Researchers Discover Link Between Schizophrenia, Autism and Maternal Flu

[Guest guest]

Didn't prego moms just masturbate too much? Maybe it was the lead in

the BOBs made in China?

>

> http://www.physorg.com/news110641743.html

>

[Guest guest]

So theoretically they're saying that the flu shot could also " trick "

the maternal immune system, right? Either way, sham city. Flu's always

been around and some other past strain should have " replicated " this

response at some point in history, right? Where's the (staggering,

yawning and snoring as I ask this) fifty year old autists?

> >

> > http://www.physorg.com/news110641743.html

> >

>

[Guest guest]

The Flu is basically a severe cold, so if thats so, anyone with a cold

while they are P.G. could have a child with autism? The common cold is

a virus too!

In EOHarm , " searchingforserenity111 "

<searchingforserenity111@...> wrote:

>

> http://www.physorg.com/news110641743.html

>

[Guest guest]

WHO THE HELL COULD REACH?????

> Didn't prego moms just masturbate too much?

[Guest guest]

http://www.enn.com/health/article/23610Researchers Discover Link Between Schizophrenia, Autism and Maternal Flu

RELATED ARTICLES

Maternal antibodies may contribute to autismNew research shows how chronic stress worsens neurodegenerative disease courseUV light may offer "double whammy" for cancerIndia stops further trials of HIV vaccine

/health/article/23610 PASADENA, Calif.- A team of California Institute of Technology researchers has found an unexpected link connecting schizophrenia and autism to the importance of covering your mouth whenever you sneeze.

It has been known for some time that schizophrenia is more common among

people born in the winter and spring months, as well as in people born

following influenza

epidemics. Recent studies suggest that if a woman suffers even one

respiratory infection during her second trimester, her offspring's risk

of schizophrenia rises by three to seven times. Since

schizophrenia and autism have a strong (though elusive) genetic

component, there is no absolute certainty that infection will cause the

disorders in a given case, but it is believed that as many as 21

percent of known cases of schizophrenia may have been triggered in this

way. The conclusion is that susceptibility to these disorders is

increased by something that occurs to mother or fetus during a bout

with the flu.

Now, researchers have isolated a protein that plays a pivotal role in

that dire chain of events. A paper containing their results, "Maternal

immune activation alters fetal brain development through

interleukin-6," will be published in the Oct. 3 issue of the Journal of

Neuroscience. Surprisingly, the finger of blame does not point

at the virus itself. Since influenza infection is generally restricted

to the mother's respiratory tract, the team speculated that what acts

as the mediator is not the mother's infection per se but something in

her immune response to it. To prove this, they triggered an

artificial immune response in pregnant mice--giving them a faux case of

the flu. The trigger they used was a snippet of double-stranded RNA

called poly(I:C), which fools the immune system into thinking there has

been an infection by an RNA virus. A single, mid-gestation

injection of poly(I:C) creates a strong immune response in a pregnant

mouse. When her offspring reach adulthood, they display behavioral and

tissue abnormalities similar to those seen in schizophrenia in humans.

Though there might be some disagreement over what it means for a mouse

to be schizophrenic, these abnormalities are generally marked by

inappropriateness of response and difficulty in coping. For instance,

afflicted mice often show antisocial tendencies, have trouble

internalizing basic cause-and-effect connections, and are anxious about

entering wide-open spaces or interacting with novel objects. Moreover,

some of these abnormal behaviors are corrected by antipsychotic drug treatment. These behaviors then pose a new question, what in the mother's immune response caused the abnormalities?

At the cellular level, the innate immune response is driven by proteins

called cytokines, which are produced by the body in response to

infection. The researchers speculated that something was being

transmitted to the fetus by one or more cytokines produced by the

mother in response to her infection. "It's known that humans

that are treated--say, for cancer--with an experimental cytokine

treatment can display very significant changes in behavior," says

H. , Biaggini Professor of Biological Sciences and senior

author of the paper. "So we know cytokines can have dramatic effects,

of the kind you see in schizophrenia." The team tried injecting the pregnant

mice with individual cytokines, rather than with poly(I:C). It turned

out that after a single dose of a specific cytokine known as

interleukin-6 (or IL-6), a mouse would give birth to offspring who, at

maturity, exhibited the familiar schizophrenia- and autism-like

behaviors. To confirm the role of IL-6, Steve , the lead

researcher, gave fake colds (poly(I:C)) to two groups of pregnant,

IL-6-free mice. One group had received anti-IL-6 antibodies which

blocked IL-6; the other consisted of so-called IL-6 knockout mice (mice

whose genetic makeup prevents them from synthesizing IL-6). In both

groups, offspring grew up normal, showing that IL-6 is necessary for

the maternal poly(I:C) treatment to alter fetal brain development and

subsequent behavior in the offspring. The decision to try

injecting IL-6 was a long shot. "It is really unexpected that a single

injection of a single cytokine would exert such a powerful effect,"

says . The scientists are still unsure what it is about

increasing IL-6 levels in the mother that causes undesirable effects in

her offspring. "The most obvious possibility is that IL-6 acts directly

on the fetal brain," the paper's authors say, but they acknowledge that

the cytokine might also alter the transfer of materials across the placenta

or might even alter the maternal immune system that gave rise to it, in

effect triggering a low-grade rejection of the developing fetal tissue

by the mother's body. Once the exact role of IL-6 has been

nailed down, there will still be more work to be done. The researchers

are hunting for ways of preventing cytokines like IL-6 from inflicting

their damage on the developing or maturing brain--perhaps via

mechanisms involving other cytokines. "We could certainly

imagine that there would be anti-inflammatory cytokines that would be

involved, that would be acting in the opposite direction," suggests

. "We haven't tested those yet, but we would like to. We also

want to test anti-inflammatory drugs in the postnatal offspring to see

if we can normalize their behavior." The paper's authors are

and , a graduate student in biology at Caltech;

Li, now a graduate student at the University of California

Medical Center, San Francisco, who participated in the project as part

of a Caltech Summer Undergraduate Research Fellowship; and Drs.

Krassimira Garbett and Karoly Mirnics, both of the Department of Psychiatry and the Vanderbilt Kennedy Center for Research on Human Development, Vanderbilt University. The research was supported by the National Institute of Mental Health and by the McKnight, Cure Autism Now, and Autism Speaks foundations. ###