A surprising and somewhat perplexing new study has revealed that healthy relatives of schizophrenics actually display some of the same neurological imbalances as sufferers, yet don’t seem to experience any symptoms of the disorder. This discovery poses something of a riddle to researchers seeking the causes – and cure – of schizophrenia, while at the same time offering clues that could help to solve this brain-teasing puzzle.
Schizophrenia is a heritable disease, and as such, the genes that make people susceptible to the disorder are often shared among family members. However, there is a difference between being a carrier and a sufferer of a genetic disorder, and lead study author Katharine Thakkar says this research “hints at what kinds of things have to go wrong” for a person with a genetic vulnerability to schizophrenia to develop full-blown symptoms.
Though these symptoms and their causes can vary greatly, previous research has indicated that schizophrenia is largely produced by imbalances of certain neurotransmitters. For instance, glutamate, which causes neurons to become active, and GABA, which inhibits these neurons, are thought to play crucial roles in regulating brain function. As such, any disruption to the harmony between these two neurotransmitters can produce serious cognitive impairments.
To conduct their study – which appears in the journal Biological Psychiatry – the team used magnetic resonance spectroscopy to observe activity in the brains of 21 schizophrenic patients, as well as 23 healthy people who were closely related to schizophrenics, and 24 healthy non-relatives.
Results showed that, like the schizophrenics, those who were related to sufferers had lower glutamate levels than the control group. However, unlike those with schizophrenia, their relatives displayed normal levels of GABA.
All of this raises a number of fascinating questions regarding the roles of both glutamate and GABA in schizophrenia, while also leaving researchers somewhat stumped as to why the glutamate deficiency seen in some people doesn’t seem to have any consequences. Furthermore, exactly how these healthy relatives manage to maintain regular GABA levels despite being genetically vulnerable to schizophrenia is something that is going to take some explaining.
While it may take some time to solve this conundrum, this study does at least provide a useful starting point for scientists, and in the words of Thakkar, “gives us more specific clues into what kinds of systems we want to tackle when we’re developing new treatments for this very devastating illness.”