Assessment & Research

Brain glutathione and GABA+ levels in autistic children.

Song et al. (2024) · Autism research : official journal of the International Society for Autism Research 2024
★ The Verdict

Brain GSH and GABA+ levels measured via MR spectroscopy do not differ between autistic and neurotypical children, so these metabolites are unlikely ASD biomarkers.

✓ Read this if BCBAs who follow neuroimaging biomarker work or consult on multidisciplinary autism assessment teams.
✗ Skip if Clinicians focused solely on skill-based interventions with no interest in biological markers.

01Research in Context

01

What this study did

Song et al. (2024) scanned 8- to 12-year-old kids with and without autism. They used MR spectroscopy to measure two brain chemicals: glutathione (an antioxidant) and GABA+ (the main calming chemical). They checked four brain areas: frontal, parietal, temporal, and occipital lobes.

02

What they found

The kids' brains looked the same. GSH and GABA+ levels did not differ between the autism and control groups in any of the four regions. The authors conclude these chemicals are unlikely to serve as autism biomarkers.

03

How this fits with other research

Nijs et al. (2016) saw the same null result for GSH in autistic adults, so the finding now spans both kids and adults. Maier et al. (2022) and Harada et al. (2011) disagree: they found higher and lower frontal GABA, respectively, in autistic participants. The clash may come from age (adult vs. child), scanner settings, or small sample sizes. Taylor et al. (2017) adds nuance: they found lower GABA only in the sensorimotor cortex, hinting that any GABA differences are region-specific, not whole-brain.

04

Why it matters

If you hoped to use a quick brain-chemical scan to confirm an autism diagnosis, this paper says don't count on it. Instead, keep assessing behavior directly. The mixed GABA picture also reminds us that autism neurochemistry is patchy, not uniform, so sensory or motor interventions tied to GABA should stay targeted and evidence-based.

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02At a glance

Intervention
not applicable
Design
quasi experimental
Sample size
101
Population
autism spectrum disorder, neurotypical
Finding
null
Magnitude
negligible

03Original abstract

Autism spectrum disorder (ASD) is a neurodevelopmental condition characterized by social communication challenges and repetitive behaviors. Altered neurometabolite levels, including glutathione (GSH) and gamma-aminobutyric acid (GABA), have been proposed as potential contributors to the biology underlying ASD. This study investigated whether cerebral GSH or GABA levels differ between a cohort of children aged 8-12 years with ASD (n = 52) and typically developing children (TDC, n = 49). A comprehensive analysis of GSH and GABA levels in multiple brain regions, including the primary motor cortex (SM1), thalamus (Thal), medial prefrontal cortex (mPFC), and supplementary motor area (SMA), was conducted using single-voxel HERMES MR spectroscopy at 3T. The results revealed no significant differences in cerebral GSH or GABA levels between the ASD and TDC groups across all examined regions. These findings suggest that the concentrations of GSH (an important antioxidant and neuromodulator) and GABA (a major inhibitory neurotransmitter) do not exhibit marked alterations in children with ASD compared to TDC. A statistically significant positive correlation was observed between GABA levels in the SM1 and Thal regions with ADHD inattention scores. No significant correlation was found between metabolite levels and hyper/impulsive scores of ADHD, measures of core ASD symptoms (ADOS-2, SRS-P) or adaptive behavior (ABAS-2). While both GSH and GABA have been implicated in various neurological disorders, the current study provides valuable insights into the specific context of ASD and highlights the need for further research to explore other neurochemical alterations that may contribute to the pathophysiology of this complex disorder.

Autism research : official journal of the International Society for Autism Research, 2024 · doi:10.1002/mrm.27742