COLUMBIA U. (US) — Research points to a relationship between lead exposure and schizophrenia and raises questions about other environmental toxins.
Scientists say their findings suggest a synergistic effect between lead exposure and a genetic risk factor, and open an avenue to better understanding the complex gene-environment interactions that put people at risk for schizophrenia and other mental disorders.
In 2004, work by scientists at the Columbia University’s Mailman School of Public Health suggested a connection between prenatal lead exposure in humans and increased risk for schizophrenia later in life. But a big question remained: how could lead trigger the disease?
Based on his own research, Tomás R. Guilarte, senior author of the new study, believed the answer was in the direct inhibitory effect of lead on the N-methyl-D-aspartate receptor (NMDAR), a synaptic connection point important to brain development, learning, and memory.
His research in rodents found that exposure to lead blunted the function of the NMDAR. The glutamate hypothesis of schizophrenia postulates that a deficit in glutamate neurotransmission and specifically hypoactivity of the NMDAR can explain a significant portion of the dysfunction in schizophrenia.
Genetic risk and exposure
In the new study, Guilarte, professor and chair of the department of Environmental Health Sciences, and his co-investigators, including researchers at Johns Hopkins School of Medicine, focused on mice engineered to carry the mutant form of Disrupted-in-Schizophrenia-1 (DISC1), a gene that is a risk factor for the disease in humans. Results appear online in Schizophrenia Bulletin.
read more at http://www.futurity.org/lead-exposure-may-trigger-schizophrenia/