Higher Levels and Glutamate to Schizophrenia
According to a new study published in the April issue of the journal Neuron, a team of researchers from the CUMC (Columbia University Medical Center), in the United States, has discovered that higher levels of glutamate could be responsible for the onset of schizophrenia in predisposed patients. Glutamate is a neurotransmitter that plays a key role in the long-term increase in the strength of nerve impulses through previously used pathways. Glutamate also plays a part in the memory and learning processes.
The findings of the researchers include a treatment strategy that could possibly slow down or even prevent the progression of schizophrenia and other psychotic disorders related to schizophrenia, and a possible diagnostic tool that would identify the patients who are at risk for schizophrenia. The senior author of the study, neurology professor Scot Small, reports that “Previous studies of schizophrenia have shown that hypermetabolism and atrophy of the hippocampus are among the most prominent changes in the patient’s brain”. Small also notes that his most recent study reveals that the aforementioned changes occur in the early stages of the disease, thus making an early diagnostic possible.
In order to locate the process, the research team from Columbia University used neuroimaging techniques in mouse models and human patients. Their first study involved a group of 25 patients who were at risk for the onset of schizophrenia. The research team studied their brains and the changes that occurred during the onset and development of the disease. A pattern was discovered in patients whose condition progressed towards schizophrenia: the activity of the glutamate neurotransmitter increased in the hippocampus first; Secondly, the metabolism of the hippocampus increased; thirdly the hippocampus atrophied.
Researchers used laboratory mouse models with schizophrenia in order to see if the increased levels of glutamate had other effects on the hippocampus as well. However, they discovered that the increase of glutamate had the same effect as it had on humans. Firstly the hippocampus became hypermetabolic and lastly, it began to atrophy.
In theory, the abnormal levels of the neurotransmitter and the hypermatabolism of the hippocampus can be seen through neuroimaging, thus being able to detect the early stages of schizophrenia. Treatment for patients with a high risk of schizophrenia onset could include the control of glutamate release. The president of the American Psychiatric Association, professor Jeffrey Lieberman, says that there have been treatment schemes for schizophrenia that were based on the reduction of glutamate levels, however, those schemes were only used on patients with a later stage of the disease, rather than an early stage. Professor Bita Moghaddam, from the University of Pittsburgh, affirms that if glutamate is responsible for the onset of schizophrenia, it could also explain why the psychotic episodes caused by the disease appear after periods of stress, due to the fact that glutamate levels increase during stress.