Genetics, Duke University Medical Center His primary area of research involves identifying the complex genetic factors that give rise to cardiovascular disease and multiple sclerosis, Dr. Gregory’s group is also applying high-resolution genomic arrays to the discovery of chromosomal abnormalities and identification of epigenetic factors associated with autism.

For decades scientists have relied on traditional genetic approaches to identify genes that contribute to the development of autism. These approaches have included collecting extended, multi-generation families that contain one or more individuals with autism. Once a sufficient number of these families have been collected, hundreds of DNA markers that can highlight differences between us all at a genetic level (a bit similar to DNA fingerprinting used in CSI) are used to identify a region of the genome is linked with the disorder in the families. More recently, higher resolution technologies that benefitted from the completion of the human genome project have been developed to allow us to look at hundreds of thousands of markers simultaneously. This approach differs from the family-based approach in that it uses thousands of unrelated cases and age/sex/ethnicity matched controls. Together, both approaches have been successful in identifying genes, or at least regions of our chromosomes, that play a role in the development of autism. However, we know that many more genes will likely contribute to autism spectrum disorders (ASDs) and that not all mechanisms that disrupt the normal function of a gene will be based on a single DNA mutation or a variant present in the general population.

My group at the Duke Center for Human Genetics recently embarked on a journey to identify autism genes using an approach that looks at chromosome content, and yet we reached an interesting finding using another technique that doesn’t rely on the sequence of our DNA. For many years it has been known that ASDs can be caused by loss (deletion) or gain (duplication) of chromosomes. These genomic rearrangements can be large or small and some have been shown to cluster in particular regions of the genome, for example on the long arm of chromosome 15 (15q11-13). Our journey began by assessing the genomic content of 119 unrelated autistic children from families that we had collected over a number of years. We used genomic microarrays (microscope slides with printed content spanning our genome) to identify novel or common regions of deletion or duplication within one autistic child from each family. Although we identified a handful of novel regions and confirmed dozens of rearrangements that have increasingly been shown to exist within the ‘normal’ population, we decided to focus on a single deletion in one individual. The deletion, which contained five genes, sparked our interest because one of the genes, the oxytocin receptor (OXTR), had been previously implicated in autism. Previous studies using the traditional genetic approaches (mentioned above) had shown that OXTR was genetically associated with autism, other studies had shown that levels of oxytocin (a neurotransmitter that the receptor binds to OXTR) is important for pro-social behavior and that a knock-out of the receptor in mice can affect this behavior, and very recent studies have tested the supplementation of oxytocin in adults with autism.

After identifying the deletion in the one affected child we screened his family to see if it was novel and causative of his autism, or if he inherited the deletion from his parents. Somewhat disappointingly, his mother also had the deletion, but interestingly she had self reported obsessive compulsive disorder (OCD) for which OXTR has also been implicated. Although we could have stopped the journey at this point, we decided try a different approach. Previous studies have shown that OXTR is controlled in the liver by a chemical group (methyl –CH3) that sits on top of the DNA but which doesn’t change its sequence (click here for more information on epigenetic changes as they relate to autism). The phenomena of DNA methylation is a normal mechanism by which our cells silence parts of the genome that they don’t want to be active (mainly repeat and retro-viral sequences) but they also use it as a switch to turn on or turn off genes for protein production. Significant in our journey was that the child with autism who had the OXTR deletion also had an affected brother. This is significant because when we assessed the methylation status of the whole family we noticed that the affected brother has very high levels of methylation in five different CG bases (among the A’s C’s G’s and T’s of our genome where the methyl group resides) in a 1,600 base pair window that had previously been identified as being methylated in the liver OXTR.

Differential methylation isn’t a novel finding as a possible cause of autism. Previous studies in Rett syndrome, which has ASD like symptoms, have shown that mutations in the methyl CpG binding protein 2 (MECP2) gene not only contributes to the development of Rett syndrome but that these mutations affect the normal functioning of the gene which regulates the expression of other genes by altering their DNA methylation state. Additionally, imprinting (the silencing of a maternal or paternal copy of a chromosome by DNA methylation) has also been established as the basis for the development of Angelman and Prader-Willi syndromes that, again, have ASD like symptoms. Our next step was to validate the observation that increased methylation of OXTR in the affected brother may be a causal mechanism of autism. We expanded our analysis to include evaluation of the methylation status of OXTR in the peripheral blood of 20 controls and 20 individuals with autism, and in a second dataset of the post-mortem samples of temporal cortex tissue (a center for language and learning) in eight controls and eight children with autism. In both datasets we were pleased to see that the individuals with autism had higher levels of methylation than the controls. We next measured the level of gene expression of OXTR because we would expect that increased DNA methylation would result in decreased gene expression – which it did in a very small number of samples that we could test.

So you’re asking yourself, how, if all these other studies had pointed to OXTR being implicated in autism, is this discovery significant? Well, we hope that we have found a unique autism-associated DNA methylation signature in a receptor for a neurotransmitter that is important in social cognition in autism. The next more exciting journey will be to substantiate what we have found in a larger number of samples and to establish if oxytocin treatment can help

Intestine, Leaky Gut, and Autism: A Serendipitous Association of a Planned Design?

April 14, 2010 3 comments

We have asked several scientists who gave presentations at the April 10-11 DAN! conference in Baltimore to share their research and perspectives from the meeting with you here on the blog.  The following piece is from Dr. Alessio Fasano, M.D. Dr. Fasano is a Professor of Pediatrics and the Director of the Mucosal Biology Research Center at the University of Maryland.  Dr. Fasano also leads the Center for Celiac Research, which includes a multidisciplinary team of gastroenterologists, pediatricians, dieticians and nurses who work together to develop individualized treatment plans for people with Celiac Disease.

The Intestine and ASD

The human intestine is a deceptively complex organ.  It is lined by a single layer of cells exquisitely responsive to stimuli of innumerable variety, and is populated by a complex community of microbial partners, far more numerous than the cells of the intestine itself.  Under normal circumstances, these intestinal cells form a tight, but selective barrier to “friends and foes”: microbes and most environmental substances are held at bay, but nutrients from the essential to the trivial are absorbed efficiently (1,2).  Moreover, the tightness of the epithelial barrier is itself dynamic, though the mechanisms governing and effecting dynamic permeability are poorly understood.  What is becoming increasingly clear is that an intestinal barrier defect (i.e., leaky gut) is associated with a large number of local and systemic disorders, including Autism Spectrum Disorders (ASD) (3).

Regulation of Intestinal Permeability

Intestinal permeability is mainly dependent on the functional state of intercellular tight junctions, sort of gates between neighboring cells that regulate trafficking of molecules and cells from the external environment into our body. To meet the diverse physiological challenges to which the intestinal epithelial barrier is subjected, these gates must be capable of rapid and coordinated responses.  This requires the presence of a complex regulatory system that orchestrates the opening and closing of the gates between cells.  While knowledge of the gates’ composition and assembly has progressed significantly during the past decade, relatively little is known about their regulation in health and disease in response to exposure to a variety of environmental stimuli.  The discovery of zonulin, a molecule that reversibly modulates the gates’ opening, sheds light on how the intestinal barrier function is regulated in health and disease (4).  The two major environmental stimuli triggering the production of zonulin in the small intestine are the presence of microorganisms (i.e., proximal bowel contamination) and exposure to gluten.

New evidence suggests that this exaggerated production of zonulin is responsible, at least in part, for the leaky gut causing abnormal passage of gluten and other “bad guys”, including casein, underneath the gut cell lining (2). This uncontrolled access of substances that do not belong to our body may lead to the onset of autoimmune and inflammatory diseases, including ASD, in genetically predisposed individuals (2). [Read more more about autoimmune disorders and autism]

ASD and Diet

ASD are heterogeneous neurodevelopmental disorders that affect approximately 1% of the general population (5).  It is generally agreed that there are multiple causes for ASD, with both genetic and environmental components involved.  Gastrointestinal (GI) symptoms are frequently experienced by subjects with ASD, but their prevalence, nature and, therefore, best treatments remain elusive (6,7).  The most frequent GI symptoms experienced by subjects with ASD include constipation, gastroesophageal reflux, gastritis, intestinal inflammation (autistic entrocolitis), maldigestion, malabsorption, flatulence, abdominal pain or discomfort, lactose intolerance, enteric infections, among others.  Of the almost 50 complementary and alternative treatments proposed for ASD, seven (antifungal therapy, chelation, enzymes, GI treatments, intestinal parasite therapy, nutritional supplements, and dietary options for autism) are specifically focused to the GI tract.  It is worthwhile to note that in a recent informal survey conducted by the Autism Research Institute involving more than 27,000 parents of autistic kids, avoidance of gluten and/or casein were among the most frequent treatments implemented in their children, with a with a better:worse ratio of 30:1 and 32:1, respectively.

Intestine, Microbiome, and Leaky Gut

A possible unifying theory to “connect the dots” of all the factors mentioned above would link changes in the gut microorganism ecosystem with leaky gut, passage of digestion products of natural food such as bread and cow’s milk that would activate immune inflammatory cells that cause inflammation both in the intestine (autistic enterocolitis) and the brain (ASD).  Alternative to the inflammatory hypothesis, it has been proposed that the defect in the intestinal barrier in ASD patients allows passage of neuroactive peptides of food origin (gliadorphin and casomorphins) into the blood and then into the cerebrospinal fluid to interfere directly with the function of the CNS.  No matter which theory turns out to be correct, changes in the intestinal microbiome and the consequent leaky gut seem to be common denominators.

The Gluten Free Diet

Given the fact that ASD is a complex and heterogeneous condition, it is instrumental to stratify children affected by autism to identify subgroups that can benefit of specific therapeutic interventions, like a gluten free diet.  Therefore, it would be highly desirable to develop specific biomarkers to help identify who would benefit the most by implementing specific interventions, including the gluten free diet.  The ingestion by genetically susceptible individuals of gluten from wheat and of similar proteins present in barley and rye can cause immune reaction leading to small bowel inflammation.  It is the interplay between genes and the environmental triggers that leads to this inflammation. This inflammatory process is initially driven by special immune cells called neutrophils (a type of white blood cell), soldiers that are called immediately into the gut to fight the uncontrolled passage of invaders through the gates stuck open because of gluten-dependent zonulin release.  Once neutrophils intercept the invader, they try to eliminate it by causing inflammation that is not necessarily limited to the gut, since these “armed” immune cells can subsequently migrate in other tissues and organs, including skin, liver, joints, heart, and brain, causing inflammation also in the organs where they migrated.  Therefore, the strict avoidance of gluten-containing grains is the best approach to avoid these inflammatory processes that can be responsible of specific clinical outcomes, including ASD, in a subgroup of individuals genetically at risk to react to gluten.

Alternative Therapeutic Strategies

Alternative therapeutic strategies to a gluten-free diet include the oral use of the zonulin inhibitor larazotide and probiotics.  Larazotide, a sort of wax that blocks the hole in which the zonulin key locks in to open the gates in between intestinal cells, has already been successfully explored in an animal model of autoimmunity and, more recently and preliminarily, in celiac disease patients through double-blind, randomized, placebo-controlled human clinical trials (2). Probiotics are “good bacteria” typically found in dairy products like yogurt and are claimed to have several beneficial effects related to their capability of either reducing the risk or treating disease (8). Although the safety of probiotics naturally present in yogurt has never been in question, the more recent use of probiotics, like lactobacilli or bifidobacteria, delivered in high numbers to consumers with potentially compromised health has raised the question of safety.  The safety of these probiotics has been reviewed by qualified experts in the field. The general conclusion is that the potential of physiological harm of lactobacilli and bifidobacteria is quite low.  While the initial use of probiotics was based on anecdotal reports of their beneficial effects, we have more recently witnessed a series of more rigorously designed clinical trials documenting the potential use of probiotics for the treatment of a variety of pediatric disorders, including enteric infectious diseases, allergic and atopic disorders, and intestinal inflammatory diseases.   The two most studied probiotics are lactobacillus GG and bifidobacteria BB12, and there have been a large number of studies with these organisms in the pediatric population, whit consistent good safety data (ie., lack of side effects) but mixed efficacy (8). The inconsistent positive therapeutic results may be related to the fact that each probiotic organism has different effects, and, therefore, they cannot be used indiscriminately for each disorder.  Indeed, different conditions may be triggered by different microbiota composition and, therefore, may require different probiotics to be effectively treated.  By performing more detailed studies to link gut microbiota composition to certain conditions, such as ASD, we will be able to decipher the host-microbe cross-talk and, therefore, we will be able to customize probiotic treatment for specific conditions (i.e.; personalized medicine).

All the aforementioned therapeutic strategies are viable interventions and, therefore, it would be desirable to perform well-designed multi-center studies to stratify children with ASD to establish which subgroup of patients would benefit of these treatments.  This approach will allow customizing treatments to maximize the chance of success by targeting the subpopulation of ASD children that would benefit the most from a gluten free diet, the use of larazotide, or to choose the proper probiotic(s) to re-establish a healthy gut ecosystem capable to decrease or completely ameliorate the clinical presentations of ASD.

References

  1. Fasano A. Pathological and therapeutical implications of macromolecule passage through the tight junction. In Tight Junctions.  Boca Raton, FL:  CRC Press, Inc., 2001, p. 697-722.
  2. Fasano A. Physiological, pathological, and therapeutic implications of zonulin-mediated intestinal barrier modulation: living life on the edge of the wall. Am J Pathol.173:1243-52, 2008.
  3. White JF. Intestinal pathophysiology in Autism. Exp Biol Med 228:639–649, 2003.
  4. Wang W, Uzzau S, Goldblum SE, Fasano A. Human zonulin, a potential modulator of intestinal tight junctions. J Cell Sci 2000;113:4435-4440.
  5. Prevalence of autism spectrum disorders – Autism and Developmental Disabilities Monitoring Network, United States, 2006.Autism and Developmental Disabilities Monitoring Network Surveillance Year 2006 Principal Investigators; Centers for Disease Control and Prevention (CDC). MMWR Surveill Summ. 2009;58:1-20.
  6. Buie T, Campbell DB, Fuchs GJ, III, et al Evaluation, Diagnosis, and Treatment of Gastrointestinal Disorders in Individuals With ASDs: A Consensus Report. Pediatrics 2010;125;S1-S18.
  7. Buie T, Fuchs GJ, III, Furuta GT, Kooros K, Levy J, Lewis JD, Wershil BK, Winter H. Recommendations for Evaluation and Treatment of Common Gastrointestinal Problems in Children With ASDs. Pediatrics 2010;125;S19-S29
  8. Guarner F Prebiotics, probiotics and helminths: the ‘natural’ solution? Dig Dis. 2009;27:412-7. .
Categories: Science Tags: , , ,

Autism Research Institute/DAN! Conference from a Father’s Perspective

April 13, 2010 8 comments

This is a guest post by Pat Kemp, Autism Speaks’ Executive Vice President – Awareness and Events. Pat, who is married, has three children and a stepson. One of his children is a young adult who has autism.

Twenty-five years ago when I first heard the word “autism,” there was nowhere to turn. No internet, most doctors didn’t know, psychologists had heard of it in grad school but weren’t sure what it really was. The support groups back then were primarily mothers seeking people in similar circumstances looking for that one hour of respite with other people dealing with similar situations. What was I to do? I was a father, working full-time with two other older children, searching feverishly to find any kernel of information to save my son with autism. I went to the library, frantically searching for information that would guide me through the process of saving my child who was rapidly fading away before my very eyes. After pushing and prodding, virtually panicking; I discovered that there was someone in San Diego named Bernard Rimland who started an organization called Autism Research Institute. I called and called until I spoke with him ‘live.’ He was kind, gentle, and understanding of my family’s plight. What he did was to give me ‘hope’ because he was collecting data to try to determine a path or paths to help families like mine whose children were fading away. I collected and sent Dr. Rimland all the data that I could gather from my son with hopes that it could lead to ‘something’ that may help him.

Well, as the advertising tagline said  “We’ve come a long way baby,”  I was impressed and amazed at what I saw at the Autism Research Institute/DAN! Conference this past weekend in Baltimore. There were hundreds of attendees searching for answers, including many fathers and grandparents. There were many experts in their respective fields sharing their knowledge, answering questions.  No matter where you stand on the autism topic, you would have appreciated the sense of community that was there. Much has changed since I started this journey into autism a quarter century ago with my son. With technological advances, I am now able to post this blog and share my experience. But I couldn’t help think to myself during the conference that this was the “House that Bernard Rimland built” many years before. Though there remains so much yet to do, it may never have occurred without the vision of one person, Bernard Rimland, who was kind enough to answer my phone call. This one person who gave me and my family hope. Thank you Dr. Rimland. You would have been proud of what I witnessed this past weekend.

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