Author Topic: NIH Federally-Funded Autism & Mercury Studies FY 2005-2009  (Read 3098 times)

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Offline Satyagraha

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NIH Federally-Funded Autism & Mercury Studies FY 2005-2009
« on: September 28, 2009, 08:22:07 pm »
NIH Autism & Mercury 2005-2009 Index

All studies were found using the NIH CRISP search engine. (Engine will be unavailable after 10/31/09).
To run a search, go to: http://crisp.cit.nih.gov/crisp/crisp_query.generate_screen
To replicate the results for this thread, search on this criteria:
(autism | thimerosol | mercury) 2005-2009



1  AMARAL, DAVID: Animal models of autism
     NIH Study #1
     NIH Study #2
     NIH Study #3
     NIH Study #4
     NIH Study #5

2  BIRNBAUM, EVA: Biomarkers of Response to Environmental Stressors: Measurement of Environmental E
     NIH Study #1
     NIH Study #2

3  CHUSUEI, CHARLES: Role of Selenocystine in Lead Toxicity
     NIH Study #1

4   CICCO-BLOOM, EMANUEL: NEUROTOXICANT EFFECTS ON CELL CYCLE REGULATION OF NEUROGENESIS
     NIH Study #1  Posted here: http://forum.prisonplanet.com/index.php?topic=137555.msg827763#msg827763
     NIH Study #2
     NIH Study #3

5   CORY-SLECHTA, DEBORAH: Core--Neurotoxicology
     NIH Study #1  Posted here: http://forum.prisonplanet.com/index.php?topic=137555.msg827767#msg827767
     NIH Study #2
     NIH Study #3

6   CROEN, LISA: Prenatal and Neonatal Biologic Markers for Autism
     NIH Study #1
     NIH Study #2
     NIH Study #3

7   FREEDMAN, JONATHAN: Comparative Genomic Responses to Environmental Stressors
     NIH Study #1
     NIH Study #2

8   HAMMOCK, BRUCE: Core--analytical biomarkers (xenobiotics) facility
     NIH Study #1
     NIH Study #2
     NIH Study #3

9   HARRY, GAYLIA: Environmentally Induced Alterations In Neuron And Glia Development and Aging
     NIH Study #1

10   HERTZ-PICCIOTTO, IRVA: Environmental epidemiology of autism
     NIH Study #1
     NIH Study #2
     NIH Study #3
     NIH Study #4
     NIH Study #5

11   KININGHAM, KINSLEY: Mechanism of Thimerosal Induced Neurotoxicity
     NIH Study #1

12   O'HALLORAN, THOMAS:    Metalloregulation by MerR and Fur Protein Families
     NIH Study #1

13   PESSAH, ISAAC: Molecular and cellular mechanisms of autism
     NIH Study #1
     NIH Study #2
     NIH Study #3
     NIH Study #4
     NIH Study #5

14   PESSAH, ISAAC: Annual Autism, Genes and the Environment Conference
     NIH Study #1

15   RAHBAR, MOHAMMAD: Epidemiological Research on Autism in Jamaica
     NIH Study #1

16   SCHANTZ, SUSAN: Neurobehavioral Teratology Society: Symposium on Pesticides and Metals
     NIH Study #1

17   SHARP, FRANK   : Core D: Molecular Genomics Core
     NIH Study #1
     NIH Study #2
     NIH Study #3
     NIH Study #4

18   SILBERGELD, ELLEN: Mercury-Induced Immune Dysfunction in Autism/ASD
     NIH Study #1  Posted here: http://forum.prisonplanet.com/index.php?topic=137555.msg827749#msg827749

19   SILBERGELD, ELLEN: Genetic Susceptibility to Mercury-Induced Immune Dysfunction in Autism & ASD
     NIH Study #2  

20   SWEDO, SUSAN: Studies of Autism and Related Disorders
     NIH Study #1
     NIH Study #2
And  the King shall answer and say unto them, Verily I say unto you, 
Inasmuch as ye have done it unto one of the least of these my brethren,  ye have done it unto me.

Matthew 25:40

Offline Satyagraha

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Mercury-Induced Immune Dysfunction in Autism/ASD
« Reply #1 on: September 28, 2009, 08:28:50 pm »
Abstract
 
Grant Number:  1R21ES014857-01
Project Title:  Mercury-Induced Immune Dysfunction in Autism/ASD
PI Information: SILBERGELD, ELLEN K. [email protected]  PROFESSOR

Abstract:
DESCRIPTION (provided by investigator):


The overall goal of this research is to test the hypothesis that there are differences in response to the immunotoxic effects of mercury compounds in humans, and that susceptibility determinants are enriched in families with cases of autism/autism spectrum disorders (ASD).

This research is relevant to understanding preventable risk factors for autism/ASD, based upon the hypothesis that mercury compounds by themselves do not cause autism/ASD but may contribute to the risks of autism/ASD through their immunotoxic properties, in combination with genetic susceptibility and co-exposures to other risks, such as infections.

Based upon extensive findings of genetically determined susceptibility to mercury immunotoxicity  in rats and mice, we hypothesize that there is a range of susceptibility for mercury-induced immunotoxicity in human populations.

We specifically hypothesize, based upon the experimental literature by us and others, that individuals within families with multiple cases of autism/ASD, will have heightened responsiveness to the immunotoxic effects of mercury compounds.

The eventual goal of this research is to identify candidate genes that influence individual responsiveness to the immunotoxic effects of mercury compounds. In order to accomplish this goal there is a primary need to define the phenotype of mercury-induced immunotoxicity, which is the goal of this project.

We will test in vitro responsiveness to mercury in PBMCs obtained from volunteers.

Responses will be measured by FACS analysis of cell surface markers and by ELISA measurements of released cytokines. A dose-response curve will be carried out, in vitro, in order to determine the slope for each individual. Replicability will be assessed by repeat measures of the same individuals; method validation will be completed by analysis of a new set of individuals.

The overall relevance of the in vitro system will first be tested by comparing PBMCs from men and women (cycling, in the luteal phase). In the second phase, we will test the hypothesis that patients with autism are more susceptible to mercury-induced immunotoxicity by comparing in vitro responses of PBMCs among family trios (autism cases plus parents) with unrelated controls.

Accomplishing the goals of this project will be the first stage in developing a broader study of gene-environment interactions in autism, as well as a targeted search for candidate genes related to mercury susceptibility in humans.

Public Health Relevance:
This Public Health Relevance is not available.

Thesaurus Terms:
autism, family genetics, gene environment interaction, genetic susceptibility, immunopathology, immunotoxicity, mercury, phenotype
gender difference, lymphocyte, monocyte
clinical research, enzyme linked immunosorbent assay, flow cytometry, human subject, patient oriented research

Institution:  JOHNS HOPKINS UNIVERSITY
 W400 Wyman Park Building
 BALTIMORE, MD 21218
Fiscal Year:  2006
Department:  ENVIRONMENTAL HEALTH SCIENCES
Project Start:  01-AUG-2006
Project End:  31-JUL-2008
ICD:  NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES
IRG:  NAME

And  the King shall answer and say unto them, Verily I say unto you, 
Inasmuch as ye have done it unto one of the least of these my brethren,  ye have done it unto me.

Matthew 25:40

Offline Satyagraha

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Re: NIH Federally-Funded Autism & Mercury Studies FY 2005-2009
« Reply #2 on: September 28, 2009, 08:38:03 pm »
Abstract
 
Grant Number:  1P01ES011256-010001
Project Title:  NEUROTOXICANT EFFECTS ON CELL CYCLE REGULATION OF NEUROGENESIS
PI Information:  CICCO-BLOOM, EMANUEL DI.   

Abstract:
DESCRIPTION (provided by applicant):


 The investigators hypothesize that neurotoxic metals and teratogens disrupt neurogenesis in developing forebrain and hindbrain systems in vitro and in vivo, acting to inhibit proliferation by altering mitogenic growth factor receptors and cell cycles signaling pathways.

There are increasing numbers of children who experience problems with learning, social interactions, and self-regulation, and exhibit difficulties with fine and gross motor control. Normal brain development depends on interactions among multiple factors including those from genetic, neurochemical, biochemical, social, and environmental sources.

Significantly, recent studies indicate that environmental toxicants injure the developing brain, potentially contributing to cognitive and motor deficits. Toxicants affecting the brain, neurotoxicants, may act at multiple time windows, eliciting immediate stage-dependent effects in specific systems that influence subsequent ontogenetic processes as well.

However, while negative effects of neurotoxicants on cell migration, differentiation, and survival have been well-characterized, little is known about the effects on the generation of neurons (neurgenesis) and underlying pathogenetic mechanisms.

As child neurologists, the investigators frequently evaluate children for abnormal brain development in clinic, concerned about attention, learning, behavior, and autism spectrum disorders. Further, as a member of the Scientific Advisory Board of the National Alliance for Autism Research (NAAR), a community family advocacy organization, they provide targeted basic and clinical research support. This current proposal represents a new direction for basic research in the investigators laboratory, which has focused on defining mechanisms that control generation of distinct neuronal populations from dividing precursors.

Previously, they examined both positive and negative regulators of precursor proliferation in the developing nervous system, defining growth factor and neuropeptide effects in culture and in vivo. Further, they employed neuronal populations in forebrain and hindbrain regions involved in learning, memory and motor functions in the fetus as well as the developing postnatal animal.

Based on extensive studies, the investigators now turn attention to the effects of well-characterized neurotoxicants, including lead and mercury, and model teratogen, valproic acid, on neurogenesis in the embryo and the newborn, defining mediating mitogenic and cell cycle pathways and designing new model systems.

Public Health Relevance:
This Public Health Relevance is not available.

Thesaurus Terms:
cell cycle, cell growth regulation, embryo /fetus toxicology, neurogenesis, neurotoxicology
DNA replication, apoptosis, biological signal transduction, cell proliferation, cyclin dependent kinase, environmental toxicology, fibroblast growth factor, growth factor receptor, lead poisoning, methylmercury, neuron, prosencephalon, rhombencephalon, teratogen, valproate
immunocytochemistry, immunoprecipitation, laboratory rat, terminal nick end labeling, tissue /cell culture, western blotting

Institution:  UNIV OF MED/DENT NJ-R W JOHNSON MED SCH
 ROBERT WOOD JOHNSON MEDICAL SCH
 PISCATAWAY, NJ 088548021
Fiscal Year:  2001
Department:   
Project Start:  30-SEP-2001
Project End:  29-SEP-2006
ICD:  NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES
IRG:  ZES1

And  the King shall answer and say unto them, Verily I say unto you, 
Inasmuch as ye have done it unto one of the least of these my brethren,  ye have done it unto me.

Matthew 25:40

Offline Satyagraha

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Re: NIH Federally-Funded Autism & Mercury Studies FY 2005-2009
« Reply #3 on: September 28, 2009, 08:43:06 pm »
Abstract
 
Grant Number:  5P30ES001247-289014
Project Title:  Core--Neurotoxicology
PI Information: CORY-SLECHTA, DEBORAH A. [email protected]  PROFESSOR

Abstract:

The basic research goal of the Neurotoxicology Core is to understand the nature of the effects of environmental chemicals on nervous system function, their consequences over the life span, the mechanisms by which these effects are produced, and the risks they pose to human health.

A key element in this goal is to understand the contribution of combined effects of genetic predisposition and environmental chemical exposures on neurological dysfunctions, particularly as it relates to neurodegenerative diseases.

The research within this Core involves both basic neuroscience research and neurotoxicology and explores the age spectrum from development to aging. The general theme of the Core is that both early and late stages of life represent periods of potentially enhanced vulnerability to neurotoxic effects. Embedded within this theme is the emerging concept that neurological effects of toxic exposures may not manifest themselves until years after exposure, and that toxicants interact in complex ways with the genetic composition of the human to influence the nature and severity of functional outcomes.

The Core consists of seven members of which five are continuing members and two are new members, drawn from the Departments of Neurology, Environmental Medicine, and Obstetrics-Gynecology. The members have been chosen on the basis of their productivity, commitment to multidisciplinary neuroscience research, and experience in areas of thematic interest to the Center.

In the past funding period, the Core was called the Neurobehavioral Toxicology Research Core to reflect its focus on behavioral toxicology. The present Core, now named the Neurotoxicology Core, has expanded its focus to include a broader spectrum of issues, ranging from mechanisms, genetic predispositions and contributions to human diseases, and human risk assessment, while maintaining strengths in behavioral toxicology.

Of particular note are the inclusions of sophisticated molecular biology and neurochemistry into the battery of Core skills. The present proposal continues to advance the traditional strengths in metal neurotoxicology, while venturing into several new initiatives as well.

A major change is the plan to recruit a new faculty to replace Dr. Cory-Slechta as Core Director. The individual will be selected to further integrate the neurotoxicology and basic neuroscience. Another change is the new initiative into molecular neuroscience and genetic-toxicant interactions, which has been developed through the addition of Drs. Federoff and Gelbard to the Core.

This group will focus particularly on toxicant contributions to the development of neurodegenerative disorders. The major thematic areas of the Neurotoxicology Core are the following:

1) Neurochemical mechanism of lead-induced behavioral toxicology (Cory-Slechta). This project examines the neurochemical and neuroanatomical sites through which lead alters neural functions. Work had identified neurotransmitter alterations, neural pathways and behavioral deficits in animal models of lead exposure.

2) Environmental neurotoxicant genetic interaction: murine model (Federoff). This work would test the hypothesis that neurotoxicants interact with yet uncharacterized genetic determinants to produce selective vulnerability. Focusing on the dopamine transporter (DAT), the principal investigator will engineer a population of dopaminergic neurons overexpressing DAT by means of a somatic mosaic approach and directed gene expression to compare the responses of expressing and non-expressing neurons in the same animal.

3) A murine model of genetic and environmental neurotoxicant action (Richfield). This project would look at the role of the alpha-synuclein gene and gene product in Parkinson?s disease using the somatic mosaic approach. Studies will determine whether mice overexpressing alpha-synuclein show an enhanced dopaminerigic vulnerability when exposed to low does of paraquat.

4) Genotype and phenotype of autism spectrum disorders (Rodier). This project will continue the investigator?s work linking injury during early development (as early as neural tube fusion) and specific genes with the development of the autism disorders. Work will continue to examine the valproic acid model of brain injury (which phenocopies some aspects of autism spectrum disorders), and the toxicant involves the HOX family of genes.

5) The role of inflammation and oxidative stress in human immunodeficiency virus type 1- associated neurologic disease (Gelbard). This project has been investigating how HIV type 1 results in neurotoxicity. In the proposed research, the principal investigator would examine the role of tumor necrosis factor alpha (TNF-a) and platelet activating factor (PAF) in the pathogenesis of neurotoxicity. Future plans include the development of TNF-overexpressing mice by somatic mosaic methods, and subsequent examination of neuronal death under various challenges.

6) Neurobehavioral and developmental effects of methylmercury exposure (Clarkson). This represents a continuation of the large human study of methylmercury exposure via fish and its consequences on development. This is one of two definitive epidemiological studies of human methylmercury exposure, which will continue and expand during the next funding period. In addition, the project director will continue his involvement in a prospective study of mercury exposure via dental amalgams.

7) Persisting functional consequences of neurotoxicant exposure during early development (Weiss). This work will continue studies of developmental exposure to several classes of toxicants. These will include solvents in addition to ongoing work in metals, endocrine disruptors (e.g., TCDD), and drugs (e.g., cocaine).

Public Health Relevance:
This Public Health Relevance is not available.

Thesaurus Terms:
biomedical facility, environmental toxicology, nervous system disorder, neurotoxicology
environmental contamination, environmental health, neural degeneration

Institution:  UNIVERSITY OF ROCHESTER
 517 Hylan Bldg., Box 270140
 ROCHESTER, NY 14627
Fiscal Year:  2002
Department:   
Project Start:  01-APR-2002
Project End:  31-MAR-2003
ICD:  NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES
IRG:  EHS

And  the King shall answer and say unto them, Verily I say unto you, 
Inasmuch as ye have done it unto one of the least of these my brethren,  ye have done it unto me.

Matthew 25:40

Offline trailhound

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Re: NIH Federally-Funded Autism & Mercury Studies FY 2005-2009
« Reply #4 on: September 28, 2009, 08:59:28 pm »
Quote
Project Title:  Core--Neurotoxicology
PI Information: CORY-SLECHTA, DEBORAH A. [email protected]  PROFESSOR

Abstract:

The basic research goal of the Neurotoxicology Core is to understand the nature of the effects of environmental chemicals on nervous system function, their consequences over the life span, the mechanisms by which these effects are produced, and the risks they pose to human health.

A key element in this goal is to understand the contribution of combined effects of genetic predisposition and environmental chemical exposures on neurological dysfunctions, particularly as it relates to neurodegenerative diseases.

The research within this Core involves both basic neuroscience research and neurotoxicology and explores the age spectrum from development to aging. The general theme of the Core is that both early and late stages of life represent periods of potentially enhanced vulnerability to neurotoxic effects. Embedded within this theme is the emerging concept that neurological effects of toxic exposures may not manifest themselves until years after exposure, and that toxicants interact in complex ways with the genetic composition of the human to influence the nature and severity of functional outcomes.

The Core consists of seven members of which five are continuing members and two are new members, drawn from the Departments of Neurology, Environmental Medicine, and Obstetrics-Gynecology. The members have been chosen on the basis of their productivity, commitment to multidisciplinary neuroscience research, and experience in areas of thematic interest to the Center.

In the past funding period, the Core was called the Neurobehavioral Toxicology Research Core to reflect its focus on behavioral toxicology. The present Core, now named the Neurotoxicology Core, has expanded its focus to include a broader spectrum of issues, ranging from mechanisms, genetic predispositions and contributions to human diseases, and human risk assessment, while maintaining strengths in behavioral toxicology.

Of particular note are the inclusions of sophisticated molecular biology and neurochemistry into the battery of Core skills. The present proposal continues to advance the traditional strengths in metal neurotoxicology, while venturing into several new initiatives as well.

A major change is the plan to recruit a new faculty to replace Dr. Cory-Slechta as Core Director. The individual will be selected to further integrate the neurotoxicology and basic neuroscience. Another change is the new initiative into molecular neuroscience and genetic-toxicant interactions, which has been developed through the addition of Drs. Federoff and Gelbard to the Core.

This group will focus particularly on toxicant contributions to the development of neurodegenerative disorders. The major thematic areas of the Neurotoxicology Core are the following:

1) Neurochemical mechanism of lead-induced behavioral toxicology (Cory-Slechta). This project examines the neurochemical and neuroanatomical sites through which lead alters neural functions. Work had identified neurotransmitter alterations, neural pathways and behavioral deficits in animal models of lead exposure.

2) Environmental neurotoxicant genetic interaction: murine model (Federoff). This work would test the hypothesis that neurotoxicants interact with yet uncharacterized genetic determinants to produce selective vulnerability. Focusing on the dopamine transporter (DAT), the principal investigator will engineer a population of dopaminergic neurons overexpressing DAT by means of a somatic mosaic approach and directed gene expression to compare the responses of expressing and non-expressing neurons in the same animal.

3) A murine model of genetic and environmental neurotoxicant action (Richfield). This project would look at the role of the alpha-synuclein gene and gene product in Parkinson?s disease using the somatic mosaic approach. Studies will determine whether mice overexpressing alpha-synuclein show an enhanced dopaminerigic vulnerability when exposed to low does of paraquat.

4) Genotype and phenotype of autism spectrum disorders (Rodier). This project will continue the investigator?s work linking injury during early development (as early as neural tube fusion) and specific genes with the development of the autism disorders. Work will continue to examine the valproic acid model of brain injury (which phenocopies some aspects of autism spectrum disorders), and the toxicant involves the HOX family of genes.

5) The role of inflammation and oxidative stress in human immunodeficiency virus type 1- associated neurologic disease (Gelbard). This project has been investigating how HIV type 1 results in neurotoxicity. In the proposed research, the principal investigator would examine the role of tumor necrosis factor alpha (TNF-a) and platelet activating factor (PAF) in the pathogenesis of neurotoxicity. Future plans include the development of TNF-overexpressing mice by somatic mosaic methods, and subsequent examination of neuronal death under various challenges.

6) Neurobehavioral and developmental effects of methylmercury exposure (Clarkson). This represents a continuation of the large human study of methylmercury exposure via fish and its consequences on development. This is one of two definitive epidemiological studies of human methylmercury exposure, which will continue and expand during the next funding period. In addition, the project director will continue his involvement in a prospective study of mercury exposure via dental amalgams.

7) Persisting functional consequences of neurotoxicant exposure during early development (Weiss). This work will continue studies of developmental exposure to several classes of toxicants. These will include solvents in addition to ongoing work in metals, endocrine disruptors (e.g., TCDD), and drugs (e.g., cocaine).

Public Health Relevance:
This Public Health Relevance is not available.

Thesaurus Terms:
biomedical facility, environmental toxicology, nervous system disorder, neurotoxicology
environmental contamination, environmental health, neural degeneration

Institution:  UNIVERSITY OF ROCHESTER
 517 Hylan Bldg., Box 270140
 ROCHESTER, NY 14627
Fiscal Year:  2002
Department:   
Project Start:  01-APR-2002
Project End:  31-MAR-2003
ICD:  NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES
IRG:  EHS

 I was wondering why they were giving cocaine to the lab rats at Emory...

mercury exposure via dental amalgams.

 I hate to think about what might be in my mouth :P i remember sitting in the dentists chair with a big styrofoam dish of fluoride in my mouth...i knew i didnt like it then. Now I have to be nasty with my dentist before she understands im not doing the shot of fluoride.


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