NEW YORK, N.Y. (February 8, 2010) –- Autism Speaks, the
world's largest autism science and advocacy organization has
released its annual list of the 10 most significant research
achievements to have impacted autism during the previous year.
Every year, Autism Speaks documents the progress made toward its
mission to discover the causes and treatment for autism spectrum
disorders, and compiles a list of the 10 most significant research
achievements to have impacted autism during the previous year. The
2009 list contains important results from clinical and
epidemiological research together with advances in gene discovery
and effective treatments which will combine to shape the future of
autism research for 2010 and beyond." Compelling autism research
comes from across the United States and around the world with
funding from a variety of public sources, such as the National
Institutes of Health, and private sources such as Autism Speaks,"
explained Autism Speaks Chief Science Officer Geraldine Dawson,
Ph.D. "These findings illustrate that we are indeed making progress
toward understanding the causes and effective treatments for autism
spectrum disorder. At the same time, we recognize that progress is
not nearly fast enough and we need more answers."
"With the latest report from the U.S. Centers for Disease
Control and Prevention (CDC) stating that autism now affects 1 in
every 110 American children, we know that the prevalence of autism
spectrum disorder (ASD) is, in fact, dramatically increasing,"
stated Autism Speaks President Mark Roithmayr, "and it is
imperative that the federal government, primarily through the
National Institutes of Health (NIH) and CDC, quickly and
significantly increase funding for autism research." While the
economic downturn threatened to slow progress, NIH research funds
resulting from President Obama's stimulus efforts encouraged
scientists to submit tens of thousands of NIH research
applications, many of which focused on autism research. "I applaud
the thousands of families nationwide who joined Autism Speaks Walks
and raised funds to support autism research efforts, enabling us to
move forward despite the economic challenges," Roithmayr added.
"Working together – families, scientists, professionals,
government officials – are making progress through science
and advocacy."
"This past year we witnessed several important advances in
autism research, from the discovery of autism susceptibility genes
to alarming new autism prevalence estimates to novel findings about
effective treatments for autism spectrum disorders," said Vice
President of Research, Sophia Colamarino, Ph.D. "While a few of the
studies selected may not have achieved a large amount of publicity,
each advanced how we think about autism in some important way."
With input from Autism Speaks' Scientific Advisory Committee,
Autism Speaks science staff culled through thousands of
publications to arrive at these choices. The 2009 compilation is
designed to be considered in its entirety and is not arranged to
suggest a ranking.
Autism Epidemiology – converging findings show that
autism prevalence is now one percent
In 2009, two major studies using different research
methodologies yielded strikingly similar and eye-opening results
showing that ASD affects approximately one percent of children in
the United States. Based on data collected just four years earlier,
it was found that ASD affected 1 out of every 150 children in the
U.S. The new results represent a 57% increase in ASD prevalence in
a relatively short period of time. Both studies also found that ASD
continues to be four times more common in boys than girls.
The first study, published in Pediatrics, was authored by
U.S. Department of Health and Human Services (HHS) and the CDC and
collected data through the National Survey of Children's Health
(NSCH) on parent-reported diagnosis of ASD. Among a nationally
representative sample of 78,000 children aged 3 to 17 years, the
investigators found that 1 in 91, or an estimated 673,000 children
in the U.S. had an ASD. While concerns lingered over the
parent-reported nature of the data, this large-scale study set the
stage for another major publication on ASD prevalence with similar
results. A second study from CDC researchers released new
prevalence data collected by the Autism and Developmental
Disabilities Monitoring Network (ADDM), a series of surveillance
sites throughout the U.S. that maintain medical and service records
on children with autism. By abstracting data and subjecting those
records to stringent clinical evaluation, the authors found that
approximately 1 in 110 children, 1 in 70 boys, met the criteria for
ASD. This 1 in 110 statistic, based on data collected in 2006,
represents a 57 percent increase from the 1 in 150 statistic which
was based on data collected by the ADDM network in 2002 using
identical research methods to the current study.
Through 2009, a number of publications on autism epidemiology
sought to investigate the reasons for the dramatic increase
witnessed in autism prevalence. Researchers from Columbia
University reported that approximately 25 percent of the rise in
autism caseload in California between 1992 and 2005 could be
directly attributed to changes in diagnostic criteria that resulted
in a shift from mental retardation diagnosis to autism diagnosis.
Thus, converging evidence from this study and others around the
world suggests that while changes in diagnostic practice may
account for a portion of the increase, they cannot alone explain
the rise in autism prevalence, and that other factors, including
environmental factors, likely play a role.
According to Dr. Colamarino, "The prevalence studies of 2009
helped shed additional light on the immense nature of the autism
public health crisis. With one percent of the U.S. population
affected by ASD, and emerging data suggesting that one percent of
the global population may be affected by ASD, not only is there
tremendous need for funding to support research into the causes and
treatments of ASD, these findings call attention to the necessity
for more accessible diagnostic and intervention services for the
growing population of those affected."
Early Intervention for Toddlers with ASD – first
randomized clinical trial of early intervention for toddlers shown
to be effective for improving cognition, language and adaptive
behavior
Although previous studies have found that early intervention can
be helpful for preschool-aged children, interventions for children
who are toddlers are just now being tested. As 2009 came to a
close, results were published in Pediatrics from the first
controlled study of an intensive early intervention appropriate for
children with ASD who are less than 2 1/2 years of age, showing
that a novel early intervention program was effective for improving
IQ, language ability, and adaptive behavior in children as young as
18 months.
The intervention, called the Early Start Denver Model, combines
applied behavioral analysis (ABA) teaching methods with
developmental 'relationship-based' approaches, blending the rigor
of ABA with play-based routines that focus on building a
relationship with the child. Children in the study were separated
into two groups, one that received 20 hours a week of the
intervention – two two-hour sessions five days a week –
from University of Washington specialists. They also received five
hours a week of parent-delivered therapy. Children in the second
group were referred to community-based programs for therapy.
Researchers closely monitored the progress of both groups.
At the beginning of the study there was no difference in
functioning between the two groups. At the conclusion of the study,
the IQs of the children in the intervention group had improved by
an average of close to 18 points, compared to only seven points in
the comparison group. The intervention group also had a nearly
19-point improvement in receptive language (listening and
understanding) compared to approximately 10 points in the control
group. Whereas only one child in the community-based intervention
group had an improved diagnosis, seven of the children in the
intervention group had enough improvement in overall skills to
warrant a change in diagnosis from autism to the milder condition
known as pervasive developmental disorder not otherwise specified
(PDD-NOS).
While the youngest children in the study were 18 months old,
this particular intervention is designed to be appropriate for
children with ASD as young as 12 months of age. Given that the
American Academy of Pediatrics recommends that all 18- and 24-
month-old children be screened for ASD, it is crucial that we are
able to offer parents effective therapies for children within this
age range. "This study strongly affirms the positive outcomes of
early intervention and the need for the earliest possible start,"
concluded Dr. Colamarino.
The First Successful Genome-Wide Association Studies for
Autism – new technologies lead to discovery of new autism
genes involved in brain development
Advances in technology and analytical methods over the past
several years have enabled a better understanding of genetic risk
factors for ASD. New methods, called Genome-Wide Association
Studies (GWAS), have now made it possible to perform comparisons of
populations of individuals affected by a condition versus a
non-affected group and identify single changes in DNA nucleotides
as specific genetic risk factors. In Spring and Fall of 2009,
autism researchers reported the first successful application of
GWAS technology to ASD.
GWAS is a powerful analysis technique that allows researchers to
sift through hundreds of millions of bits of genetic data to
identify changes to the genetic code that are associated with a
disease. Because the approach is not based on any specific
biological hypothesis, scientists can cast the broadest
experimental net possible, and use sophisticated statistical
methods to establish the disease association. In April 2009, a
large team of scientists led by investigators at Children's
Hospital of Philadelphia, reported results from the first
successful GWAS study in autism. Because tens of thousands of DNA
samples are required for GWAS to produce meaningful results, the
researchers collaborated with members of the Autism Genome Project,
and pooled samples from the Autism Speaks-funded Autism Genetic
Resource Exchange (AGRE) combined with many other collections. The
result was identification of a DNA variant associated with the
genes cadherin 10 and 9, which are responsible for creating
molecules that facilitate the formation of neuronal connectivity.
This finding is consistent with accumulating evidence suggesting
abnormal interactions between neurons may be at the core of the
deficits seen in autism.
The idea that faulty connections between neurons plays a major
role in ASD was further supported with the publication of the
second autism GWAS study in October. Also working with AGRE and
members of the Autism Speaks-funded Autism Genome Project, a
collaboration led by investigators from Boston's Autism Consortium
and Johns Hopkins University used a very different statistical
approach to discover an association between ASD and the gene
semaphorin-5A. Similar to the cadherins identified in the first
study, semaphorin 5A is thought to play an important role in neural
development.
These two groundbreaking studies confirm the potential for GWAS
to make successful contributions to our understanding of autism
genetics. "Remarkably, out of the approximately 20,000 different
human genes the experiments could have identified, the genetic
variations that were uncovered are genes involved in brain
development, serving to expand and reinforce our current thinking
about the biological mechanisms underlying autism," explained Dr.
Colamarino.
Studies of Genetic Copy Number Variations Reveal New
Biological Pathways – the ubiquitin pathway is linked to
autism for the first time
One of the newest different types of genetic variation to be
appreciated are submicroscopic DNA deletions or duplications called
copy number variants (CNV). In a companion paper to the GWAS study
published in Nature in April 2009, researchers led by
Children's Hospital of Philadelphia scientists took advantage of
their expansive set of genetic data to conduct additional analyses
that would explore CNVs in the autism genome. Along with revealing
genes involved in biological pathways previously connected to ASD,
their results also surprisingly implicated a new cellular pathway,
known as the 'ubiquitin pathway,' in the pathology of autism.
Genes are the instructions that create proteins. Proteins are in
turn the functional end of our biology. By studying autism
genetics, researchers are not only uncovering factors that can be
used to assess the risk of developing autism, they are
simultaneously unlocking the mystery of what biological pathways
underlie ASD. To date, the majority of autism-associated CNVs have
been found to lie in genes whose proteins help neurons adhere to
each other and establish proper connections. Results of this newest
and largest CNV study continued to confirm this association,
finding several CNV in neuronal adhesion and synapse-related
genes.
The second major class of genes in which the investigators
uncovered CNV is the ubiquitin pathway. The ubiquitin system is
primarily involved with altering protein function and disposing of
unused molecules within cells. At first glance, the report of CNVs
associated with the ubiquitin pathway was somewhat surprising, even
if one of the genes in the pathway, UBE3A, has previously been
linked to ASD because of its involvement in Angelman Syndrome.
However, the authors note that one of the major roles of the
ubiquitin pathway is to regulate the turnover of synaptic
components, especially those related to plasticity and learning,
including the cell-adhesion molecules identified by both their GWAS
and CNV analyses. Thus, the authors speculate that the two
different types of gene networks their CNV analyses identified may
actually be functionally related.
"Taken together, the genetic findings of 2009 are helping to
refine our understanding of autism," explained Dr. Colamarino. "Not
only is the discovery of CNV in genes that govern the ubiquitin
pathway a new finding in autism, the fact that this can be
functionally related to other autism genetic discoveries,
specifically through a role in synapse activity, suggests that many
of these seemingly disparate and individually rare mutations are
converging at the level of biology." Identification of the various
different types of genetic mutations may define different
subclasses of autism and reveal individual opportunities for future
therapeutic development, as well as suggest the possibility of
developing a more general approach to treatment by focusing on the
common biological pathways.
Combined Therapies Hold Promise for More Effective Treatments
– medication and parent training are more effective for
reducing serious behavioral problems in children with autism than
medication alone
Large-scale autism studies have sought FDA approval for drugs
that target core or associated symptoms for autism, however few
have proven successful. In 2009, a paper in the Journal of the
American Academy of Child and Adolescent Psychiatry
demonstrated the first successful randomized controlled trial for a
combined treatment approach for ASD, showing that combined
pharmacological and behavioral treatment was more effective than
pharmacological treatment alone for reducing challenging
behaviors.
A new multi-site study by the Research Units on Pediatric
Psychopharmacology Autism Network, the same group that conducted
the pivotal studies leading to the approval of risperidone for
reducing aggression and irritability in children and adolescents
with autism, investigated whether combining risperidone treatments
with a simultaneous behavioral intervention would be more effective
than medication alone. Their 24-week study of 124 children ages
4-13 compared a treatment regime of risperidone alone with a
combined treatment regimen of risperidone and a parent training
program that followed the principles of applied behavioral
analysis. While both the combined and medication-only treatments
reduced the severity of non-compliant behaviors, the combined
therapy resulted in a significantly greater reduction while using
lower doses of risperidone. The combined therapy was also better at
reducing other challenging behaviors, such as irritability and
hyperactivity.
"This study provides hope for a wider range of available
treatments and greater flexibility for clinicians who should be
encouraged to use combined approaches in cases where medications or
behavioral interventions are not effective on their own," explained
Dr. Colamarino. Confirming the effectiveness of coordinated
treatments that take full advantage of the benefits of both
pharmaceutical and behavioral approaches also demonstrates the
continued need to support research establishing the most effective
treatments in all realms. "The vast majority of clinical trials
conducted to date have only addressed how an individual treatment
compares to a placebo. Very few studies have been conducted that
make head-to-head comparisons of two or more treatments as was done
here, so the success of this trial will also serve to highlight the
utility of "comparative effectiveness trials" for determining the
best treatments for ASD," she concluded.
Genetic Findings Lead to a New Mouse Model of Autism –
mice carrying a mutation in a gene linked to autism display some
subtle and specific features of the disorder
In the most recent wave of autism genetic studies, the gene
neurexin-1alpha has been linked to ASD perhaps more often than any
other, drawing attention to our need to better understand how its
biological function relates to ASD. In 2009 researchers completed
the first detailed behavioral characterization of mice lacking the
neurexin-1alpha gene, discovering analogies to at least one core
domain of ASD.
Over the past few years, researchers studying ASD from a variety
of angles have honed in on what appears to be a central role for
proper synaptic functioning in the biology of ASD. Synapses are the
specialized sites of nerve cell communication within the brain.
Importantly, it is believed that the ability of synapses to
regularly change their communication properties is what underlies
learning and memory and other forms of neuroplasticity. Scientists
have discovered that several genes responsible for producing
molecules that are active at synapses are altered in individuals
with ASD. The first synapse genes linked to ASD were the
"neuroligins," and in the last two years, no less than eight
genetic studies have – incredibly – also implicated
abnormalities in a gene, neurexin-1alpha, that produces binding
partners of the neuroligin proteins. Neurexin proteins work in
tandem with the neuroligin proteins to govern proper operation of
synapses. This provides independent support for the role of
synaptic function in ASD, and it also makes researchers fairly
confident that understanding the complicated biological role of the
neuroligin-neurexin signaling pathway will provide important
insight into brain function in ASD.
Researchers from Stanford University and UT Southwestern Medical
Center, Dallas studied mice lacking neurexin-1alpha, looking for
signs of any ASD-related symptoms. First, focusing on the synapse,
they confirmed subtle disruptions in neurotransmission between
brain cells that may be expected to impact brain function. Then in
examining behaviors of the mice, they found that although the mice
appeared fairly typical, they actually had a nearly two-fold
increase in stereotyped grooming behaviors (considered a mouse
version of human repetitive behaviors), linking the gene to at
least one core behavioral feature of ASD. Finally, in a somewhat
unexpected result, the researchers tested the animals in several
different situations, but found no deficits in social behaviors or
anxiety. Fascinatingly, this result contrasts with their earlier
work in mice with a specific neuroligin mutation, which showed
abnormalities in social behavior but no changes in repetitive
behaviors. This could mean that the neurexin-1alpha gene plays a
unique role in stereotyped behaviors. Alternatively, the currently
generated neurexin-1alpha mouse mutant may not fully mimic the
human ASD mutation. All of these are possibilities that future
research will now be in position to address.
Dr. Colamarino reflected on how many animal models exist of the
genetic disorders that share overlap with ASD (such as Fragile X,
Tuberous Sclerosis etc.) and how these models have been responsible
for some of the most exciting results to emerge in recent years
regarding the treatment of neurodevelopmental disorders. "However
the creation of model systems of so-called 'idiopathic' autism,
autism that is not related to another known medical disorder, is
still in the beginning stages, so the characterization of each
novel model adds a significant new tool for the research
community." Because the animals display some unusual
characteristics that are conceptually similar to individuals with
ASD, lessons from such mice stand to improve our ability to
understand and treat ASD in humans. They also demonstrate that ASD
can be dissociated into individual 'phenotypes' which may be
independently modeled and studied. "In this way," explained Dr.
Colamarino, "characterization of mouse models with mutations in
genes for neuroligins and neurexins, both of which regulate
synapses in the brain, highlights how genetic findings can be
successfully and immediately leveraged into new autism research
opportunities."
Mitochondrial Dysfunction, Autistic Regression… and
Fever – individuals with mitochondrial dysfunction and autism
found to have high rate of autistic regression
Mitochondria are responsible for producing most of the energy
the body uses for every day metabolic functions. More attention has
recently been focused on a potential link between ASD and
dysfunctional mitochondria. A study published in 2009 in the
Journal of Child Neurology further examined this link,
finding that a subgroup of patients with mitochondria disorders may
be at increased risk for autistic regression, especially around
periods of fever.
Mitochondria are intimately tuned to the environment in which
they reside and are built to respond quickly to fluctuations in the
state of that environment. To characterize a relationship between
mitochondria disorders and ASD, researchers from Atlanta identified
a group of 28 children who had been diagnosed with both ASD and
mitochondrial disease. The most common clinical observation in
children with both ASD and mitochondria disorder was "hypotonia,"
or muscles with low tone, followed closely by "fatigue with
activity." They also found that approximately 60 percent (17 of 28)
of these children experienced a regressive form of ASD, a rate of
regression that is over two times greater than what is observed in
ASD in general. Notably, 12 of those 17 regressions occurred in
conjunction with having suffered a fever within a two week period
of the regression. However, this regression did not appear to be
necessarily linked to vaccinations, as two-thirds of the children
that regressed with fever had not received vaccination, and of
those who did receive a vaccination, none regressed without also
having a fever.
Although a small study, this report illuminates potentially
useful new commonalities between children with both an ASD and
mitochondria disorder, suggesting that children with mitochondrial
disease may be at increased risk for autistic regression and that
increased risk may be associated with some fever-response pathway.
Although this paper did not establish the temporal relationship
between fever and autistic regression, fever-induced regression is
a well-known feature of metabolic disorders overall, and the study
brings another angle to the already intriguing relationship of
fever and autism. In 2008, researchers reported that some children
with ASD actually improve around periods of fever, suggesting that
subgroups of ASD exist in which the individuals react differently
to fever.
"In light of this new data, it is clear we need more research
into the body's complex cascade of metabolic and immune actions
that accompany fever, how those relate to the biology of autism,
and the appropriateness of fever management," commented Dr.
Colamarino. "By showing that a subgroup of individuals with
mitochondria disorders may be at risk for autistic regression, the
publication highlights the continued need for enhanced awareness of
the clinical signs of mitochondrial dysfunction as well."
Later Language Acquisition in Nonverbal Individuals with
Autism – contrary to early beliefs, individuals with autism
can acquire spoken language after age five
A common belief of many parents and clinicians is that, if a
child with ASD has not developed communicative speech by 5 years of
age, the prognosis for future development of speech is extremely
poor. In 2009 scientists challenged this belief by conducting a
comprehensive review of the research literature to search for
reports of individuals who were reported to have acquired speech at
age 5 or older. One-hundred sixty-seven such cases were identified,
changing the way in which we view language development in
individuals with ASD.
Early theories of brain development held that the period before
age five represents a unique time in development during which
language acquisition is possible, a critical period for language.
Yet, recent longitudinal neuroimaging research has shown that the
brain has a prolonged development, with major changes occurring
during adolescence, and we now know that the capacity for neural
generation extends even into adulthood. While the field of
neuroscience has revised its notions of neuroplasticity and
development accordingly, the field of ASD has held onto the notion
of an early critical period for language acquisition. This paper
published in the Journal of Cognitive and Behavioral
Neurology, however, provides a very different perspective.
The authors identified in the published literature 167
individuals with ASD who used speech for the first time after age
five. Many of these children had been offered language intervention
based on either traditional or naturalistic applied behavior
analysis during the elementary school years, with the intensity of
intervention ranging from 30 minutes/week to 30 hour/week. Others
had been taught sign language or provided with Picture Exchange
Communication System (PECS) training, computer-based training, or
speech-language therapy. Children who developed phrase speech were
found to have been in treatment longer than those who only achieved
single word speech. In virtually all cases, significant time and
effort put into treatment was necessary for speech to develop.
According to their records, many of these children learned to "use
phrases," "answer simple questions," "make spontaneous requests,"
use "complete sentences," and "speak in spontaneous, complex
sentences."
Although the age at which speech developed was variable (ranging
from 6-12 years), once the child began speaking, subsequent
improvement was often quite rapid. This suggests that achieving
initial sound production and words can provide an important
springboard for the development of subsequent speech. According to
Dr. Colamarino, "This important paper offers hope for the many
children who have not yet developed speech by age five, dispelling
the belief that older individuals with ASD cannot respond well to
speech interventions and providing a much more positive prognosis
for individuals with ASD."
Language Regression in Autism - losing language skills is
found to be specific to children with ASD
Similar to ASD, language learning difficulties are associated
with children with Specific Language Impairment (SLI),
developmental language disorder that is not associated with
deafness, autism, or general developmental delay. Overlapping
behaviors and challenges have been shown in children with ASD and
those with SLI, making people wonder what features of language
impairment, if any, are specific to autism. An important new study
was published in 2009 investigating language development in
children with ASD and SLI, which showed that the loss of language
skills is highly specific to children with ASD.
Published in the Journal of Child Psychology and
Psychiatry, the study included 368 children with ASD and SLI
from the United Kingdom. Parents were interviewed using the Autism
Diagnostic Interview – Revised, which provided a detailed
developmental history of the child and included information on loss
of language skills (i.e. the milestone of acquiring either single
words or short phrases was reached but then language development
plateaued or was lost). The authors found that whereas 15 percent
of children with ASD showed loss of language, only 1% of children
with SLI showed similar patterns of loss. Curiously, they found
that those children with ASD who later lost language skills
acquired either single words or short phrases significantly earlier
than those children with ASD who showed no signs of language
loss.
The study reveals a surprisingly strong specificity for language
regression and ASD, perhaps indicating that even though language
impairment is common to both ASD and SLI, they may involve
different biological mechanisms. "Most importantly, these findings
have immediate clinical implications," explained Dr. Colamarino,
"suggesting that the presence or absence of language regression can
be useful information in the differential diagnosis of ASD versus
SLI for children presenting to their doctors with language
difficulties."
Association of Family History of Autoimmune Disease and
Autism Spectrum Disorders – use of large Danish database adds
another link between autism and the immune system
A 2009 study published in Pediatrics used the nationwide
psychiatric health registry in Denmark to re-examine the potential
link between autoimmune diseases, particularly in the mother, and
ASD. Using a sample size over ten times larger than previously
studied, their findings confirmed an association between autoimmune
disease and ASD.
Multiple research approaches have been used throughout the years
to uncover a potential relationship between immune function and
autism, and while producing very intriguing data, the size of these
studies has been limited and the findings have not always been
replicated. This study utilized the nationwide health care system
in Denmark to focus on the relationship between familial autoimmune
diseases and ASD, including virtually all of the children born in
the country between 1993 and 2004 (over 680,000 children). After
locating those with diagnoses of an ASD, the authors used other
databases to track down information on the presence or absence of
twenty-six different autoimmune disorders in the parents or
unaffected siblings. Their results confirmed previously reported
links between familial type 1 diabetes and ASD, as well as between
rheumatoid arthritis and ASD, discovering for the first time that
rheumatoid arthritis in the mother, but not the father, is
associated with increased risk for ASD. The authors also uncovered
the first association between ASD and untreated celiac disease in
mothers.
By using one of the largest and most comprehensive national
health databases, this study provides additional clues regarding
the association between immune system dysregulation and ASD. The
associations found with specific autoimmune diseases and whether
the disease is present in mothers versus fathers provide important
clues about the biological mechanisms that may lead to autism. For
instance, because the risk of ASD was increased only when the
mothers, but not the fathers, had rheumatoid arthritis, the authors
hypothesize that the link to autism may be due to exposure to
maternal antibodies secreted during pregnancy, or other alterations
within the prenatal environment. A relatively new focus in the
search for the causes of ASD is the complex interaction between the
immune function of a mother during pregnancy and the biological
impact this may have on the early brain development of her child.
In contrast, the association between type 1 diabetes and ASD was
found if either parent was diabetic indicating that this link may
be explained by a genetic factor that is related to both diabetes
and autism. "This study suggests that looking at the associations
with familial autoimmunity may be used to narrow down the search
for autism risk factors, both genetic and environmental," said Dr.
Colamarino.
"Not only does this research provide insights into causes and
treatments, it provides a scientific context to prioritize funding
for further research" remarked Dr. Dawson. "Autism research is a
slow and incremental process. We see that epidemiological, genetic
and environmental discoveries proceed simultaneously, with findings
in one, advancing the other. To proceed in all areas of autism
research concurrently requires a tremendous level of funding
support." Autism Speaks has committed more than $141 million to
date to fund research into the causes, diagnosis and treatment for
autism through 2014. It is currently funding research into
potential genetic and environmental risk factors involved with
autism, identification of the biological pathways that underlie
autism, as well as improved methods of early diagnosis and new
treatment models." Read more about Autism Speaks' science portfolio
here and the annual letter from the Chief Science Officer here.
Further Dr. Dawson explained that money spent on research is
well spent. According to a 2007 Harvard School of Public Health
study, it costs approximately $35 billion each year to care for
people with autism – a number that has clearly increased over
the past two years with the rising prevalence among the youngest
people with ASD and a growing demand for housing, work skills and
opportunities, healthcare, and other services that simply do not
exist for adults with ASD. In FY 2008, total federal spending on
autism research was just $177 million, expected to increase to $282
million in FY 2009 due to a one-time infusion of $89 million in
stimulus spending. During his campaign, President Obama committed
to $1 billion of annual federal spending on autism by 2012. In
October 2009, the President identified autism as one of his
administration's top three public health priorities. Increased
funding for autism research that defines causes and leads to
effective treatments will clearly offset the growing cost to the
public associated with caring and services for the still increasing
number of individuals with autism.
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