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“Healing Autism: No Finer a Cause on the Planet”

November 8, 2001        News Morgue Search  www.feat.org/search/news.asp

RESEARCH

·        Scientists Announce Creation for Autism

·        Researchers To Use Genomic Tech On Toxins/Disease

Susceptibility Link

ABSTRACTS (non-IMFAR)

·        Aminoglycoside Antibiotics And Autism: A Speculative Hypothesis

·        EEG Finding with Autism

 

 

Scientists Announce Creation for Autism

http://www.eurekalert.org/pub_releases/2001-11/uocd-sac110801.php

San Diego, Calif. – Autism experts around the world will reportedly establish the first and only scientific organization dedicated to researching autism spectrum disorders, marking perhaps one of the most significant steps in the quest to unravel this puzzling disorder. The society will be organized at the inaugural International Meeting for Autism Research (IMFAR) conference being held Nov. 9 and 10 at the San Diego Convention Center.

The scientific community’s newest society, the International Society for Autism Research (ISAR) will formalize its charter and elect its first president during the two-day autism research conference being held Nov. 9 and 10. Organizers of the society foresee ISAR as a major stimulus in attaining the highest quality interdisciplinary research on autism spectrum disorders by fostering collaboration among scientists and healthcare professionals.

“Those of us who have focused our research efforts on autism spectrum disorders have not had the benefit of sharing and discussing our findings with each other in a forum dedicated to this disorder,” said Sally Rogers, an autism expert and a psychologist at the University of Colorado School of Medicine’s Department of Psychiatry who is one of the founders of ISAR. “We absolutely must have a dialog to keep research, not only moving forward, but also to a much higher level.”

The new society will support international research through the sharing of information, findings and new ideas. Organizers anticipated that once the society is formalized this weekend, members will immediately work to establish a scientific journal for publication of peer-reviewed research as well as an annual scientific meeting and a regular newsletter. Pending a vote of the founding members, membership will likely be limited to scientists and researchers who hold graduate degrees from accredited universities and who have either authored a peer-reviewed journal article related to autism, have extramural funding to carry out research related to autism or have other scientific credentials that can be submitted to the membership committee for review.

“The formation of this new society signals a new era of cooperation and communication in the multidisciplinary research of autism,” said David G. Amaral, research director at the UC Davis M.I.N.D. Institute and professor of psychiatry at UC Davis School of Medicine. “This is an extremely complicated neurodevelopmental disorder which will only be understood through the dedicated effort of the various types of researchers and clinicians who will be attending ISAR. I think this day will be a landmark in the treatment of patients with autism.” More information about the IMFAR conference can be viewed at IMFAR’s virtual newsroom at www.newswise.com/vpr/mtg2001.ucm.html.

The International Meeting for Autism Research (IMFAR) is being promoted as the first-ever scientific research conference specifically devoted to the topic of autism. The conference is underwritten collaboratively by the Cure Autism Now Foundation, the UC Davis M.I.N.D.

Institute and the National Alliance for Autism Research (NAAR). Its mission

is to provide a unique opportunity for researchers, advocates, health care

professionals, service providers and others affected by autism to discuss

and promote new research into the condition. www.imfar.org In order to reach

the IMFAR virtual newsroom, please log onto

http://www.newswise.com/vpr/mtg2001.ucm.html

 

 

 

 

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Researchers To Use Genomic Technology On Toxins/Disease Susceptibility Link

Hutchinson Center, University Of Washington join in $37 Million national

effort to study health impact of toxic substances

[They intend to study mercury, which is specifically included in this

announcement.  However, not specifically mentioned with the “disease

susceptibility” factor is the immune system component.  How would they

otherwise be able to control for the effects of immune weakening viral

infections? Along with the efforts of the new researcher’s organization ISAR

(see above article), these developments represent ever more new hope for

finding the cause of autism soon. -LS]

http://www.fhcrc.org/news/science/2001/11/05/Toxico.htm

The Fred Hutchinson Cancer Research Center, in collaboration with the University of Washington, has been selected to participate in a federally funded, $37 million research consortium to study how individual genetic makeup affects one’s response to various environmental agents, from asbestos to tobacco smoke. Such research will help answer puzzling questions such as why some people who have never smoked a cigarette develop lung cancer, while others who have smoked heavily for years never show signs of the disease.

The Hutchinson Center/UW Toxicogenomics Consortium, part of a research collective involving a handful of academic institutions nationwide, will receive more than $7 million in funding over five years from the National Institute of Environmental Health Sciences, or NIEHS, headquartered in Research Triangle Park, N.C.

Each member of the NIEHS Toxicogenomics Research Consortium brings its own area of expertise, but collectively the group will use the tools of genomics to obtain a fundamental understanding, on a genome-wide scale, of the mechanisms of environmentally induced disease processes. Researchers will attempt to better understand how disease occurs; how to identify potential environmental hazards; how to predict potential disease; how to identify exposed individuals; and how to prevent disease.

The long-range goal of the Hutchinson Center/UW partnership is to shed light on genetic differences that make some people more sensitive than others to various environmental exposures.

The Seattle-based consortium will exploit the combined strengths of the Hutchinson Center and University of Washington in DNA-microarray technology – the use of so called “gene chips” to monitor the expression of thousands of genes at once – and the UW’s long-standing expertise in toxicology and environmental-health sciences.

The principal investigator of the Seattle consortium, an expert in both environmental sciences and DNA-array technology, is Helmut Zarbl, Ph.D., member of the Hutchinson Center’s Human Biology and Public Health Sciences divisions. His work focuses on using DNA-array technology to determine whether particular genes are sensitive to the actions of chemical toxicants and how these genes are involved in cancer development. Genes that are sensitive to a particular toxic substance can be identified by an increase or decrease in their expression level after exposure.

“The ultimate goal is to predict an individual’s risk of cancer based on their genetic profile and environmental exposures,” said Zarbl, also an associate professor of pathology and toxicology at UW.

“If a person carries a combination of genes that puts them at higher risk with a particular environmental exposure, then we may be able to develop methods of intervention such as dietary modifications, chemopreventive agents or drugs to counter the effects of exposure,” he said. “Or, among individuals we identify as highly susceptible, we may give them information on the types of occupations they should avoid, for example, or the types of exposures to which they may be particularly sensitive.”

Co-principal investigator of the consortium is David Eaton, Ph.D., director of the NIEHS-funded UW Center for Ecogenetics and Environmental Health.

“Many chronic diseases – such as most cancers, Parkinson’s disease and Alzheimer’s disease – are caused by complex interactions between genetics and the exposures to factors in our environment,” said Eaton, a professor of environmental health and associate dean for research in the UW School of Public Health and Community Medicine.

“For example, recent research has shown that genetic factors alone account for only 20 to 40 percent of our risks for developing some form of cancer. Factors in our environment, such as diet, smoking and chemical pollutants, interact with our genetics to account for the other 60 to 80 percent of risk.

“The work of the Hutchinson Center/UW Toxicogenomics Consortium can help us better understand genetic differences that make some people more sensitive to environmental exposures.”

The consortium’s four laboratory-based projects will focus on the effects of various toxic substances on breast-cancer development, how exposures to certain pesticides may affect behavior in children, environmental factors that may harm the developing nervous system, and the development of laboratory tests that can replace animal testing.

Below are brief descriptions of each project:

Project 1: Many environmental factors can harm the development of the nervous system in infants before and after birth. These factors can include exposure to metals such as methyl mercury, nutritional changes, and physical factors such as hyperthermia (exposure to excessive heat, which can occur if a pregnant woman experiences a high fever). Adverse neurodevelopmental effects of exposures can range from behavioral changes to major birth defects such as spina bifida. The goal of this project is to use genomic approaches to improve the understanding of how environmental factors can damage the developing nervous system and so improve our ability to identify and prevent birth defects. (Project leaders: Elaine Faustman, Ph.D., professor of environmental health, UW; Philip Mirkes, Ph.D., research professor of pediatrics, UW.)

Project 2: The goal of this project is to gain a better understanding of how exposures to certain pesticides can affect the behavior of children.  The researchers are focusing on the HDL-associated plasma enzyme paraoxonase, which provides protection from the effects of exposures to some organophosphates, a group of chemicals that includes the pesticides chlorpyrifos and diazinon. Children produce very little paraoxonase enzyme until they are about a year old, and so are extremely vulnerable to these chemical exposures. (Project leaders: Clement Furlong, Ph.D., research professor of medical genetics, UW; Lucio Costa, Ph.D., professor of environmental health, UW.)

Project 3: This project aims to develop tests for toxic exposure and stress responses using liver cells cultured in the laboratory. Because the liver processes nearly all chemicals that enter the body, the expression of genes in liver cells could predict how a given exposure would affect one’s health. To see if their cell-culture systems accurately model the toxic effects of chemical exposures, the researchers will compare the results of tests using cultured cells to those using rodents. One of their ultimate goals is to develop laboratory tests that can replace animal testing.  (Project leader: Curtis Omiecinski, Ph.D., professor of environmental health, UW.)

Project 4: This project will use DNA-microarray technology to map and identify genes that influence susceptibility to environmental toxins that cause breast cancer. Relatively few women diagnosed with breast cancer –between 5 percent and 10 percent – carry BRCA1 and BRCA2, the so-called “breast-cancer genes” that have been linked to an inherited form of the disease. However, up to half of all women are believed to carry genetic mutations that may make them susceptible to various environmental exposures linked with breast-cancer growth. Researchers hope that by identifying such genes in rats – and ultimately, humans – they’ll better understand how to identify sensitivity to environmental breast-cancer risk factors in the majority of women. (Project leader: Helmut Zarbl, Ph.D., member of the Hutchinson Center’s Human Biology and Public Health Sciences divisions and principal investigator of the Hutchinson Center/UW Toxicogenomics Consortium.)

Each research project is supported by an infrastructure of technology cores that will provide a range of materials and services. A tissue-acquisition core, directed by UW pathology professor Peter Rabinovitch, M.D., Ph.D., will provide access to genetically defined tissues and cell cultures. A DNA-expression array core, led by Zarbl, will compare the molecular fingerprints of cells exposed to different doses of environmental agents.

Another important strength of the consortium is the combined Hutchinson Center/UW expertise in bioinformatics and statistics, which will be key in analyzing data that ultimately will contribute to a national microarray gene-expression database. The consortium’s bioinformatics core will be co-directed by Steven Self, Ph.D., member of the Hutchinson Center’s Public Health Sciences Division; and Roger Bumgarner, Ph.D., director of the UW Center for Expression Arrays and research assistant professor in the Department of Microbiology.

A toxicology core, directed by Terry Kavanagh, Ph.D., associate professor of environmental health at UW, will coordinate the development of standardized methodologies in expression-array analysis to be used across the national consortium’s participating universities as well as the NIEHS.

Other academic institutions participating in the NIEHS Toxicogenomics Research Consortium are the University of North Carolina at Chapel Hill;

Oregon Health and Science University in Portland; Duke University in Durham, N.C.; and the Massachusetts Institute of Technology in Cambridge.

“We know that we can stretch the research dollar by having scientists at NIEHS and grantees at universities work in concert,” said Kenneth Olden, Ph.D., director of NIEHS. “But perhaps more important, we know that bringing ideas together in science increases the advances we achieve.”

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Aminoglycoside Antibiotics And Autism: A Speculative Hypothesis.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ui ds=11696245&dopt=Abstract <-- address ends here.  Manev R, Manev H.  Department of Psychiatry, The Psychiatric Institute The University of Illinois at Chicago, Chicago, IL 60612, USA.

HManev@psych.uic.edu

Background: Recently, it has been suspected that there is a relationship between therapy with some antibiotics and the onset of autism; but even more curious, some children benefited transiently from a subsequent treatment with a different antibiotic. Here, we speculate how aminoglycoside antibiotics might be associated with autism.

Presentation: We hypothesize that aminoglycoside antibiotics could a) trigger the autism syndrome in susceptible infants by causing the stop codon read through, i.e., a misreading of the genetic code of a hypothetical critical gene, and/or b) improve autism symptoms by correcting the premature stop codon mutation in a hypothetical polymorphic gene linked to autism.

Testing: Investigate, retrospectively, whether a link exists between aminoglycoside use (which is not extensive in children) and the onset of autism symptoms (hypothesis “a”), or between aminoglycoside use and improvement of these symptoms (hypothesis “b”). Whereas a prospective study to test hypothesis “a” is not ethically justifiable, a study could be designed to test hypothesis “b”.

Implications: It should be stressed that at this stage no direct evide nce supports our speculative hypothesis and that its main purpose is to initiate development of new ideas that, eventually, would improve our understanding of the pathobiology of autism.

PMID: 11696245 [PubMed - as supplied by publisher]

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EEG Finding with Autism

Paroxysmal discharges on EEG in young autistic patients are frequent in

frontal regions

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11694957&dopt=Abstract  Hashimoto T, Sasaki M, Sugai K, Hanaoka S, Fukumizu M, Kato T.  Department of Education for Handicapped Children, Naruto University of Education, 748 Nakashima, Takashima, Naruto-cho, Naruto-city, Tokushima 772-8502, Japan.

EEGs were recorded in 86 autistic patients during sleep. Epileptic discharges were observed in 37 cases (43%). Twenty-seven (73%) of these 37 cases had localized spikes, 8 had multiple spike foci, one had generalized spikes, and one had both multiple spike foci and generalized spikes.  Forty-seven epileptic discharge foci were registered in 36 cases, the exception being one with generalized spikes.

Thirty-six (76.6%) of the registered 47 epileptic discharge foci were in the frontal region, one (2.1%) in the temporal region, 7 (14.1%) in the centro-parietal region, and 3 (6.4%) in the occipital region. Twenty (55.6%) of the 36 frontal spikes were at midline (11 at Fz and 9 at Cz), 8 on the left side, and 8 on the right side. The dipole of midline spikes was in the deep midline frontal region. These results suggest that frontal dysfunctions are important in the mechanism of symptoms in autism.

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