Research

MRS (magnetic resonance spectroscopy) in schizophrenia

April 9, 2026 9 min read

Most people know MRI as a way of taking pictures of the brain. Far fewer know that the same scanner can also measure the chemical composition of small brain regions — without contrast injection, without radiation, and in a single sitting. That technique is magnetic resonance spectroscopy (MRS), and over the past two decades it has become an important tool for studying the chemistry of schizophrenia.

In one sentence

MR spectroscopy lets researchers non-invasively measure concentrations of brain metabolites — including glutamate, GABA, glutathione, and N-acetylaspartate — and has produced some of the most cited recent evidence implicating glutamate dysfunction in schizophrenia.

How MRS works

MR spectroscopy uses the same nuclear magnetic resonance physics as MRI but reads out the signal differently. Each chemical in the brain has a slightly different magnetic environment, producing a distinct frequency in the recorded signal. By analysing those frequencies, researchers can identify and quantify several metabolites within a defined voxel — typically a cube a few centimetres on a side.

The most commonly measured metabolites in schizophrenia research include:

MRS at higher field strengths (3T, 7T) gives better separation of overlapping peaks, which has been particularly important for distinguishing glutamate from glutamine and for measuring GABA reliably.

What MRS has shown in schizophrenia

Glutamate

The largest and most replicated MRS finding in schizophrenia concerns glutamate. Multiple meta-analyses, including the influential 2016 paper by Merritt and colleagues in JAMA Psychiatry, have shown:

These findings have helped anchor the glutamate hypothesis of schizophrenia in direct human evidence, complementing pharmacological models based on NMDA antagonists like ketamine. See our piece on the glutamate hypothesis.

GABA

GABA MRS has produced more variable findings. Some studies show reduced GABA in prefrontal regions in schizophrenia, consistent with post-mortem findings of altered parvalbumin-positive interneurons. Other studies have not replicated this. The technical demands of GABA MRS — particularly editing techniques like MEGA-PRESS — partly explain the variability.

NAA

Reduced NAA, often in prefrontal and hippocampal regions, has been one of the longest-standing MRS findings in schizophrenia. NAA is sometimes interpreted as a measure of neuronal integrity, though it is also affected by mitochondrial function and brain energetics. Reduced NAA has been observed in chronic schizophrenia and to a lesser extent in first-episode patients, suggesting both early and progressive components.

Glutathione

Glutathione is the brain's most abundant antioxidant. Several MRS studies have shown reduced cortical glutathione in schizophrenia, supporting models that include oxidative stress as a contributor. This has fed interest in N-acetylcysteine (NAC), a glutathione precursor, as an adjunctive treatment. See our pieces on NAC in schizophrenia.

Energy metabolism

Phosphorus MRS (31P-MRS) and proton MRS measures of creatine and lactate have suggested altered brain energy metabolism in schizophrenia. This has informed renewed interest in metabolic interventions including the ketogenic diet.

Limitations and caveats

MRS findings come with important caveats:

From MRS to drug development

One of the practical impacts of MRS findings has been to motivate clinical trials of glutamate-modulating agents in schizophrenia. The 2024 FDA approval of xanomeline-trospium (Cobenfy), a muscarinic-targeted antipsychotic, was not directly based on MRS data, but the broader push beyond dopamine that the approval reflects is informed by MRS evidence of glutamate dysfunction.

Several clinical trials have used MRS as a pharmacodynamic biomarker — measuring how a candidate drug changes brain glutamate or GABA — to test target engagement before committing to large efficacy studies. This is one of the more promising applications of MRS for drug development.

Clinical use

MRS is not used to diagnose schizophrenia. There are some narrow clinical applications — for example, measuring NAA in suspected mitochondrial disorders or differentiating tumour types — but psychiatric clinical use is essentially non-existent. The findings remain a research tool.

A note on what MRS measures

MRS measures total tissue concentrations within a voxel. It does not directly measure synaptic neurotransmitter release, the rate of metabolic flux, or function. Interpretations linking MRS measurements to specific functional changes require care.

Where the field is going

Several directions are active:

For more imaging perspectives, see our pieces on fMRI, PET imaging, and brain volume changes.


This article is for educational purposes only and is not medical advice, diagnosis, or treatment. Always consult a qualified mental health professional. If you or someone you know is in crisis, call or text 988 in the US, or your local emergency number.

Frequently asked questions

Is MRS the same as MRI?
MRS uses the same scanner as MRI but produces a chemical readout instead of an anatomical image. Both rely on nuclear magnetic resonance physics; the difference is in how the signal is processed and presented.
Does MRS expose me to radiation?
No. MRS, like MRI, is non-ionising. The main practical considerations are the magnetic field, the noise of the scanner, and the time required (often longer than a standard MRI).
What is the most replicated MRS finding in schizophrenia?
Elevated glutamate (or glutamate+glutamine) in the medial frontal cortex and basal ganglia in clinical high-risk and first-episode samples, with patterns that may shift with treatment and chronicity.
Will MRS ever be used clinically for schizophrenia?
It is unlikely to be a standalone diagnostic test, but MRS may eventually inform treatment selection — for example, identifying patients with glutamate elevations who may benefit from glutamate-modulating treatments.

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