More News On The Research Front

This reposted article is from the website of the Brain and Behavior Research Foundation. For the latest discoveries involving MI, I recommend checking out their site: www.bbrfoundation.org . This reposted article deals with possible causes and, hopefully, treatment of schizophrenia. My son and I participated in a schizophrenia study from Johns Hopkins. It could possibly be the one cited here. Anyway, it’s another baby step in the march for a cure.

Johns Hopkins Researchers Link Two Biological Risk Factors For Schizophrenia

Release Date: 07/17/2012

Johns Hopkins researchers say they have discovered a cause-and-effect relationship between two well-established biological risk factors for schizophrenia previously believed to be independent of one another.

The findings could eventually lead researchers to develop better drugs to treat the cognitive dysfunction associated with schizophrenia and possibly other mental illnesses.

Researchers have long studied the role played in the brain’s neurons by the Disrupted-in-Schizophrenia 1 (DISC1) gene, a mutation with one of the strongest links to an increased risk of developing the debilitating psychiatric illness.

In a study published in the journal Molecular Psychiatry, the laboratory of Mikhail V. Pletnikov, M.D., Ph.D., in collaboration with the laboratory of Solomon H. Snyder, M.D., D.Sc., instead looked at the role the DISC1 gene plays in glia cells known as astrocytes, a kind of support cell in the brain that helps neurons communicate with one another.

“Abnormalities in glia cells could be as important as abnormalities in neuronal cells themselves,” says Pletnikov, an associate professor of psychiatry and behavioral sciences at the Johns Hopkins University School of Medicine, and the study’s leader. “Most gene work has been done with neurons. But we also need to understand a lot more about the role that genetic mutations in glia cells play because neuron-glia interaction appears crucial in ensuring the brain operates normally.”

Besides the paranoia and hallucinations that characterize the disease, schizophrenics have cognitive deficits, leaving them unable to think clearly or organize their thoughts and behavior.

Previous studies found that one of the roles of astrocytes is to secrete the neurotransmitter D-serine, which helps promote the transmission of glutamate in the brain, believed to be a key to cognitive function. Schizophrenics have decreased glutamate transmission. It appears, Pletnikov says, that people with DISC1 mutations associated with the psychiatric illness are faster to metabolize D-serine, which leads to a decrease in the apparently crucial transmitter.

In clinical trials, other researchers are trying to boost D-serine levels in people with schizophrenia to see if they can boost cognitive function.

In the new study, the Johns Hopkins researchers found that DISC1 is directly involved in regulating the production of D-serine by the enzyme known as serine racemase.

The researchers found that DISC1 normally binds to serine racemase and stabilizes it. The mutant DISC1 in patients with schizophrenia cannot bind with serine racemase, and instead destabilizes and destroys it. The result is a deficiency of D-serine.

The Hopkins researchers bred mice with the mutant DISC1 protein expressed only in astrocytes and, as predicted, the animals had decreased levels of D-serine. These mice also showed abnormal behavior “consistent with schizophrenia,” Pletnikov says. For example, the rodents showed sensitivity to psycho-stimulants that target glutamate transmission. By treating the mice with D-serine, the scientists were able to ameliorate the schizophrenic-like symptoms. Mice without the DISC1 mutation in astrocytes had normal D-serine levels.

Pletnikov says that in the future, researchers hope that they can target the unstable junction between the abnormal DISC1 and serine racemase. If drugs, for example, can be found to increase glutamate transmission in humans, doctors may be able to improve cognitive function in schizophrenics. He says a DISC1 mutation may also be an important risk factor in other psychiatric disorders.

“Abnormal glutamate transmission is believed to be present in patients with bipolar disorder, major depression and possibly anxiety disorders, so our findings could apply to other psychiatric diseases,” he says.

Along with Pletnikov and Snyder, other Hopkins scientists involved in the research include Ting Martin Ma; Sofya Abazyan, Pharm.D.; Bagrat Abazyan, M.D.; Chunxia Yang, B.S.; Saurav Seshadri, Ph.D.; and Akira Sawa, M.D., Ph.D.

The study is funded by monies from the American Recovery and Reinvestment Act (ARRA MH083728); the Brain and Behavior Research Foundation Independent Investigator and Young Investigator Awards; U.S. Public Health Service Grants MH18501, P20 MH084018, P50 MH094268, R01 MH069853, R01 MH092443, R21 MH085226 and RC1 MH088753; and the Cell Science Research Foundation in Japan. It is also supported by the SR/RUSK foundation, the Stanley Foundation and the Maryland Stem Cell Research Fund.

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About waywardweed

I am a consumer and parent of two sons, one with a mental illness and the other a third-year law student.
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2 Responses to More News On The Research Front

  1. Gledwood says:

    I’ve always wanted to take part in some kind of research study. I have 2 conditions they could study: schizoaffective disorder and opiate dependency. I asked the methadone clinic again and again why no new treatments are ever trialled in our area and got no real answer except that because there is no big teaching hospital in this part of London we just don’t come under the right catchment area, which is pretty pathetic.

    When you see an outpatient psychiatrist here you nearly always get a trainee. And then when you see another doctor 3 months later you get a totally different person, and I get the impression a lot of them haven’t got the faintest interest in psychiatry anyhow, they’re doing it purely because you have to do a bit of everything to get a medical degree. Hardly “ideal” treatment is it… But this is Britain and medicine here is FREE! That’s probably the best thing about living in the UK compared to America. Just about everything else “sucks” as you Americans would say… 😉

  2. waywardweed says:

    Hi Gledwood,
    I’m not certain where I first heard about the study I partcipated in, but if I had to guess I’d say I read about it in NAMI’s magazine. Just in case you don’t know, NAMI is the National Association on Mental Illness, probably the largest organization of its kind in the US. They often list various research projects going on. The study was done out of Johns Hopkins which is in Baltimore, Maryland, just outside of Washington DC. It’s about a ten-hour drive from where I live but I didn’t have to go there. The researchers traveled to the volunteers. Someone I know recently spent two months in the DC area, participating in a study where they provided room and board. I’ve heard good and bad things about the British and Canadian heathcare system. Ours isn’t so hot either because there are so many insurance plans, it’s a pain to keep up. And, of course, they are not cheap. Yeah, I like the word “suck.” I’m sure you have a comparable one in England.

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