Monday, September 7, 2009

Ginni Pigs

Hi Everyone,
I hope you are all doing well, I am doing good. I get a newsletter everyday from NAMI. This is a really important one. I had to share it with you here. As some of you know my mother's story, for the first time today I am going to share my personal story with you. I don't think I have even talked about this with anyone but Pete and his family. It is hard for me, but now I am free of the shame, so here I go, taking a deep breath. When I graduated High School I wanted to go off to College like all my friends and my older brother Albert. I tried to save money but I worked part time at South Shore Hospital and made pretty good money, but I used it to pay for my first leather jacket, my car etc. When I applied for student loans to go to college they told me that my Dad made too much money, something must of changed in three years because my brother Albert was able to get student loans and then a scholarship. So again I saved some money for a semester at Massasoit College, then my brakes went on my car, I had to use that money instead of paying for College. Eventually I gave up on myself and my dreams to be a writer, Journalist. Before I knew it I met Pete and I moved out of my parents house to live with him and have Christa. Things were all well with me until about the time Christa was 2 years old. I started having anxiety attacks to the point that I could not leave the house. My biggest fear had come to life. I am going to suffer the rest of my life like my mother. This was 5 yrs before her new treatment proved to me that she was bipolar with hallucinations, because if she was truly a Paranoid Schizophrenic as first diagnosed I don't think lithium would have worked on her the way it did. I was a full time Mom with Christa and one day I saw a commercial for a Anxiety Clinic at Mass General and it was for free. I had no health insurance at time. So I called, had a huge attack as I entered the Doctor's Office. They gave me many big pills in a big bottle, I went home took one, and immediately felt better, I couldn't function without them. To make a long story short, I became addicted. There I was with no one to turn to for help, I wanted to go to detox, I was a mess. So I decided to withdraw myself at home. Bad idea, don't ever do it. After a few ambulance rides to the hospital. I eventually had a seizure in front of Christa and I could have died from a heart attack. I then turned to Alcohol to help ease the withdrawals. Even a stupider Idea, but being young and scared with no support system, you do what you have to do to survive. I was such a Party Girl in High School, it helped me escape the pain of my childhood. I did experiment with drugs, like Pot and anything else. But I could only handle Alcohol. When I knew I was to become a mother, I did calm down while pregnant and after she was born until the Anxiety took over me, it was the only way I could leave the house I just needed one drink and I could go to family functions and to the store. God finally intervened and I went to Highpoint in Plymouth Ma. It was the worst thing I have ever experienced. I will never take a narcotic again in my life unless I truly have to. A social worker and a counselor reassured me that I did not have any signs of Schizophrenia and I was put on Prozac. I started my life over and it has been good since then. Today I realized when posting this information that both my mother and I were Ginni pigs in a way as treatment for mental illness progressed. I have always physically been her clone, now I know why I felt that bond and love for her. We were one in the same. Just a generation apart. Thanks for reading my story and visiting my blog. Take Care, Janet :)

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Schizophrenia Linked to Over-expression of Gene in Fetal Brain Excess of Shortened Forms Could Lead to Abnormal Brain Development Gene over-expressed in fetal brain

A gene called DISC1, (for "disrupted in schizophrenia") has been a leading contender among possible genetic causes since it was implicated in a large Scottish clan two decades ago. The DISC1 gene codes for a protein important for brain development, as well as for mood and memory - functions that are disturbed in schizophrenia. However, until now there have been few clues as to how DISC1 might increase risk for the chronic mental disorder.

A new study suggests how impaired expression of DISC1 might wreak havoc during early critical periods as the developing brain gets wired up. NIMH researchers have discovered that previously unknown shortened forms of the gene were expressed 2.5 times more in the fetal brain than after birth. By contrast, other forms were expressed more evenly across development. The shortened forms were also over-expressed in brains of adults who had schizophrenia.

"These shortened forms may result in a functionally aberrant and truncated protein that is more highly expressed in the brains of people with schizophrenia" explained NIMH's Dr. Joel Kleinman, who led the research.

Drs. Kleinman, Barbara Lipska, Kenji Nakata, Daniel Weinberger and colleagues, report on their discoveries in postmortem brain tissue online, during the week of August 24, 2009 in the Proceedings of the National Academy of Science (PNAS).
Background

The new findings may help explain the molecular roots of the illness in the Scottish clan, in which more than half of the members developed schizophrenia or other serious mental disorders. Previous studies had traced their disease, in part, to a different aberration, a mismatch called a translocation, in which a chunk of genetic material from one chromosome gets attached to another chromosome. But this has never been seen in other families. A translocation, like the shorter messenger RNA forms, would result in shortened forms of DISC1 protein. So other affected families and the Scottish clan could in fact share a similar illness process, say the researchers.
Results of This Study

The researchers linked several illness-implicated variations in the DISC1 gene to the shorter forms of DISC1 products, called messenger RNAs, that transform the gene into protein. The results suggest that variations in the DISC1 gene boost risk for schizophrenia by producing shortened messenger RNAs that are predominantly expressed during the formative period when the fetal brain is taking shape.
Significance

"Our results cast a new light on apparent failures to replicate findings that have long plagued psychiatric genetics" said Kleinman. "We discovered that different genetic variations can result in the same or similar messenger RNAs and protein. That means that different studies could turn up different variations and still be pointing to the same underlying disease process. So some findings thought to be non-replications may ultimately prove to be replications."

Since at least a half-dozen genes implicated in schizophrenia by the NIMH group interact with DISC1, the downstream adverse effects of impaired DISC1 on brain systems are likely considerable, said Kleinman.
What's Next

One of the suspect gene variants associated with a shortened messenger RNAs is detectable in white blood cells, raising the possibility that it could someday be used as a genetic marker for the illness.

NIMH's Dr. Joel Kleinman explained how the DISC1 gene may increase risk for schizophrenia at a recent NIMH seminar.
Reference

Nakata K, Lipska BL, Hyde TM, Ye T, Fink E, Morita Y, Vakkalanka R, Bareboim M, Sei Y, Weinberger DR, Kleinman JE. DISC1 splice variants are upregulated in schizophrenia and associated with risk polymorphisms. Aug 24, 2009 PNAS.

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