Re:Neuro damage following exposure to Thrimerosal based vaccines

[Guest guest]

> Neurodevelopmental Damage Following Exposure to Thimerosal-Based Vaccines

> in

> Mice Vulnerable to Autoimmune Disease

> PI: Mady Hornig, University of California, Irvine Collaborator: W. Ian

> Lipkin, University of California, Irvine, and Columbia University

> Dramatic increases in reported diagnoses of autism, a chronic and

> disabling neuropsychiatric disorder characterized by abnormalities in social

> interaction, learning, and behavior, have occurred state-, nation- and

> worldwide over the past decade. Although the basis of the disorder is

> unknown, genetic, immune and infectious factors are proposed to be

> important. One hypothesis is that pre- or early postnatal infection and/or

> exposure to toxins or vaccines results in aberrant brain development.

> his project explores an animal model of autism based on early exposure

> to toxins present in certain vaccines (ethylmercury present in thimerosal

> additive) with or without concurrent immune challenge (polyvalent vaccinal

> antigens) by repetitive bolus administration that mimics the early childhood

> immunization schedule. Similarities between sequelae of organic mercury

> exposure and autism include stereotypic behaviors; abnormal responses to

> novel environment; abnormal taste preferences; disturbed spatial learning;

> growth delay; hippocampal, cerebellar, and amygdalar pathology;

> autoantibodies to brain components, and increased frequency in males. Using

> this model, we will probe the mechanisms by which early toxic and immune

> disruptions alter brain architecture and function.

> Specific aims include:

> 1) characterize the behavioral, cognitive, and motoric deficits

> associated with early thimerosal/polyvalent vaccine exposure;

> 2) map the neurodevelopmental histopathology using stereologic

> methods;

> 3) evaluate the role of cytokines, apoptosis-related products,

> metallothioneins (a group of proteins that bind mercury), glutathione, and

> other soluble factors as potential mediators of brain damage following toxic

> and/or immune challenge; and

> 4) establish the biological basis for neonatal identification of

> vulnerability to neural damage following toxic and/or immune challenge

> through assessment of baseline levels of cytokines, metallothioneins, and

> other soluble factors.

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