Autism Speaks awards research grants, virus link to be explored

[HysteryDiagnosis]

http://www.digitaljournal.com/article/301838

In a 2009 Digital Journal interview with Dr. Hossein Fatemi, Professor of Psychiatry, Pharmacology and Neuroscience at the University of Minnesota Medical School - who has been studying the link between the H1N1 influenza virus and autism and schizophrenia since 1998 - this link was confirmed in mice.

"We asked a simple question," Dr. Fatemi said. "If we infect pregnant mice at various gestations with H1N1, does it cause abnormalities in the offspring's brain development. The experiment looked at the impact of H1N1 infection on brain genes in the hippocampus and in the cerebellum."

Dr. Fatemi found a direct connection between flu infection and the onset of autism, schizophrenia, and other gray and white matter afflictions.

"A large number of brain genes were affected significantly in both the hippocampus and cerebellum," said Dr. Fatemi.
Citing a CDC study on the Autism Speaks web sited, the disorder is growing at an alarming rate - afflicting 1 in 110 American children, 1 in 70 of whom are boys.

Read more: http://www.digitaljournal.com/article/301838#ixzz1ADEtBLWj

[lumberjack_jeff]

1. Typo in the original article.

"One in 110 American children, and one in 70 American boys."

[HysteryDiagnosis]

2. One of the things I think that is missing from the equation, however

this comes close is the body burden of lead, Hg, etc that the mother passes to the infant during gestation. Since a weakened metallothionein protein is associated with ASD and since it assists in the removal of heavy metals... it would seem logical to chelate or at least check a woman's body burden prior to her becoming pregnant.

She collects toxins during a 20 or 30 year period and then unloads a certain amount over a 9 month period. Lead very much looks like calcium to the body, and Hg (silver fillings) installed into pregnant ewes shows up in the calves in less than 24 hours. Calves may not be the correct term here but it works for me.

[lumberjack_jeff]

3. I suspect that there's an environmental trigger.

That works both in utero and on infants. It may be a combination of triggers which act on people who are genetically vulnerable to it.

It could be that only minute amounts of the trigger are enough to present the conditions in vulnerable kids. In other words, I doubt that a test is ever going to definitively tell a mother that her offspring will have the condition, nor do I think that chelation will be a solution.

[Odin2005]

4. One should be skeptical of any study funded by Autism Speaks.

They are a scam organization that fills it's coffers by whipping up hysteria of a nonexistent "autism epidemic".

[HysteryDiagnosis]

5. I hate scam artists and I am not kidding.

http://www.ncbi.nlm.nih.gov/pubmed/20941330





MBio. 2010 Oct 5;1(4). pii: e00176-10.
Induction of Toll-Like Receptor 3-Mediated Immunity during Gestation Inhibits Cortical Neurogenesis and Causes Behavioral Disturbances.
De Miranda J, Yaddanapudi K, Hornig M, Villar G, Serge R, Lipkin WI.
Abstract

Maternal infection during pregnancy with a wide range of RNA and DNA viruses is associated with increased risk for schizophrenia and autism in their offspring. A common feature in these exposures is that virus replication induces innate immunity through interaction with Toll-like receptors (TLRs). We employed a mouse model wherein pregnant mice were exposed to polyinosinic-polycytidylic acid , a synthetic, double-stranded RNA molecular mimic of replicating virus. Poly(I ⋅ C) inhibited embryonic neuronal stem cell replication and population of the superficial layers of the neocortex by neurons.

Poly(I ⋅ C) also led to impaired neonatal locomotor development and abnormal sensorimotor gating responses in adult offspring. Using Toll-like receptor 3 (TLR3)-deficient mice, we established that these effects were dependent on TLR3. Inhibition of stem cell proliferation was also abrogated by pretreatment with the nonsteroidal anti-inflammatory drug (NSAID) carprofen, a cyclooxygenase (COX) inhibitor. Our findings provide insights into mechanisms by which maternal infection can induce subtle neuropathology and behavioral dysfunction, and they may suggest strategies for reducing the risk of neuropsychiatric disorders subsequent to prenatal exposures to pathogens and other triggers of innate immunity.



Ann Clin Psychiatry. 2009 Jul-Sep;21(3):148-61.
Phenotypic expression of autoimmune autistic disorder (AAD): a major subset of autism.
Singh VK.
Brain State International Research Center, Scottsdale, AZ 85260, USA. [e-mail]
Abstract

BACKGROUND: Autism causes incapacitating neurologic problems in children that last a lifetime. The author of this article previously hypothesized that autism may be caused by autoimmunity to the brain, possibly triggered by a viral infection. This article is a summary of laboratory findings to date plus new data in support of an autoimmune pathogenesis for autism.

METHODS: Autoimmune markers were analyzed in the sera of autistic and normal children, but the cerebrospinal fluid (CSF) of some autistic children was also analyzed. Laboratory procedures included enzyme-linked immunosorbent assay and protein immunoblotting assay.

RESULTS: Autoimmunity was demonstrated by the presence of brain autoantibodies, abnormal viral serology, brain and viral antibodies in CSF, a positive correlation between brain autoantibodies and viral serology, elevated levels of proinflammatory cytokines and acute-phase reactants, and a positive response to immunotherapy. Many autistic children harbored brain myelin basic protein autoantibodies and elevated levels of antibodies to measles virus and measles-mumps-rubella (MMR) vaccine. Measles might be etiologically linked to autism because measles and MMR antibodies (a viral marker) correlated positively to brain autoantibodies (an autoimmune marker)--salient features that characterize autoimmune pathology in autism. Autistic children also showed elevated levels of acute-phase reactants--a marker of systemic inflammation.

CONCLUSIONS: The scientific evidence is quite credible for our autoimmune hypothesis, leading to the identification of autoimmune autistic disorder (AAD) as a major subset of autism. AAD can be identified by immune tests to determine immune problems before administering immunotherapy. The author has advanced a speculative neuroautoimmune (NAI) model for autism, in which virus-induced autoimmunity is a key player. The latter should be targeted by immunotherapy to help children with autism.
PMID: 19758536

[semillama]

6. If you hate scam artists, then why you constantly reference them?

Such as the Geiers and Andrew Wakefield? Inquiring minds would like to know.

[HysteryDiagnosis]

7. ... not even close. n/t

[semillama]

9. Way to duck the question. n/t

[HysteryDiagnosis]

10. Duck duck goose for you too. n/t

[Teaser]

11. Data may be good but

I am not a disorder.

[trotsky]

8. All the more reason to vaccinate and avoid getting the real flu!

Thanks, HD, for being a strong proponent of vaccination!