Washington, June 3 : Harvard researchers have found a genetic link to the risk of developing psychiatric disorders such as schizophrenia, bipolar disorder and depression.
The new study supported by NARSAD, the world's leading charity dedicated to mental health research, provides new insights into how genes work to impair various aspects of attention, memory and perception.
Previous studies based on two major famines in the 20th century, the Dutch Hunger Winter of 1944-45 brought about by the Nazi occupation in World War II and the Chinese famine in 1959-61, the scientists found that the incidence of schizophrenia among children born to women who were pregnant during these famines increased two-fold.
Deborah L. Levy, Ph.D., associate professor of psychology in the Department of Psychiatry at Harvard Medical School and director of the Psychology Research Laboratory at McLean Hospital has found that schizophrenia traits are common in families.
Levy is studying families to detect relatives who are carriers of the genes for schizophrenia and bipolar disorder, even though these individuals don't have the diseases themselves.
"One of the key issues in any genetic study is to distinguish individuals who are gene carriers from individuals who are not gene carriers," said Dr. Levy.
In single gene disorders, such as cystic fibrosis and Huntington's disease, 25 percent and 50 percent of family members, respectively, have the same illness.
In contrast, only 6.5 percent of family members of people with schizophrenia actually have the illness, which means most relatives don't have symptoms of the illness but may still be gene carriers.
For the study, the team is focussing on four discernable schizophrenia-related traits that occur in well family members at a much higher rate than schizophrenia itself: difficulty following a slow moving target with one's eyes, syntax errors or idiosyncratic use of language, subtle anomalies involving the midline of the face , and difficulty filtering out noises and other irrelevant stimuli (a condition known as sensory gating).
They have found that idiosyncratic use of language (a trait similar to the thought disorder observed in schizophrenia) occurs in 37 percent of clinically unaffected first-degree relatives of individuals with schizophrenia.
This rate is almost six times higher than schizophrenia in the same families.
When the rates for thought disorder and schizophrenia and related clinical conditions were combined, the proportion of potential gene-carrying relatives came close to 50 percent, consistent with a dominant gene, and much higher than the 6.5 percent rate of schizophrenia in the same families.
"With diseases like schizophrenia and bipolar disorder, identifying the genes is just the starting point," Dr. Levy.
"The ultimate goal is to discover the biological processes these genes initiate in the brain, ultimately leading to better treatments in the future."
The researchers believe that these findings would help in developing novel therapies targeted to specific patients and to specific genes.
Lead researcher Donald C. Goff, M.D., director of the Schizophrenia Clinical and Research Program at Massachusetts General Hospital identified a link between low blood levels of folate and negative schizophrenia symptoms, folate is involved in many different chemical pathways in the brain, including keeping levels of the amino acid homocysteine low.
When homocysteine levels are too high, this interferes with the functioning of receptors located all over the brain that are critical to learning, memory, brain development, and general neural processing.
"We now have the techniques to determine how genes combine to produce schizophrenia symptoms," said Dr. Roffman.
"As we gain a better understanding of individual biogenetic pathways, we can identify high-risk groups and those most likely to benefit from specific treatments," he added.
The study was presented at NARSAD's 3rd annual Boston Mental Health Research Symposium at the Harvard Medical School.