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SCHAFER AUTISM REPORT "Healing Autism:
No Finer a Cause
on the Planet"
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RESEARCH - News Article
* Autism Project Draws Praise, Funding
Questions
RESEARCH - Abstracts. Contains technical
language.
* Use of Complementary And Alternative
Treatments For Children With
Autistic Spectrum Disorders Is Increasing.
* Model of Autism: Increased Ratio of
Excitation/Inhibition
In Key Neural Systems.
* Molecular Dissection Of The Amygdala And
Its Relevance To Autism.
* The Amygdala & Autism: Implications
From Non-Human Primate Studies
* Bioinformatic Analysis Of Autism
Positional Candidate Genes Using
Biological Databases And Computational
Gene Network Prediction.
* Hearing Impairment And Psychopathological
Disorders In Children
And Adolescents. Review of the Recent
Literature.
* Increases In Social Initiation Toward An
Adolescent With Autism:
Reciprocity Effects.
* Infections, Toxic Chemicals And Dietary
Peptides Binding To
Lymphocyte Receptors And Tissue Enzymes
Are Major Instigators
of Autoimmunity In Autism.
Autism Project Draws Praise,
Funding Questions
[By Barbara Feder Ostrov and Jessica
Portner for the
A federal plan designed to find the cause of
autism within 10 years and create new treatments for many patients drew praise
from parents and experts around
Autism affects as many as 1.5 million
Americans, according to estimates based on federal statistics. In
The so-called federal autism “road map”
establishes priorities for scientific research on the causes of autism,
detecting it early and developing the most effective treatments. Its goals are
ambitious: Federal officials hope not only to find the cause of autism within
seven to 10 years, but also to prevent up to a quarter of all autism cases and
create therapies that will allow 90 percent of autistic children to speak. The
plan, developed by an interagency autism committee at the National Institutes
of Health, has no price tag yet, and lawmakers have not discussed how much they
might spend on it.
Experts are discussing the plan at a
major autism conference this week in
“We really don't know that much about
autism. There aren't a lot of facts,” said David Amaral, a University of
California-Davis autism expert who worked on the plan. “This will set us on a
journey to start uncovering some of those facts. We have a catastrophic problem
on our hands.” The plan will help coordinate previously disorganized research
efforts and help spur lawmakers to set aside more money for the fight against
autism, said Amaral, research director at UC-Davis' Medical Investigation of
Neurodevelopment Disorders (MIND) Institute.
“Before, there was no attempt to pull it
all together,” Amaral said. “You have to have a plan before you can even
request additional funding.” Some parents are skeptical that money will be
coming soon. Rick Rollens, parent of an autistic child who helped found the
MIND Institute, said he was encouraged that the government's overall plan could
jump-start autism research around the country. But its goals will not be
realized, he said, unless the government devotes a minimum $500 million toward
research, identification and treatment.
“There is no dollar amount dedicated to
this, and it is a public health crisis,” he said. “Short of that, anything
would be window-dressing.” Rollens and other parents of autistic children
regard the disease as an epidemic that threatens not only their children's
futures but
Some epidemiologists believe that better
diagnosis and changing demographics help explain the rise in autism cases, but
UC-Davis and state researchers have found that those factors alone cannot
account for the spike in cases.
“There is a sense of urgency in
Researchers also will work on ways to
screen children early for the disease, when intensive therapies can seemingly
work miracles for some children. Children will be followed for years to
determine the most effective behavioral therapies and medical treatments.
Scientists also hope to categorize different types of autism to more
effectively target drugs and other therapies, Amaral said.
Gaynelle Grover of
“I am glad something like this is
happening,” Grover said. “It's difficult for a parent with a child who wants
answers now. As a child grows, it gets harder and harder for the parents and
the child. The window of opportunity is when children are very young.” The
plan, to be refined at this week's autism summit in
“We're finally starting to get a critical
mass of researchers,” said Amaral. “Over the next decade, we're going to see
some real progress.”
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* * *
Use of Complementary And
Alternative Treatments For Children With Autistic Spectrum Disorders Is
Increasing.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ui
ds=14606219&dopt=Abstract
Levy SE, Hyman SL.
Division of Child
Development and Rehabilitation, Children's Seashore House, Children's
Interventions considered to
be
New treatments emerge, older treatments
become less popular, and the cycle recurs.
Data supporting new treatments should be
scrutinized for scientific study design, clinical safety, and scientific
validity.
Many families approach the clinician
armed with brochures, handouts, and printouts from Web sites that are dedicated
to the care and support of parents and children with ASD.
A recent web search using "autism
and detoxification" resulted in almost 8,000 sites.
The Defeat Autism Now! (DAN!) Project
arose in 1995 from collaboration of members of the Autism Research Institute.
The DAN! Project advocates a specific and
extensive protocol for diagnosis and treatment and can be viewed at http://www.autism.com/ari/#dan.
The scientific validation and support for
many interventions is incomplete and disparate from the recommendation in the
Families should be encouraged to discuss
all proposed investigations or treatments they wish to try with their primary
care provider so the practitioner can serve as the medical home (Sidebar, page
688).
The clinician should communicate and
collaborate with the family and educational professionals to encourage
objective identification of what works.
With increasing access to health
information and societal pressure for families to actively participate in their
health management, continued growth of interest in
Clinicians must remember that parents may
have different beliefs regarding the effectiveness of treatment and different
tolerance for treatment risks.
Practitioners must keep avenues of
communication open, remain open-minded, and not assume a "don't ask, don't
tell" posture in the context of providing a medical home to the increasing
number of children diagnosed with autism.
PMID: 14606219 [PubMed - in process]
* * *
Model of Autism: Increased
Ratio of Excitation/Inhibition In Key Neural Systems.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ui
ds=14606691&dopt=Abstract
Rubenstein JL, Merzenich MM.
Nina Ireland Laboratory of
Developmental Neurobiology, Center for Neurobiology and Psychiatry, Department
of Psychiatry,
Autism is a severe
neurobehavioral syndrome, arising largely as an inherited disorder, which can
arise from several diseases.
Despite recent advances in identifying
some genes that can cause autism, its underlying neurological mechanisms are
uncertain.
Autism is best conceptualized by
considering the neural systems that may be defective in autistic individuals.
Recent advances in understanding neural
systems that process sensory information, various types of memories and social
and emotional behaviors are reviewed and compared with known abnormalities in
autism.
Then, specific genetic abnormalities that
are linked with autism are examined.
Synthesis of this information leads to a
model that postulates that some forms of autism are caused by an increased
ratio of excitation/inhibition in sensory, mnemonic, social and emotional
systems.
The model further postulates that the
increased ratio of excitation/inhibition can be caused by combinatorial effects
of genetic and environmental variables that impinge upon a given neural system.
Furthermore, the model suggests potential
therapeutic interventions.
PMID: 14606691 [PubMed - in process]
* * *
Molecular Dissection Of The
Amygdala And Its Relevance To Autism.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ui
ds=14606693&dopt=Abstract
Zirlinger M, Anderson D.
Division of Biology,
California Institute of Technology, Pasadena, CA 91125, USA.
The limbic system, and in
particular the amygdala, have been implicated in autism.
The amygdala is a complex structure that
in rodents consists of at least 12 different nuclei or subnuclei.
A comparative analysis of amygdala
neuroanatomy in normal vs.
autistic brains would be aided by the
availability of molecular markers to unambiguously recognize these different
amygdala substructures.
Here we report on the development of methods
to identify genes enriched in the central, lateral and medial nuclei of the
rodent amygdala.
Our results suggest that laser-capture
microdissection of specific amygdala subnuclei, when combined with linear
amplification of cRNA probes for oligonucleotide microarray hybridization, can
efficiently identify genes whose expression is confined to these substructures.
Importantly, many of these genes were
missed in previous gene expression-profiling experiments using whole amygdala
tissue.
The
isolation of human orthologs of these subnucleus-specific genes, and/or the
application of these methods directly to human tissue, may provide useful
markers for characterizing neuropathological correlates of autism, as well as
for identifying molecular differences between normal and autistic brains.
PMID: 14606693 [PubMed - in process]
* * *
The Amygdala And Autism:
Implications From Non-Human Primate Studies. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ui
ds=14606694&dopt=Abstract
Amaral DG, Bauman MD,
Schumann CM.
Department of Psychiatry and
Behavioral Sciences and Center for Neuroscience, The M.I.N.D. Institute, University
of California at Davis, Davis, CA 95817, USA. dgamaral@ucdavis.edu
Brothers (1990) has proposed
that the amygdala is an important component of the neural network that
underlies social behavior.
Kemper and Bauman (1993) identified
neuropathology in the amygdala of the postmortem autistic brain.
These findings, along with recent
functional neuroimaging data, have led Baron-Cohen et al.
(2000) to propose that dysfunction of the
amygdala may be responsible, in part, for the impairment of social behavior
that is a hallmark feature of autism.
Recent data from studies in our
laboratory on the effects of amygdala lesions in the adult and infant macaque
monkey do not support a fundamental role for the amygdala in social behavior.
If the amygdala is not essential for the
component processes of social behavior, as seems to be case in both non-human
primates and selected patients with bilateral amygdala damage, then it is
unlikely to be the primary substrate for the impaired social behavior of
autism.
However, damage to the amygdala does have
an effect on a monkey's response to normally fear-inducing stimuli, such as
snakes, and removes a natural reluctance to engage novel conspecifics in social
interactions.
These findings lead to the conclusion
that an important role for the amygdala is in the detection of threats and
mobilizing an appropriate behavioral response, part of which is fear.
Interestingly, an important comorbid
feature of autism is anxiety (Muris et al. 1998). If the amygdala is
pathological in subjects with autism, it may contribute to their abnormal fears
and increased anxiety rather than their abnormal social behavior.
PMID: 14606694 [PubMed - in process]
* * *
Bioinformatic Analysis Of
Autism Positional Candidate Genes Using Biological Databases And Computational
Gene Network Prediction.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ui
ds=14606695&dopt=Abstract
Yonan AL, Palmer AA, Smith
KC, Feldman I, Lee HK, Yonan JM, Fischer SG, Pavlidis P, Gilliam TC. Columbia
Genome Center, Columbia University, New York, NY 10032, USA.
Common genetic disorders are
believed to arise from the combined effects of multiple inherited genetic
variants acting in concert with environmental factors, such that any given DNA
sequence variant may have only a marginal effect on disease outcome.
As a consequence, the correlation between
disease status and any given DNA marker allele in a genomewide linkage study
tends to be relatively weak and the implicated regions typically encompass
hundreds of positional candidate genes.
Therefore, new strategies are needed to
parse relatively large sets of 'positional' candidate genes in search of actual
disease-related gene variants.
Here we use biological databases to
identify 383 positional candidate genes predicted by genomewide genetic linkage
analysis of a large set of families, each with two or more members diagnosed
with autism, or autism spectrum disorder (ASD).
Next, we seek to identify a subset of
biologically meaningful, high priority candidates.
The strategy is to select autism
candidate genes based on prior genetic evidence from the allelic association
literature to query the known transcripts within the 1-LOD (logarithm of the
odds) support interval for each region.
We use recently developed bioinformatic
programs that automatically search the biological literature to predict
pathways of interacting genes (PATHWAYASSIST and GENEWAYS).
To identify gene regulatory networks, we
search for coexpression between candidate genes and positional candidates.
The studies are intended both to inform
studies of autism, and to illustrate and explore the increasing potential of
bioinformatic approaches as a compliment to linkage analysis.
PMID: 14606695 [PubMed - in process]
* * *
[Hearing Impairment And
Psychopathological Disorders In Children And Adolescents. Review of the recent
literature] [Article in French]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ui
ds=14615703&dopt=Abstract
Bailly D, Dechoulydelenclave
MB, Lauwerier L.
Federation de Psychiatrie de
l'Enfant et de l'Adolescent, Hopital Sainte-Marguerite, 270, boulevard
Sainte-Marguerite, Faculte de Medecine de Marseille, 13009 Marseille.
OBJECTIVE: - Hearing
impairment is a multifaceted condition with medical and social aspects.
If the neuropsychiatric impact of
deafness on children has been investigated by researchers from a variety of
fields and backgrounds, their conclusion is that children with hearing
impairment follow many different developmental pathways.
The aim of this paper is to examine the
relationships between hearing impairment and mental health and the effect of
impaired communication on family development.
Method - From a review of the literature,
the authors examine the relationships between hearing impairment and mental
disorders in children and adolescents in terms of prevalence, clinical features
and etiological factors.
The fami-ly dynamics and the
parents-child interactions were also explored.
RESULTS: - The assessment of psychiatric
disorders in hearing-impaired children sets some methodological pro-blems.
Accurate evaluation is hampered by the
immature language exhi-bited by many hearing-impaired children and by the
difficulties that may be encountered in establishing rapport if the child does
not understand the examiner's verbal exchanges.
Several authors point out the lack of
communication skills and experiences with hearing-impaired children on the part
of many examiners.
In addition, delays have been observed for
the development of social maturity in hearing-impaired children and the
parents' descriptions may reflect their own worries, rather than the
emotional-behavioral functioning of the child.
The measurement of psychiatric symptoms
is then compromised insofar as many of the assessment procedures are highly
verbal and were standardized for normal-hearing children.
These difficulties may explain that the
pre-valence rates of mental disorders in hearing-impaired children and
adolescents found in the literature vary from 15% to 60%.
If autism and deafness may both confound
each others' dia-gnosis, several studies also point out the high comorbidity
observed between these 2 conditions.
The significance of this association
remains unclear.
Many of the authors conclude that hearing
impairment is unlikely to be an etiological factor in autism.
However, auditory impairment may be a
marker for brain damage in autism.
Although some studies showed high rates
of depression and anxiety disorders, particularly social phobias, in deaf and
hard-of-hearing children and adolescents, most of the studies conclude that the
prevalence of affective disorders in hearing-impaired children and adolescents
is comparable with estimates of prevalence for hearing young people.
A number of studies have suggested that
deaf children show greater degrees of impulsivity than hearing children.
However, it seems that this background of
greater impulsivity does not lead to higher rates of attention-deficit/hyperactivity
disorder (ADHD) among deaf children.
Using standardized instruments to
estimate the prevalence of ADHD in this population, recent studies conclude
that deaf children with hereditary deafness are not at greater risk of developing
ADHD but that children with acquired deafness are, and that this difference is
probably related to the medical conditions and family climates distinguishing
these two groups.
Psychotic disorders are no more common
among hearing-impaired young people than among young people with normal
hearing.
However, some recent studies showed that
the presentation of schizophrenia can differ in deaf people because of the high
frequency of visual hallucinations observed in them.
Lastly, if primitive personality has been
described as being more prevalent among hearing-impaired children and
adolescents, most of the studies found a normal range of emotional-behavioral
functioning in them.
In summary, if varying incidences of
emotional disturbances and behavioral problems have been reported for
hearing-impaired children and adolescents, except autism, it seems that
children with hearing impairment experience the same range of mental health
problems as hearing children.
A variety of demographic, medical and
educational factors were investigated as possible etiological factors for the
psychiatric disorders observed in hearing-impaired children.
Factors such as medical conditions,
degree of deafness, communication ability and social deprivation may play a
role.
However, many studies also emphasize that
a number of other variables, including educational methods, parental adaptation
and parental support, may have an impact, positive or negative, on the
deve-lopment of the hearing-impaired child.
By this way, numerous investigations have
shown that deaf children of deaf parents attain better emotional and cognitive
development than do deaf children of hearing parents.
CONCLUSION: - A number of questions
remain about the neuropsychiatric and psychosocial aspects of
hearing-impairment in children.
For instance, few studies have been
conducted to examine the impact of the different methods of communication and
education on the psychosocial adjustment of deaf children.
However, this review clearly show that
appropriate and effective management can occur only when the mental health
professionals are know-ledgeable and sensitive to the unique characteristics
and experiences of hearing-impaired children and adolescents.
PMID: 14615703 [PubMed - in process]
_______________________________________________________
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* * *
Increases In Social
Initiation Toward An Adolescent With Autism: Reciprocity Effects.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ui
ds=14622895&dopt=Abstract
McDonald ME, Hemmes NS.
The Graduate Center and
Queens College, City University of New York, and The Genesis School, 270
Washington Ave., Suite 6, 11804, Plainview, NY, USA
Level of spontaneous social
initiating by three adult caregivers toward a youth with autism was studied
during a program to increase the youth's level of social initiating.
The adult participants were three staff
members of a program for individuals with autism; they were assigned to the
classroom of the youth participant, but none was directly involved in his
educational program.
Under a multiple-baseline across subject
design, in combination with a multi-element design, the youth's social
initiations toward each adult were systematically reinforced.
Two sessions were conducted daily: one in
which prompts, token reinforcers, and verbal praise for the youth's social
behavior were presented (baseline and training sessions), and one in which
prompts were absent and only verbal praise was presented (probe sessions).
Frequency of spontaneous initiating
toward the youth increased for each adult during treatment when the youth's
frequency of initiating toward a given adult increased.
It was higher during training vs. probe
sessions, where level of social initiating by the youth was also higher.
PMID: 14622895 [PubMed - in process]
* * *
Infections, Toxic Chemicals
And Dietary Peptides Binding To Lymphocyte Receptors And Tissue Enzymes Are
Major Instigators Of Autoimmunity In Autism.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ui
ds=14611720&dopt=Abstract
Vojdani A, Pangborn JB,
Vojdani E, Cooper EL.
Lab. Comparative Immunology,
Dept. Neurobiology, UCLA Medical Center, Los Angeles, CA, USA.
Similar to many complex
autoimmune diseases, genetic and environmental factors including diet,
infection and xenobiotics play a critical role in the development of autism.
In this study, we postulated that
infectious agent antigens such as streptokinase, dietary peptides (gliadin and
casein) and ethyl mercury
(xenobiotic) bind to
different lymphocyte receptors and tissue enzyme (DPP IV or CD26).
We assessed this hypothesis first by
measuring IgG, IgM and IgA antibodies against CD26, CD69, streptokinase (SK),
gliadin and casein peptides and against ethyl mercury bound to human serum
albumin in patients with autism.
A significant percentage of children with
autism developed anti-SK, anti-gliadin and casein peptides and anti-ethyl
mercury antibodies, concomitant with the appearance of anti-CD26 and anti-CD69
autoantibodies.
These antibodies are synthesized as a
result of SK, gliadin, casein and ethyl mercury binding to CD26 and CD69,
indicating that they are specific.
Immune absorption demonstrated that only
specific antigens, like CD26, were capable of significantly reducing serum
anti-CD26 levels.
However, for direct demonstration of SK,
gliadin, casein and ethyl mercury to CD26 or CD69, microtiter wells were coated
with CD26 or CD69 alone or in combination with SK, gliadin, casein or ethyl
mercury and then reacted with enzyme labeled rabbit anti-CD26 or anti-CD69.
Adding these molecules to CD26 or CD69
resulted in 28-86% inhibition of CD26 or CD69 binding to anti-CD26 or anti-CD69
antibodies.
The highest % binding of these antigens
or peptides to CD26 or CD69 was attributed to SK and the lowest to casein
peptides.
We, therefore, propose that bacterial
antigens (SK), dietary peptides (gliadin, casein) and Thimerosal (ethyl
mercury) in individuals with pre-disposing HLA molecules, bind to CD26 or CD69
and induce antibodies against these molecules.
In conclusion, this study is apparently
the first to demonstrate that dietary peptides, bacterial toxins and xenobiotics
bind to lymphocyte receptors and/or tissue enzymes, resulting in autoimmune
reaction in children with autism.
PMID: 14611720 [PubMed - in process]
_________________________________________________________________
Lenny Schafer, Editor mailto:edit@doitnow.com
Edward Decelie Debbie
Hosseini Richard Miles Ron Sleith Kay Stammers
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