Concentrations of Cortical <scp>GABA</scp> and Glutamate in Young Adults With Autism Spectrum Disorder

Kolodny, Tamar; Schallmo, Michael-Paul; Gerdts, Jennifer; Edden, Richard A.E.; Bernier, Raphael; Murray, Scott O.

doi:10.1002/aur.2300

Cited by 51 publications

(40 citation statements)

References 146 publications

(187 reference statements)

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“…Our study included 28 young adult participants on the autism spectrum (18 males, 10 females), and 35 NT comparison participants (21 males, 14 females). Data from these participants with ASD [58][59][60] and NTs 12,[58][59][60][61] were included in our recently published work. All participants were assessed by clinicians with extensive experience with ASD, under the supervision of a doctorallevel clinical psychologist who had achieved research reliability in the gold standard tools used to diagnose ASD.…”

Section: Methodsmentioning

confidence: 99%

Weaker neural suppression in autism

et al. 2020

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Abnormal sensory processing has been observed in autism, including superior visual motion discrimination, but the neural basis for these sensory changes remains unknown. Leveraging well-characterized suppressive neural circuits in the visual system, we used behavioral and fMRI tasks to demonstrate a significant reduction in neural suppression in young adults with autism spectrum disorder (ASD) compared to neurotypical controls. MR spectroscopy measurements revealed no group differences in neurotransmitter signals. We show how a computational model that incorporates divisive normalization, as well as narrower top-down gain (that could result, for example, from a narrower window of attention), can explain our observations and divergent previous findings. Thus, weaker neural suppression is reflected in visual task performance and fMRI measures in ASD, and may be attributable to differences in top-down processing.

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Section: Methodsmentioning

confidence: 99%

Weaker neural suppression in autism

et al. 2020

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“…The definition of standard reference GSH values within the different brain areas reported could lead to a better interpretation of the altered GSH levels recorded in subjects with neurological disorders, with insight into the possible role of GSH as a biomarker and therapeutic target. Referring to the reliability previously discussed and the sensibility of MEGA-PRESS, the most reliable GSH detected values were those of studies that used this technique in brain area analysis through a comparison between groups and in clinical applications [ 3 , 10 , 67 , 74 , 77 , 83 , 95 , 96 , 97 , 98 , 99 , 100 ].…”

Section: Brain Areas Gsh Concentrationmentioning

confidence: 99%

“…However, almost all of these studies were carried out with indirect measurements of GSH in the blood or post-mortem [ 128 ]. More recent studies with 3 T MRS through the in vivo evaluation of GHS levels found no significant difference in GSH levels between patients with ASD and the controls (Durieux et al mean concentration 2.5 mM in the dorsomedial prefrontal cortex and 2.8 mM in the basal ganglia of both ASD patients and HC) [ 99 , 128 ].…”

Section: Clinical Applications Of Gsh Imagingmentioning

confidence: 99%

In Vivo Brain GSH: MRS Methods and Clinical Applications

et al. 2021

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Glutathione (GSH) is an important antioxidant implicated in several physiological functions, including the oxidation−reduction reaction balance and brain antioxidant defense against endogenous and exogenous toxic agents. Altered brain GSH levels may reflect inflammatory processes associated with several neurologic disorders. An accurate and reliable estimation of cerebral GSH concentrations could give a clear and thorough understanding of its metabolism within the brain, thus providing a valuable benchmark for clinical applications. In this context, we aimed to provide an overview of the different magnetic resonance spectroscopy (MRS) technologies introduced for in vivo human brain GSH quantification both in healthy control (HC) volunteers and in subjects affected by different neurological disorders (e.g., brain tumors, and psychiatric and degenerative disorders). Additionally, we aimed to provide an exhaustive list of normal GSH concentrations within different brain areas. The definition of standard reference values for different brain areas could lead to a better interpretation of the altered GSH levels recorded in subjects with neurological disorders, with insights into the possible role of GSH as a biomarker and therapeutic target.

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“…The possibility that there could be a neural basis for the lack of an undershoot in ASD may have significant implications for understanding the neural circuits that are disrupted and may provide specificity for long-standing speculation that disrupted inhibition contributes to ASD. Despite the evidence for disrupted inhibition, we note that this same cohort of ASD and NT subjects did not have any differences in GABA concentration in some of the same brain regions that exhibited differences in undershoot magnitude (e.g., visual, auditory, and somatomotor ROIs) as measured with MRS (Kolodny et al, 2020b). Thus, the fMRI undershoot may reflect an inhibitory process that is not captured by MRS measurements of GABA.…”

Section: Discussionmentioning

confidence: 65%

“…Other data from these same (or subsets of these) subjects have been described elsewhere (Millin et al, 2018 ; Murray et al, 2018 ; Schallmo et al, 2018 , 2019 ; Kolodny et al, 2020a , b ). Most relevant is the Millin et al’s ( 2018 ) study.…”

Section: Methodsmentioning

confidence: 98%

Late fMRI Response Components Are Altered in Autism Spectrum Disorder

Murray

Kolodny

Schallmo

et al. 2020

Front. Hum. Neurosci.

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Disrupted cortical neural inhibition has been hypothesized to be a primary contributor to the pathophysiology of autism spectrum disorder (ASD). This hypothesis predicts that ASD will be associated with an increase in neural responses. We tested this prediction by comparing fMRI response magnitudes to simultaneous visual, auditory, and motor stimulation in ASD and neurotypical (NT) individuals. No increases in the initial transient response in any brain region were observed in ASD, suggesting that there is no increase in overall cortical neural excitability. Most notably, there were widespread fMRI magnitude increases in the ASD response following stimulation offset, approximately 6-8 s after the termination of sensory and motor stimulation. In some regions, the higher fMRI offset response in ASD could be attributed to a lack of an "undershoot"-an often observed feature of fMRI responses believed to reflect inhibitory processing. Offset response magnitude was associated with reaction times (RT) in the NT group and may explain an overall reduced RT in the ASD group. Overall, our results suggest that increases in neural responsiveness are present in ASD but are confined to specific components of the neural response, are particularly strong following stimulation offset, and are linked to differences in RT.

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Concentrations of Cortical GABA and Glutamate in Young Adults With Autism Spectrum Disorder

Cited by 51 publications

References 146 publications

Weaker neural suppression in autism

Weaker neural suppression in autism

In Vivo Brain GSH: MRS Methods and Clinical Applications

Late fMRI Response Components Are Altered in Autism Spectrum Disorder

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