Experts from Johns Hopkins University published in Molecular Psychiatry their finding that a rare genetic mutation is linked to schizophrenia. They suggest a mutation of the gene Neuronal PAS domain protein 3 (NPAS3) could be responsible in some way for development of mental illnesses like schizophrenia.
The experts studied the members of a family with a high rate of mental illness. An abnormal mutation of NPAS3 was found in a number of the family members.
NPAS3 regulates and makes sure healthy neurons are consistently developed.
The researchers wanted to determine if this observed mutation had any effect on the way NPAS3 should normally function so they grew neurons with mutated and normal versions of the gene in a dish to analyze any significant differences.
The normal version had long extensions to make good neuronal connections with other cells. The mutated version had much shorter extensions.
(Joseph Nordqvist. (2013, January 24) "Gene Identified with Schizophrenia Identified." Medical News Today. Retrieved from http://www.medicalnewstoday.com/articles/255307.php.)
Researchers at the New University of Buffalo found how defects in a neurological pathway in early development might be responsible for the onset of schizophrenia later in life.
Published in Schizophrenia Research, the findings tested the hypothesis in a new mouse model of schizophrenia. It shows how gestational brain changes cause behavioral problems later in life.
The genomic pathway is the Integrative Nuclear FGFR1 Signaling (INFS). It is a central intersection for multiple pathways of up to 160 different genes thought to be involved in this illness.
Lead author Michal Stachowiak, PhD, professor in the Department of Pathology and Anatomical Sciences in the UB School of Medicine and Biomedical Sciences, believes this is the first model to explain schizophrenia from genes to development to brain structure and finally to behavior.
Stachowiak suggests it's possible 100 patients with schizophrenia will each have a different genetic mutation that causes the illness. It's possible because of the INFS interaction.
He tells us: "We think schizophrenia occurs when there is a malfunction in the transition from stem cell to neuron, particularly with dopamine neuron."
The researchers induced schizophrenia by creating an FGFR1 (fibroblast growth factor receptor) mutation in mice.
("Scientists propose first genomic explanation for schizophrenia," retrieved on January 23, 2013 from http://www.news_medical_net/news/20130123/ . . .)
Good news: Perinatal choline supplement could lower schizophrenia risk.
A random controlled trail used 93 healthy pregnant woman, half of whom took choline during the last two trimesters of pregnancy. The women's babies also received choline soon after delivery.
The results revealed the babies who received choline perinatally had a significantly lower risk of a physiologic risk factor for schizophrenia at the age of 33 days compared to the babies who had received matching placebo.
The researchers believe "several" maternal risk factors for this illness are tied to decreased availability of choline for a fetus. Often, pregnant women are advised to increase their intake of choline-rich foods like eggs and meat.
The study was published in the American Journal of Psychiatry.
Robert Freedman, MD, co-author of the study and editor of that journal, indicates longer-term follow-up is necessary to assess whether choline supplementation decreases risk for the later development of schizophrenia as well.
("Perinatal choline supplement may lower schizophrenia risk," retrieved on January 21, 2013 from http://psychcentral.com/news/2013/01/20/perinatail-choline-supplement . . .)
To end here with a healthy tip:
Amantadine, a drug approved for treating extrapyramidal symptoms, has been shown in several studies to reverse anti-psychotic induced weight gain.
(NAMI-New York State News, Ask the Doctor p. 23 Winter 2012)
Published On: February 05, 2013