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“Protecting the health and informed consent rights of
children since 1982.” =============================================
August 23, 2001 Search www.feat.org/search/news.asp
·
Cure Autism Now Announces New Environmental Influences
on Autism
Initiative
1. Comparison of
ethylmercury developmental neurotoxic properties with an established model of
methylmercury developmental neurotoxicity
2. Double-blind
placebo-controlled cross-over study of DMSA and lipoic acid for the treatment
of children with regressive autism
3. A comparative study
evaluating the dose-responsiveness effects of methylmercury and thimerosal on
select nervous, immune and enzyme parameters
4. Evaluation of
chelation effect on children with autism
5. Role of cytokines
in developmental neurotoxicit
6. Effect of mercury
on apoptosis of neuronal cells
·
Kids of Bipolar Parents May Not Face Higher Risk
Cure Autism Now is pleased to announce six new research
awards as part of an Environmental Influences on Autism Initiative. These
particular grants were made possible by a generous contribution from Sallie and
Tom Bernard, and are the result of an RFP distributed to the scientific
community to examine the possible metabolic, molecular, genetic or other response
to mercury as it relates to autism.
Exposure to mercury, a potent neurotoxin, has shown to
cause immune, sensory, neurological, motor and behavioral dysfunctions similar
to traits defining or associated with autism. Although the FDA recently removed
thimerosal from vaccines, the high number of anecdotal reports was compelling
enough to Cure Autism Now to want to establish scientific data on whether and
how mercury may play a role in causing autism, as well as how to treat its
effects.
Among the diverse research projects that Cure Autism Now
will be funding include projects focusing on molecular structure; chelation
studies using DMSA and DMPS to determine this treatment’s efficacy; the
comparative aspects of methyl vs. ethyl mercury; and animal and human
therapeutic studies. Cure Autism Now assembled a special scientific advisory
board with expertise in heavy metal toxicity who reviewed all proposals
received. We express our sincere appreciation to them, and particularly to
Chair David Baskin, M.D., for his time, dedication and integrity.
Elizabeth Tegley
Science Program Officer
Cure Autism Now
Comparison of ethylmercury developmental neurotoxic
properties with an
established model of methylmercury developmental
neurotoxicity
Jay Charleston, Ph.D., Institute of Neurotoxicology
and Neurological
Disorders
Relatively little information is known about the potential developmental
neurotoxicity of ethylmercury (EtHg), the active ingredient of thimerosal, a
bacteria static agent commonly used to preserve vaccines. Vaccination of children following the
recommended pediatrics schedule may result in exposure levels which may
contribute to neurologic deficits. The lack of adequate information about the
known neurotoxic potential of EtHg has forced the FDA to set exposure levels
based on known developmental neurotoxic effects of methylmercury (MeHg). This
assumption by the FDA assumes that MeHg and EtHg are equivalent. This hypothesis
needs to be tested.
We are currently conducting a large study of the
developmental consequence of very low levels of MeHg in a mouse model. This
project is being funded by a grant from the United States Environmental
Protection Agency (USEPA). Briefly, we are investigating subtle changes in
specific brain sites using state-of-the-art stereological methods combined with
histochemical and immunohistochemical staining techniques. We are investigating
four exposure levels at four time points. These time points are selected to
take advantage of unique temporally separated events in the developing mouse
brain representing specific neural cell proliferation and migratory sequences.
The endpoint is the quantification of neuron number in the cerebral cortex,
cerebellum and midbrain structures.
The proposed experimental design will seek to replicate
the above research model with EtHg exposure in place of MeHg exposure. This
will allow us to determine the relative equivalency of the neurotoxic effects
of these two compounds. The results will directly serve to assess if the FDA allowance
of thimerosal in vaccine preparations based on MeHg exposure risk assessment is
a reasonable decision.
Double-blind placebo-controlled cross-over study of DMSA and
lipoic acid for
the treatment of children with regressive autism
Jane M. El-Dahr, M.D., Tulane University School of
Medicine
The incidence of autism in the U.S. has increased over
the past decade
at the same time that infants were exposed to organic
mercury through the preservative thimerosal in childhood vaccines The many
parallels between autism and mercury toxicity - individual susceptibility,
delayed loss of skills, brain pathology, neuropsychiatric manifestations,
autoimmunity directed against brain components - have led to the concern that
regressive autism may represent a unique form of mercury poisoning. Anecdotal
evidence suggests that symptoms of autism may improve with chelation. We
propose to study the effect of treatment with the well-characterized chelating
agent meso-2,3-dimercaptosuccnic acid (DMSA) combined with lipoic acid in young
children with autism.
Hypothesis: Regressive autism, in some children, is the
result of early exposure to mercury and symptoms can be diminished with removal
of toxic metals. Aims: Estimate exposure to mercury in fetal and postnatal life
in children with regressive autism; measure mercury and heavy metals present at
baseline as well as released during treatment with urine, stool, and hair samples;
quantitate anti-brain antibodies pre- and post-treatment; and determine the
efficacy of this treatment to improve core autistic symptoms. Design: Double-blind placebo-controlled
cross-over with eight months in each arm. Forty children ages 2-5 years with
DSM IV autism and a history of developmental regression will be enrolled.
Standardized psychometric testing of intelligence, language, and behavior will
be done at baseline, cross-over, and completion of study and rating scales of
autistic behavior determined every two months.
A comparative study evaluating the dose-responsiveness
effects of
methylmercury and thimerosal on select nervous, immune and
enzyme parameters
Deborah Keil, Ph.D., Medical University of South
Carolina
Infantile autism (IA) is a neurodevelopmental syndrome
found in 1-5
cases of every 10,000 children with boys acquiring this
syndrome 3-5 times more than girls. The spectrum of disorders of autism
includes a range of impaired development of language and communication, unusual
behaviors, and mental retardation. A diversity of pathophysiological effects
also exist to include hyperserotoninemia, decreased T-cell proliferative
function and activation, increased soluble IL-2 levels in serum, decreased CD8+
cells, decreased NK cells, development of anti-brain autoantibodies, decreased cerebellum
volume and Purkinje cell number. Several studies indicate that the etiology of
IA is multi-factorial and includes exposure to environmental chemicals. In
particular, mercury exposure during infant and child development has been
implicated in IA, especially in the case of vaccines containing mercury.
Although mercury exposure from vaccines has been implicated in autism, this
association !
!
has been criticized due to a lack of supportive
experimental dose-response data. Thus, the proposed study will assess the
possible role of methylmercury (MeHg) and thimerosal (TH) in contributing to
the pathophysiology of IA using a mouse model to assess dose-responsive effects
in cognitive and physiological parameters that encompass nervous, immune and enzyme
pathways. This comparative approach will permit increased understanding of
deficits due to MeHg or TH after acute exposure during early developmental
stages and facilitate understanding of etiological causes of autism or other
neurodevelopmental diseases. Furthermore, this study will also improve our
understanding of the health effects attributed to different forms of mercury
and contribute to the development of toxicological risk assessment models for
detecting environmental contaminants that would adversely impact children’s
health.
Patricia Rosen, M.D., MPH, Texas Center for Autism
Research and
Treatment
Vaccine injections have been blamed as a potential source of
mercury exposure in early childhood. Based on the recommended childhood
immunization schedule the cumulative amount of mercury given to a two-year-old
child would be about 237.5 micrograms. Whether or not this could have resulted
in an increase in the incidence of autism either through exposure to mercury or
through an effect on the immune system is in question. Clinical similarities of
patients with mercury poisoning to patients with autism as reported in ARC
Research, has also caused concern. Although there is a significant safety
margin incorporated into acceptable mercury exposure limits, some children
could be exposed to a cumulative dose over the first 6 months of life that
exceeds federal guidelines on methyl mercury. We propose to do a prospective,
randomized double blind, cross over study that evaluates the effect of
chelation therapy with DMPS on neurobehavioral functioning of children with
autism. DM!
!
PS is an investigational drug that has been used in Europe
and Russia for many years (since 1958) for the treatment of heavy metal
poisoning. It has also been used in the United States on a compassionate use
basis for heavy metal poisoning when other available medicines have either been
ineffective or contraindicated. DMPS is very effective in removing mercury,
lead and other heavy metals from humans but the question to be asked is will it
help our children who have been diagnosed with autism.
Ellen Silbergeld, Ph.D., University of Maryland School
of Medicine
Methyl mercury (MeHg) is an environmental pollutant
that causes
profound neurotoxicity and has been associated with autism.
A major toxic effect associated MeHg exposure in humans is damage to the
developing nervous system, involving inhibition of cell migration. This project
will test the hypothesis that methyl mercury disrupts neurodevelopment through perturbing
cytokine-directed neural migration, resulting in permanent structural
alterations of the CNS and behavioral and cognitive dysfunction. By defining the role of inflammatory
cytokines in brain development, the results of this project may also have
implications for understanding mechanisms by which maternal infections increase
risks of autism and other perinatal brain disorders.
Leman Yel, M.D., University of California, Irvine
Organic mercury compounds are known to be toxic mainly
to the nervous
system. Recently, the similarities between the neurological
findings in mercury exposure and autism have come to attention. It has been
estimated that children are exposed to a quantity of mercury that exceeds the
safety guidelines in the first two years of life through thimerosal
(ethylmercury salicylate) in vaccines. And, a strong association between the administration
of certain vaccinations and the onset of autistic manifestations has been
noted. Autism is a multi-factorial disease in the pathogenesis of which
genetic, immunological, and environmental factors play a role. Brain biopsies
from autistic children show degeneration and a loss of neuronal cells without
any evidence of inflammation that is consistent with an apoptotic (programmed
cell death) process. Mercury accumulates in the mitochondria and disrupts cell
energetics. It has been shown to induce apoptosis by causing mitochondrial
dysfunc!
!
tion in lymphocytes. No study has been published on the
apoptotic effect of mercury in the nervous system. We hypothesize that mercury
induces apoptosis in neuronal cells and this effect is mainly via the
mitochondrial pathway. This might be
more pronounced in children with autism because of genetic susceptibility.
Thus, apoptosis due to mercury exposure may contribute to the pathogenesis of
autism. Therefore, we intend to examine the effect of thimerosal on apoptosis
induction and the signaling steps of mitochondrial pathway of apoptosis in
neuronal cells. The results would clarify the effect of a mercury compound in
neuronal cell death and degeneration, and provide a better understanding of the
potential role of mercury exposure in the pathogenesis of autism.
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