Researchers from Imperial College London and GlaxoSmithKline found that 49 genes work differently in the brains of schizophrenia patients compared to controls. The data suggests that these genes are involved in controlling cell-to-cell signaling in the brain, which would support the theory that abnormalities in the way in which cells communicate are involved in the disease.
The investigators also found that that the genes for dopamine and for myelin were not acting any differently in schizophrenia patients compared with controls. They thus believe that overproduction of dopamine in the brain or damaged nerve-cell coating may not be the cause of schizophrenia, as previously assumed.
’s drug candidates for schizophrenia, which are in Phase I and II development, target the AMPA receptor, type 1 glycine transporter, and the dopaminergic pathway.
The researchers analyzed brain tissue from 23 controls and 28 schizophrenia patients, selected from brains donated by U.K. patients being treated for schizophrenia, and compared the data to an equivalent study in the U.S. The changes they found were common to both studies. This is the biggest cohort of schizophrenia patients used for this type of study to date, according to the scientists.
This investigation is a component of a larger study looking at proteins and DNA as well as mRNA in the samples, which were taken from the two brain regions associated with schizophrenia, the frontal cortical area and the temporal cortex.
The current results appear March 3 in Molecular Psychiatry.