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Neurometabolites

What are neurometabolites?

Products of normal chemical metabolism may be altered in schizophrenia. Changes in metabolite levels may be indicative of altered biochemical activity. Magnetic resonance spectroscopy (MRS) has been used to measure levels of neurometabolites, such as N-acetylaspartate (NAA), creatine (Cr), and glutamine (Gln). These derivatives are indirect indicators of biochemical activity. Alteration in levels of NAA/Cr is associated with the protective myelin sheath surrounding neurons, which is used as a marker of neural cell viability. Decreased levels of NAA are associated with neuron death, or injury to the part of the neuron that connects to other cells, the axon. Gln is a metabolite of the neurotransmitter, glutamate (Glu).

What is the evidence on neurometabolites?

High quality evidence found a small decrease in myo-inositol levels in the medial prefrontal region in people with schizophrenia compared to controls. Moderate to high quality evidence found N-acetylaspartate levels were reduced in the frontal lobe, temporal lobe, thalamus, hippocampus, cerebellum, and cingulate cortex. Lower quality evidence also found reduced N-acetylaspartate in the parietal lobe, basal ganglia, and occipital lobe (white matter only). N-acetylaspartate may be increased in the striatum and the lenticular nucleus. There were small to medium-sized reductions in glutamate, and increases in glutamine, in the frontal cortex of people with schizophrenia, which may progress with age.

In unmedicated people with schizophrenia (drug naive or drug free), there were reductions in N-acetylaspartate in the thalamus and in frontal white matter (using <3T MRI scanners only), and medium-sized increases in glutamate+glutamine in the medial prefrontal cortex, and increases in choline in the basal ganglia. There were no changes in glutamate, creatine or myo-inositol in unmedicated patients.

In first-degree relatives of people with schizophrenia, there were N-acetylaspartate reductions in the anterior cingulate and in the hippocampus. In people at either clinical or genetic high-risk of schizophrenia, there were N-acetylaspartate reductions in the thalamus and in the N-acetylaspartate/creatine ratio in the prefrontal cortex.

October 2020

Last updated at: 3:30 am, 27th October 2020
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