Objective: To explore the possible metabolic alterations of primary motor cortices (M1) of Parkinson’s disease (PD) patients and prodromal PD using 7T proton magnetic resonance spectroscopy (MRS).

Background: Glutamate and GABAergic dysregulation exacerbates excitotoxicity and disrupts motor circuitry, both contributing to PD pathology. The primary motor cortex (M1) is critical for motor executive function. Understanding how GABA and glutamate dysregulation in M1 contribute to PD motor executive dysfunction is crucial for targeted therapeutic development to mitigate disease progression. Utilizing 7T MRS offers an advantage in quantifying GABA and glutamate levels, aiding in the precise evaluation of neurotransmitter alterations in PD.

Method: We included 17 PD patients, 16 HCs and 10 patients with idiopathic rapid eye movement sleep behavior disorder (iRBD). 7T MRS data were acquired using a stimulated echo acquisition mode (STEAM) localization technique in M1. Metabolites including glutamate (Glu), gamma-aminobutyric acid (GABA), N-acetyl aspartate (NAA), phosphocholine (PCho), and glycerophosphocholine (GPC) concentrations were quantified by using LCModel software and then corrected for the partial volume effect of cerebrospinal fluid.

Results: The results demonstrated that compared with HC, GABA of the M1 cortex was significantly lower in PD and iRBD patients (PD vs HC: 1.00±0.60 vs 1.66±0.49, p=0.003; iRBD vs HC: 1.04±0.20, p=0.005). The absolute and actual GABA concentrations in the M1 cortex of PD patients showed a decreasing trend compared to iRBD, although the difference did not reach statistically significant. The concentration of PCho+GPC in iRBD significantly decreased compared to HC (iRBD vs HC: 2.30 ± 0.25 vs 2.78 ± 0.53, p=0.045) and PD (PD vs prodromal phase PD: 2.94 ± 0.59 vs 2.30 ± 0.25, p=0.009). The concentration of Glu was significantly positively correlated with the total UPDRS III score (r=0.53, p=0.037) and UPDRS III score of the more affected side (r=0.56, p=0.025). The absolute concentrations of NAA+NAAG (r=0.58, p=0.019) and Glu+Gln (r=0.52, p=0.037) were significantly positively correlated with the total UPDRS III score.

Conclusion: These findings may shed a light on the metabolic mechanism of PD motor executive dysfunction. The motor deficits may be related to the disorder of neurotransmitter transmission and brain energy metabolism.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/the-alteration-of-gaba-and-glutamate-in-parkinsons-disease-is-related-to-motor-executive-dysfunction-a-7t-mrs-study/