Mold & Autism

In keeping within the bio-medical realm of possible Autism causes, one of the more intriguing is the theory of “infectious agents and toxins” interacting with a fetus/baby/child’s developing immune and neurologic systems resulting in changes and disruptions in those systems. The speculated result is Autism and sensory integration dysfunction, like my son.

Another article provided at the same site of Clark Seif Clark provides details of a Manhatten Beach settlement in which a family is awarded $22.6 million, claiming their son suffered brain damage because of lumber infested with toxin mold. – Sharon

Mold Education: Mold & Autism – An infection-based model of neurodevelopmental damage
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[Editor’s Comment: There are not many peer- reviewed published articles that discuss any possible relationship between fungi and autism. Of those published articles, there are very few that I can provide you access to without violating copyright laws. Here is one of the more interesting ones that I can give you.]

Perinatal exposure to infectious agents and toxins is linked to the pathogenesis of neuropsychiatric disorders, but the mechanisms by which environmental triggers interact with developing immune and neural elements to create neurodevelopmental disturbances are poorly understood. We describe a model for investigating disorders of central nervous system development based on neonatal rat infection with Borna disease virus, a neurotropic noncytolytic RNA virus. Infection results in abnormal righting reflexes, hyperactivity, inhibition of open-field exploration, and stereotypic behaviors. Architecture is markedly disrupted in hippocampus and cerebellum, with reduction in granule and Purkinje cell numbers. Neurons are lost predominantly by apoptosis, as supported by increased mRNA levels for pro-apoptotic products (Fas, caspase-1), decreased mRNA levels for the anti-apoptotic bcl-x, and in situ labeling of fragmented DNA. Although inflammatory infiltrates are observed transiently in frontal cortex, glial activation (microgliosis > astrocytosis) is prominent throughout the brain and persists for several weeks in concert with increased levels of proinflammatory cytokine mRNAs (interleukins 1, 1, and 6 and tumor necrosis factor ) and progressive hippocampal and cerebellar damage. The resemblance of these functional and neuropathologic abnormalities to human neurodevelopmental disorders suggests the utility of this model for defining cellular, biochemical, histologic, and functional outcomes of interactions of environmental influences with the developing central nervous system.

Click here for Mold Education: Mold & Autism – An infection-based model of neurodevelopmental damage


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