A novel study suggests difficulties processing auditory stimuli, genetic factors and smoking are potential risk factors for schizophrenia.
Schizophrenia has long been known to be hereditary although researchers have been unable to determine the main gene responsible for the condition.
In order to study the genetic background of schizophrenia, the frequency of particular risk genes between healthy and ill people has mostly been compared until now. In a new study, researchers used electroencephalography (EEG) to study the processing of simple acoustic stimuli (a sequence of similar clicks).
When processing a particular stimulus, healthy people suppress the processing of other stimuli that are irrelevant to the task at hand. Patients with schizophrenia exhibit deficits in this kind of stimulus filtering and thus their brains may be inundated with too much information.
As psychiatrically healthy people also filter stimuli with varying degrees of efficiency, individual stimulus processing can be associated with particular genes.
In the current study, involving over 1,800 healthy participants from the general population, psychiatrist Dr. Georg Winterer and Boris Quednow, Ph.D., examined the relationship between acoustic stimulus filtering and a known risk gene for schizophrenia: the so-called “transcription factor 4″ gene (TCF4). TCF4 is a protein that plays a key role in early brain development.
As patients with schizophrenia often smoke, the scientists also studied the smoking habits of the test subjects.
In the study sample, investigators determined that psychiatrically healthy carriers of the TCF4 gene also filter stimuli less effectively – like people who suffer from schizophrenia.
Researchers discovered that smokers who carry the risk gene display a less effective filtering of acoustic impressions. This effect was all the more pronounced the more the people smoked.
Non-smoking carriers of the risk gene, however, did not process stimuli much worse. “Smoking alters the impact of the TCF4 gene on acoustic stimulus filtering,” said Quednow, explaining this kind of gene-environment interaction. “Therefore, smoking might also increase the impact of particular genes on the risk of schizophrenia.”
The results could also be significant for predicting schizophrenic disorders and for new treatment approaches, he said. ”Smoking should also be considered as an important cofactor for the risk of schizophrenia in future studies.”
A combination of genetic (e.g. TCF4), electrophysiological (stimulus filtering) and demographic (smoking) factors could help diagnose the disorder more rapidly or also define new, genetically more uniform patient subgroups.
