Archive for the ‘autism research’ Category

By Dr. Meghan Swanson
Meghan Swanson is a Postdoctoral Fellow at the Communication & Play Laboratory at Hunter College, City University of New York

Of all the scientific/academic conferences that I’ve attended, the International Meeting for Autism Research is by far my favorite. So I was thrilled when the Autism Science Foundation selected me as an IMFAR Travel Grantee. With ASF’s generous support I traveled to IMFAR 2012 in Toronto from May 17th to 19th and these are my experiences:

The weeks and months prior to IMFAR I had my nose in the books and fingers on the keyboard preparing for my dissertation defense. On April 18th I defended my dissertation and my degree was officially awarded on April 26th. So for many reasons this year’s IMFAR meeting was different for me.  This year I attended as a newly minted Ph.D., attempting to make the transition from student to colleague.

Since I was presenting my own research on Thursday, much of the day was spent preparing and standing by my poster. Presenting posters can be such a valuable learning experience. Every year I have the “why didn’t I think of that?” moment and am so appreciative of everyone’s thoughts and enthusiasm. Recently, the study I presented at IMFAR was accepted for publication in the Journal of Autism and Developmental Delays. Click here if you’d like to read it (email mswanson@gc.cuny.edu if you would like me to email you a PDF): .

On Friday, I found myself inspired by Bernie Devlin’s talk on gene discovery. He masterfully put into picture how far we have come as a field and what the future has in store for us. Friday morning I was also able to catch a talk by the prolific Charles Nelson (Bucharest Early Intervention Project). In his talk he discussed the difficulties of doing research with baby siblings of children with autism. On average 1 in 5 of these baby siblings go on to have ASD, so if we look for endophenotypes (subclinical traits associated with autism) in these populations we may be identifying endophenotypes for “risk” of autism rather than endophenotypes for autism itself. He also spoke about a research study where he showed infants pictures of their mothers and strangers. He found that high risk infants (baby siblings) and low risk infants didn’t show the same brain patterns in response to the pictures.

In the Friday afternoon oral presentations on early developmental processes and trajectories I attended what I think was the “coolest” talk of the conference. This talk by J.D. Jones, Ami Klin, and Warren Jones introduced a new approach to analyzing eye-tracking data. The approach quantifies allocation of visual resources and used “kernel density analysis at each moment in time in TD children to create a continuously changing map of normative salience in relation to movie-content” (from abstract). As an eye-tracking researcher myself, I was fascinated by this new approach and taken aback by the ingenuity and creativity on the part of this research group.

On Saturday I saw a talk by James McPartland during the Electrophysiology oral presentations. He presented a study where he cleverly collected ERP and EEG data in a single paradigm. Participants also completed the Autism Quotient and the Reading the Mind in the Eyes Task (both are measures of the broad autism phenotype). His data analysis utilized Bayesian structural equation modeling and linked traits to behavior to brain!

On Saturday afternoon I found myself in an Educational Symposium presentation by Dr. Cathy Lord. Dr. Lord presented research that highlighted the disparity is services found across different ethnic groups. She noted that a study from 20 years ago found that African American families were receiving 10 times fewer services when compared to white families. There was also an interaction with maternal education, with low-educated African American families receiving fewer services than African American families’ higher education attainment. On a sobering note, she indicated that this gap in services was at its greatest 7 years ago, but then the gap shrank for 2 years, only to remain stable for the last 5 years. For me this talk was the perfect way to wrap up my IMFAR 2012 experience. It served as a worthy reminder that as an autism researcher my number one priority has to be the families that I serve!

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Autism Science Foundation is in the running for a $10K grant from the Chase Community Giving Contest — but we need your votes to rise to the top before September 19th!
Vote on Facebook by searching for “Autism Science Foundation” here: http://on.fb.me/TmAbbC
Vote for Autism Research
All Your Questions Answered
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On the Chase Community Giving voting page, search for “Autism Science Foundation” to find ASF’s page then click Vote and follow instructions to share with your friends to vote again!
How many times can I vote? 
All Facebook users are eligible for one vote during the contest, which ends September 19th, and an additional vote for “sharing” your vote with your Facebook friends. Finally, Chase card holders are eligible for a 3rd vote. All votes may be cast for the same charity.
How do I access additional votes?
Chase cardholders may cast their additional vote here. Also, don’t forget to “share” your vote with your friends after you’ve voted to gain an additional vote!
Thanks for Chasing Down the Causes of Autism with Autism Science Foundation!

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Today we opened our applications process for the 2013 Pre- and Post-doctoral Training Awards for graduate students, medical students and postdoctoral fellows interested in pursuing careers in basic and clinical research relevant to autism spectrum disorders. In the past three years, ASF has funded over $700,000 in pre- and post-doctoral grants.

“Pre- and post-doctoral fellowships not only build our knowledge about what causes autism and how best to treat it, but also build our future by encouraging outstanding young investigators to dedicate their careers to autism research,” said Alison Singer, president of ASF.

“We are so grateful to all our donors and volunteers who have come together to support autism research and who make these grants possible,” said Karen London, co-founder of ASF.

The proposed training must be scientifically linked to autism. ASF will consider for training purposes all areas of related basic and clinical research including but not limited to:

  • Human behavior across the lifespan (language, learning, communication, social function, epilepsy, sleep, repetitive disorders)
  • Neurobiology (anatomy, development, neuro-imaging)
  • Pharmacology
  • Neuropathology
  • Human genetics/genomics
  • Immunology
  • Molecular and cellular mechanisms
  • Studies employing model organisms and systems
  • Studies of treatment and service delivery

Applications must be received by November 16, 2012. Additional information about the RFA can be found at www.autismsciencefoundation.org/ApplyForaGrant.html.

Grant applications will be reviewed by members of ASF’s Science Advisory Board (SAB) and other highly qualified reviewers. Current SAB members include Dr. Joseph Buxbaum (Mt. Sinai School of Medicine); Dr. Emanuel DiCicco-Bloom (UMDNJ-Robert Wood Johnson Medical School); Dr. Sharon Humiston (University of Rochester); Dr. Bryan King (University of Washington, Seattle); Dr. Ami Klin (Emory University); Dr. Harold Koplewicz (The Child Mind Institute); Dr. Eric London (New York Institute for Basic Research); Dr. Catherine Lord (New York Center for Autism and the Developing Brain); Dr. David Mandell (University of Pennsylvania/CHOP); Dr. Kevin Pelphrey (Yale Child Study Center) and Dr. Matthew State (Yale Medical School).

To learn more about the ASF’s grant programs, and to read about projects funded through this mechanism in prior years, visit www.autismsciencefoundation.org

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This is a guest post from ASF Science Writer Jerri Sparks Kaiser. Jerri, a parent of four children, one of whom has autism, blogs for ASF from a parent’s perspective about the latest autism research. A former Congressional Press Secretary, Jerri is an experienced science writer and has written specifically about autism for many years. Before her life in PR, she was a trained researcher having earned her B.A. in Psychology at UCLA. She currently lives with her family in New York.

Photo Credit: Eddie~S

Bullying is something that has been around as long as adolescents have been in close proximity to each other.  Whether your children are in large schools or small schools, bullying exists.  With the recent report that ASD children are three times more likely to be bullied than their unaffected siblings, the impact of bullying has taken on a special urgency in my home. (more…)

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This is a guest post from ASF Science Writer Jerri Sparks Kaiser. Jerri, a parent of four children, one of whom has autism, blogs for ASF from a parent’s perspective about the latest autism research. A former Congressional Press Secretary, Jerri is an experienced science writer and has written specifically about autism for many years. Before her life in PR, she was a trained researcher having earned her B.A. in Psychology at UCLA. She currently lives with her family in New York.

Me: Jared, do you like to be hugged?

Jared: I don’t know.  Kind of.

Me: How does the hug make you feel?

Jared: Pretty happy, bye.

Then he hung up on me.  Such is the life of the mother of an autistic child.  It is so hard to get a conversation out of him, much less a phone conversation with its inherent lack of visual cues and persistently following him around the room.  Jared is also a teenager who wants to do his own thing.

The reason I asked Jared these questions is because a new study out of the Yale Child Study Center by Martha Kaiser (no relation) indicates that individuals with autistic traits may not process hugs as socially rewarding.  Specifically, two areas of the brain, the STS (superior temporal sulcus) and the OFC (orbitofrontal cortex), were found not to be stimulated during slow, light brushes with a watercolor brush.

In my own experience with my son Jared, I remember the day he was born when the nurse placed him in my arms.  I tried to initiate breastfeeding but Jared turned away.  I noticed then that whenever I stroked his cheek like the books said to stimulate the nursing instinct in your baby that my son turned the opposite direction.  I thought I was doing it wrong and I visited with several lactation consultants.  Nothing worked and finally my milk dried up at 12 weeks because Jared just didn’t get the sucking down properly.  I even pumped and used a crooked syringe designed to teach babies how to breastfeed, but nothing worked.  I was so immensely disappointed in myself and felt like a failure as a mother.  The unkind comments of disapproving moms at the mall when I pulled out Jared’s formula bottle added to that pain.  It is amazing how cruel people can be when they don’t know the situation.  To this day I feel like crying when I remember one woman saying “you do know that breast is best” as she shook her head at me.

What I came to realize years later is that not only did Jared have difficulty in the muscle movements needed to suck efficiently, he also did not crave that physical touch that my later born children did.  My three younger children would gently caress my arm, neck or chest area as they nursed and they would squeeze me with their other hand.  It was so enjoyable.  They also curled their body around mine as if we were still attached.  The only time Jared did that as a young infant and child was when he was terrified of something.

In fact, to this day Jared only seems to crave physical contact when he is in distress, such as when he has had a “bad moment” at school or the group home where he now lives or when he has been hospitalized for behavioral problems.  It is bittersweet that I can only get that bonding from him when he is in distress but I tell myself at least he needs me.

Recently Jared called me late at night from his group home, crying hysterically.  He had an altercation with another client at the group home, which is about an hour away from our home, and he wanted me to make him feel better.  I spoke to him in soothing tones over the phone, my heart breaking because I was not beside him to comfort him, and he slowly calmed down.  We did a visualization technique I learned from the book “When My Autism Gets Too Big.”  I guided him through deep breaths and encouraged him to close his eyes and rub his upper legs slowly as we both visualized the creek in Vail, Colorado or the beach at Martha’s Vineyard, two of our favorite vacation stays.

Then Jared asked sadly “Who is going to hug me?”  It was a remarkable thing for him to ask.  My heart was so broken by this point, but I said into the phone “I am, right now.  Wrap your arms around yourself and know that it is me.  I am coming through this phone to hug you right now.”

“Can you read me a story?” he then asked.  “Yes,” I said.  Then I recited “Good Night Moon” from memory and my son fell asleep.  Sometimes a virtual hug is all I can give my son, late at night and so far away.  Our journey with autism is not at all an easy one.  I take comfort in the fact that Jared does now ask for the occasional hug and every now and then tells me he loves me, maybe not always with words but actions.

The research may indicate there is no social reward but personally I feel the results of the study indicate a different way of expressing and processing the social reward.  Scientists just haven’t decoded the autistic brain’s response to social stimuli yet.  Different does not mean absent.

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By Matt Carey

What factors are there that may influence a child being autistic? What might increase or lower the chances that any given child will be diagnosed with autism? These are obviously major questions within the autism stakeholder communities and the autism research community. There have been indications since the 1970’s that the prenatal environment might play a key role in some part of autism. The work of Stella Chess pointed to congenital rubella syndrome as a risk factor for autism. Since then other possible exposures during pregnancy have been identified, including thalidomide, valproic acid and others. But while these exposures point to gestation as the key period for environmental risks, there is no reason to expect that they are an exhaustive list.

The journal Pediatrics released a new autism study today which presents more possible risk factors: Maternal Metabolic Conditions and Risk for Autism and Other Neurodevelopmental Disorders.  The study by authors from the University of California, Davis (including the MIND Institute) and Vanderbilt University. One thing I like about Pediatrics is that they give good lay summaries of the papers they publish, with “what is known on this subject” and “what this study adds”. In this case:

WHAT’S KNOWN ON THIS SUBJECT: Diabetes during pregnancy has been associated with general development impairments in
offspring; however, associations between autism and maternal diabetes have been inconsistent. Few studies have examined
related conditions accompanied by underlying increased insulin resistance and their association with developmental outcomes.

WHAT THIS STUDY ADDS: This population-based study in young children provides evidence that maternal metabolic conditions
are a risk factor for autism, developmental delay without autistic symptoms, and impairments in several domains of development,
particularly expressive language, after adjusting for sociodemographic and other characteristics.

The study, part of the CHARGE Study, posed the question of whether metabolic conditions (MC’s) in pregnant women pose a risk for autism and other developmental disabilities. In specific, they looked at maternal diabetes, hypertension, and obesity as risk factors. They found that in their study group, mothers who reported that they had these MC’s were more likely to have children with autism or other developmental disabilities. For autism, the risk was 60% higher (odds ratio 1.61) while for developmental disabilities the risk was over double (odds ratio 2.35) when the mother had one of these metabolic condition.

If this sounds somewhat familiar, it’s worth noting that preliminary results from this study were presented at IMFAR last year and this study was highlighted at the press conference.

The CHARGE study draws families locally to the MIND Institute by way of the regional centers, recruitment efforts by MIND personnel (my family was recruited but was just outside the catchment area at 130 miles from MIND). One strength of the CHARGE study is that they don’t rely upon existing records; they test each child (ADOS, ADI-R, Mullen Scales of Early Learning, Vineland, etc.) in-house. Information on metabolic conditions during pregnancy were taken from structured interviews with some cross-checking of medical records to confirm the accuracy of the interviews:

Demographic and medical information was obtained from the CHARGE Environmental Exposure Questionnaire
(EEQ; available for 97.6% of participants), birthfiles, and medicalrecords (available for 57.7% of participants). The EEQ is a structured telephoneadministered interview with the biological mother and includes questions about demographic characteristics,
maternal medical history, and various environmental exposures. Trained study staff extracted data from medical records

The primary focus metabolic condition was diabetes (type 2 diabetes and gestational diabetes) with obesity (body mass index >30) and hypertension also studied.

Table 2 from the paper (click to enlarge) shows the odds ratio for autism spectrum disorders (ASD) and other developmental disorders (DD) vs. typically developing (TD) for children born to mothers with diabetes and other maternal metabolic conditions:

As noted above, the odds are about 50% higher (and more, depending on condition) for ASD, and even higher for other developmental disabilities. The authors didn’t stop there. They explored how these maternal metabolic conditions might affect language and other measures of development. Table 3 (click to enlarge) shows comparisons of test scores for children with and without ASD and whose mothers had or did not have diabetes. (MSEL: Mullen Scales of Early Learning. VABS: Vineland Adaptive Behavior Scales)

Maternal diabetes may result in lower language scores, for both ASD and non-ASD kids. The authors wrote:

Within the ASD group, children of mothers with diabetes performed 0.37 SD lower on the MSEL expressive language scale compared with children of nondiabetic mothers (P = .01; Table 3); MSEL receptive language and VABS communication scores were also lower among children of diabetic mothers, with differences approaching statistical significance. No significant differences in MSEL or VABS scores were observed regarding MCs collectively among children with ASD.

The authors repeated the comparison, but for all metabolic conditions instead of just diabetes. Their Table 4 (click to enlarge) showed that there were no significant differences within the ASD group on maternal metabolic conditions. But for the non-ASD group, on every measure of the Mullens and Vineland tests, children of mothers with metabolic conditions scored lower than children whose parents did not have diabetes, obesity and/or hypertension.

This shouldn’t be surprising since the non-ASD group includes those with developmental disabilities other than ASD. So in some way this is basically telling that story in another way: maternal metabolic conditions increase the risk of developmental disabilities.

The study was relatively large, with 1004 subjects. Some of the subgroups were small, limiting the power of the study in those areas. These numbers can be found in Table 2. The most common maternal metabolic condition, by far, was obesity. The number of children whose mothers had hypertension were relatively few, leading to large confidence intervals for those odds ratios.

Another limitation is that they rely upon parent-reported medical conditions. The authors address this issue and tie together the conditions studied (diabetes, hypertension and obesity) in this paragraph:

Reliance on self-reported medical conditions was a limitation of this study. However, in the 56% of participants for
whom medical records were available, we found the 2 sources to be in good agreement. Thus, despite this limitation, we can have confidence in our results. Furthermore, although biological measurements (eg, glucose, insulin, lipids, immune biomarkers) before and during pregnancy would have been ideal, we chose conditions (T2D/GDM, hypertension, and obesity) highly indicative of increased insulin resistance as proxy measures of dysregulated metabolism and chronic inflammation because we lacked these biological measurements for most of the participants.

Without biological measurements during pregnancy the authors can’t draw specific conclusions about what behind these conditions might raise the risks of autism and developmental disorders. But they do pose some possibilities such as increased levels of glucose, fetal iron deficiency, increased levels of the cytokine interleukin-6 and others.

In the end, the authors conclude rather simply:

The prevalence of obesity and diabetes among US women of childbearing age is 34% and 8.7%, respectively. Our findings raise concerns that these maternal conditions may be associated with neurodevelopmental problems in children and therefore could have serious public health implications.

Until these results are replicated, these maternal metabolic conditions should be considered as strong potential candidates for autism risk factors. As the authors say, “these maternal conditions may be associated with neurodevelopmental problems in children”. But such a conservative conclusion takes nothing away from the potential impact of this study nor the fact that researchers can start to incorporate this new information into their models of autism etiology right away.

The paper: Maternal Metabolic Conditions and Risk for Autism and Other Neurodevelopmental Disorders
The authors: Paula Krakowiak, MS, Cheryl K. Walker, MD, Andrew A. Bremer, MD, PhD, Alice S. Baker, BA, Sally
Ozonoff, PhD, Robin L. Hansen, MD, and Irva HertzPicciotto, PhD

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This is a guest post from ASF Science Writer Jerri Sparks Kaiser. Jerri, a parent of four children, one of whom has autism, blogs for ASF from a parent’s perspective about the latest autism research. A former Congressional Press Secretary, Jerri is an experienced science writer and has written specifically about autism for many years. Before her life in PR, she was a trained researcher having earned her B.A. in Psychology at UCLA. She currently lives with her family in New York.

Photo Credit: modernaroid

For years, I’ve known about the groundbreaking research of Dr. Eric Courchesne because I studied his work in college.  When I read his recent article “The Troublesome Bloom of Autism” in Discover Magazine, however, I was astonished.  Courchesne’s latest research found that in the womb during the second trimester, and possibly the third trimester, the brains of children who are later diagnosed with autism are not experiencing the neural paring that those of typically developing children experience.  That is, the autistic brains have more neurons in the prefrontal cortex than those who do not have autism, an average of 67% more.  Specifically, this passage in the article floored me (bold mine):

“During the second trimester of pregnancy, the precursors to neurons in the brain divide furiously. Then they almost all stop, well before birth. When the brain gets bigger after delivery, all that is happening is that the individual neurons are growing and sprouting branches. The only time autistic children can get their extra neurons, in other words, is while they are in the womb. “We established a time zone,” Courchesne says.

That time zone rules out the old bad-mothering theory of autism, and the notion that vaccines trigger autism in toddlers. Courchesne suspects that fetal brains become autistic due to a combination of genetic and environmental influences that strike during the second and possibly third trimesters, just as neurons are dividing. It may be no coincidence that many of the genes thought to increase the risk of autism are also involved in the division of cells.” My son Jared’s development as an infant and toddler matches up with Dr. Courchesne’s findings.  My son had a large head at birth and his doctor was becoming increasingly concerned about his head size and even tested him for hydrocephalus.  His head circumference was literally off the charts and the area around his frontal and temporal lobes was noticeably bulging a bit.  This was in 1997 and the doctor didn’t know what to make of it since my son did not have hydrocephalus.  At the time, we just assumed he was taking after his father’s side of the family because the males are all quite stout, tall and large-boned individuals.

I had a normal pregnancy with my son and was not sick with any viruses.  I did go into labor at 37 weeks, but other than a mild case of jaundice since he was born 3 weeks early; there was nothing unusual about Jared’s birth.  I was only in labor for 3 hours and he came home from the hospital the next day.

I’ve been through the blame game, trying to discern whether or not I ate something harmful or didn’t do something right during my pregnancy.  I’ve tried to cure my son by offering him every therapy known to man, by spending inordinate amounts of time with him and money on him.  Eventually I accepted Jared for who he is, a most loving child with a lot to offer the world.  If and when the world is ready for Jared and his multivaried talents and quirks, I will be able to rest easier at night.  Courchesne’s research is helping with that because it is only through understanding the why and the how that we can begin to understand how to accept and move forward.

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Nine new projects to be funded

Today we announced the recipients of our annual pre- and postdoctoral fellowships.  Six postdoctoral and three predoctoral grants will be awarded to student/mentor teams conducting research in autism interventions, treatment targets, early diagnosis, biomarkers, and animal models. This represents a 50% increase over last year’s six pre- & postdoctoral grants.

“Last week, when the CDC announced a 23% increase in autism prevalence, the autism community demanded more research to understand what is causing autism and to develop better treatments for individuals with autism,” said ASF Co-Founder Karen London. “We are proud to be able to increase our research funding in response to this national health crisis and we are so grateful to all our donors and volunteers who have come together to support autism research and make this funding increase possible.

This year, ASF will fund $330,000 in fellowship grants. In three years of operations, we have funded $790,000 in pre- and postdoctoral grants.

“ASF attracts excellent applicants across the board, and the top choices are exceptional people representing a broad set of perspectives on autism science,” said Dr. Matthew State, Chair of the ASF Scientific Advisory Board and the Donald J. Cohen Professor of Genetics and of Psychiatry at the Yale Child Study Center & Co-Director, Yale Program on Neurogenetics.

Two projects are co-funded by the FRAXA Research Foundation and the Phelan-McDermid Syndrome Foundation. Additional direct funding for ASF’s pre- and postdoctoral grant program was provided by Bailey’s Team and the Rural India Supporting Trust.

The following projects were selected for 2012 funding:

Postdoctoral Fellowships:

  • Inna Fishman/Ralph-Axel Muller: San Diego State University
    Multimodal Imaging of Social Brain Networks in ASD
  • Karyn Heavner/Craig Newschaffer: Drexel University
    Evaluating Epidemiological and Biostatistical Challenges in the EARLI Investigation
  • Haruki Higashimori/Yongjie Yang: Tufts University
    Role of Astrocytic Glutamate Transporter GLT1 in Fragile X
    Co-funded by: FRAXA Research Foundation
  • April Levin/Charles Nelson: Children’s Hospital Boston
    Identifying Early Biomarkers for Autism Using EEG Connectivity
  • Klaus Libertus/Rebecca Landa: Kennedy Krieger Institute
    Effects of Active Motor & Social Training on Developmental Trajectories in Infants at High Risk for ASD
  • Oleksandr Shcheglovitov/Ricardo Dolmetsch: Stanford University School of Medicine
    Using Induced-Pluripotent Stem Cells to Study Phelan McDermid Syndrome
    Co-funded by: Phelan McDermid Syndrome Foundation

Predoctoral Fellowships:

  • Nina Leezenbaum/Jana Iverson: University of Pittsburgh
    Postural and Vocal Development during the First Year of Life in Infants at HeightenedBiological Risk for ASD
  • Jennifer Moriuchi/Ami Klin: Emory University Marcus Autism Center
    Gender and Cognitive Profile as Predictors of Functional Outcomes in School-Aged Children with ASD 
  • Rebecca Simon/Karen Bales: University of California, Davis  MIND Institute
    The Role of Serotonin in Social Bonding in Animal Models

Learn more about the projects selected for funding here – http://www.autismsciencefoundation.org/current-grantees.

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