Saturday, November 8, 2008



ScienceDaily (Nov. 6, 2008) — Research from the University of Pittsburgh could expand the options for controlling schizophrenia by identifying a brain region that responds to more than one type of antipsychotic drug. The findings illustrate for the first time that the orbitofrontal cortex could be a promising target for developing future antipsychotic drugs—even those that have very different mechanisms of action.


The study will be published during the week of Nov. 3 in the online edition of the journal Proceedings of National Academy of Sciences, with a print version to follow.


Bita Moghaddam, a professor in the Department of Neuroscience in Pitt's School of Arts and Sciences and the paper's lead author, found that schizophrenia-like activity in the orbitofrontal cortex—a brain region responsible for cognitive activity such as decision making—could be triggered by the two different neurotransmitters linked to schizophrenia: dopamine and glutamate. Brain activity was then normalized both by established antipsychotic medications that regulate only dopamine and by experimental treatments that specifically target glutamate.


"The orbitofrontal cortex is an area that's been somewhat neglected in schizophrenia research. This study should encourage researchers to focus on this brain region in imaging and other human studies, and also to use as a model for developing antipsychotic drugs," Moghaddam said. "Schizophrenia appears to be caused by very diverse and sometimes rare genetic mutations. Diverse mutations can end up causing the same disease if they disrupt the function of a common group of neurons or networks of neurons. We think that the key to understanding the pathophysiology of schizophrenia and finding better treatments is to identify these networks. This data suggests that the orbitofrontal cortex may be a critical component in networks affected by schizophrenia."


Working with UPMC neurology resident Houman Homayoun, Moghaddam first established that dopamine and glutamate could, separately, produce schizophrenia-like symptoms in the orbitofrontal cortex. They first simulated symptoms brought on by irregular neural receptors of glutamate. Studies within the last few years—including work by Moghaddam at Yale University—have shown that under-functioning glutamate receptors known as NMDA receptors can produce schizophrenia-like symptoms. Moghaddam and Homayoun found that stunting the NMDA receptors resulted in schizophrenia-like effects in the orbitofrontal cortex. The team also used a dose of amphetamine to simulate dopamine-related schizophrenia symptoms in the orbitofrontal cortex; schizophrenia is often linked to an excess of dopamine in the brain.


Moghaddam and Homayoun then tested the currently prescribed medication—a treatment developed more than 50 years ago that targets neural receptors of dopamine—and new experimental drugs that work on the glutamate system. They found that both medications normalized brain activity.


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COMMENT: Saying that schizophrenia is "linked to" dopamine tells us nothing. Linked how? What is the linkage? Gibberish.


The Medical Business talks only of "treatment" and "medication"; they are not even trying to help anyone be healthy - it is only about establishing you as a revenue stream.


People with scizophrenia should all take 100 mg of niacin each day after lunch, and strictly avoid high-copper foods, like oysters and liver.All multi-vitamins also have some copper, and should therefore be rejected in favor of separate vitamins and minerals in the proper forms at the appropriate times of day for each (vitamins C and B in the morning, zinc and magnesium at night, etc.) Although chocolate has some copper, a few ounces of high-cacao content chocolate is good for you (60-70%).


Drs Hoffer and Osmond have proven their "adrenochrome hypothesis", despite conventional doctors' claims to the contrary; however, their multi-gram doses are way too intense for most people, and they never explain why they put one person on 3 grams and another on 9, etc.


There is also the factor of "the schizophrenic family". This used to be called "the schizophrenic mother", but that was misogynistic/unscientific. Not that the whole family has schizophrenia, but that the family is severely dyfunctional, and the "schizophrenic" is the only member of their family who won't pretend everything's fine. He/she is a therefore made a scapegoat. (See, we didn't do anything wrong; son/daughter has schizophrenia - that's why he/she says such horrible things about us.) Learning about the psychopaths can be essential.

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