Breakthrough UK study finds lack of key brain protein affects schizophrenia
Researchers have thought all along that synaptic dysfunction causes the debilitating cognitive symptoms seen in schizophrenia; however, new imaging data suggests that these symptoms, such as loss of abilities to plan and remember, are instead caused by the lack of a brain protein that facilitates communication between neurons. It marked the first time that studies of a living brain was made and lays the track for future research pathways for novel schizophrenia treatments.
When researchers at the MRC London Institute of Medical Sciences, UK, used a newly-developed radioactive PET tracer designed to bind to specific proteins coded by a gene known as SV2A, 18 schizophrenic subjects showed significantly lower levels of the protein in two key frontal brain regions, significant because a genetic variation in the gene SV2A has previously been associated with increased schizophrenia risk.
Lead researcher Oliver Howes thinks the loss of synapses could underlie the development of schizophrenia, but as the study also established that the two most common antipsychotic medications administered to schizophrenic patients were not causing/exacerbating the condition, “synaptic function in schizophrenic patients could be hypothetically restored by boosting SV2A activity, to treat the cognitive symptoms of the disease.”(The results of animal studies affirm that common antipsychotics haloperidol and olanzapine do not affect SV2A protein levels.)
“Next we hope to scan younger people in the very early stages to see how synaptic levels change during the development of the illness and whether these changes are established early on or develop over time,” Howes said.
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