Author:
Maier Simon,Nickel Kathrin,Lange Thomas,Oeltzschner Georg,Dacko Michael,Endres Dominique,Runge Kimon,Schumann Anke,Domschke Katharina,Rousos Michalis,Tebartz van Elst Ludger
Abstract
Abstract
Introduction
Autism spectrum disorder (ASD) encompasses a heterogeneous group with varied phenotypes and etiologies. Identifying pathogenic subgroups could facilitate targeted treatments. One promising avenue is investigating energy metabolism, as mitochondrial dysfunction has been implicated in a subgroup of ASD. Lactate, an indicator of energy metabolic anomalies, may serve as a potential biomarker for this subgroup. This study aimed to examine cerebral lactate (Lac+) levels in high-functioning adults with ASD, hypothesizing elevated mean Lac+ concentrations in contrast to neurotypical controls (NTCs).
Materials and methods
Magnetic resonance spectroscopy (MRS) was used to study cerebral Lac+ in 71 adults with ASD and NTC, focusing on the posterior cingulate cortex (PCC). After quality control, 64 ASD and 58 NTC participants remained. Lac+ levels two standard deviations above the mean of the control group were considered elevated.
Results
Mean PCC Lac+ levels were significantly higher in the ASD group than in the NTC group (p = 0.028; Cohen’s d = 0.404), and 9.4% of the ASD group had elevated levels as compared to 0% of the NTCs (p = 0.029). No significant correlation was found between blood serum lactate levels and MRS-derived Lac+ levels.
Limitations
A cautious interpretation of our results is warranted due to a p value of 0.028. In addition, a higher than anticipated proportion of data sets had to be excluded due to poor spectral quality.
Conclusion
This study confirms the presence of elevated cerebral Lac+ levels in a subgroup of adults with ASD, suggesting the potential of lactate as a biomarker for mitochondrial dysfunction in a subgroup of ASD. The lower-than-expected prevalence (20% was expected) and moderate increase require further investigation to elucidate the underlying mechanisms and relationships with mitochondrial function.
Funder
Deutsche Forschungsgemeinschaft
Universitätsklinikum Freiburg
Publisher
Springer Science and Business Media LLC
Subject
Psychiatry and Mental health,Developmental Biology,Developmental Neuroscience,Molecular Biology
Cited by
1 articles.
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