Decreased BOLD signal variability in middle-aged and older adults on the Autism Spectrum
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Purpose
Autism spectrum disorder (ASD) is a lifelong neurodevelopmental disorder. Preliminary evidence suggests an increased risk for accelerated or early-onset cognitive and neurological decline in ASD. While it is well established that brain development in children, adolescents and young adults with ASD diverges from neurotypical (NT) peers, it is unknown how brain function is impacted in older adults with ASD. Understanding age-related changes of brain function in ASD is crucial to establish best practices for cognitive and health screenings in adults with ASD and develop interventions that might reduce the risk of accelerated decline. Decreases in blood-oxygenation-level-dependent (BOLD) signal variability (BSV) in typical aging have been shown across multiple studies, likely reflecting declining Gamma-Aminobutyric Acid (GABA) activity, and is associated with poorer cognitive performance. We hypothesized that adults with ASD would show reduced BSV compared to the NT group, with steeper negative age associations in the ASD than NT group.
Methods
The study assessed BSV in a cohort of adults (40-70 years), 28 with ASD and 39 age-matched NT. General linear models tested for main effects of diagnostic group (ASD, NT), age and group-by-age interactions (controlling for RMSD).
Limitations
Our cross-sectional data and small sample size highlight the need for longitudinal analyses in larger cohorts, alongside exploring links to cognitive function. Additionally, psychotropic medications used by our cohort of adults on the autism spectrum may have affected BSV.
Results
Significant group-by-age interactions were observed for the right insular, left temporal occipital fusiform, right frontal orbital and right inferior lateral occipital cortex, with BSV showing strong negative associations with age in the ASD but not NT group.
Conclusion
These findings suggest that BSV decreases may occur earlier in adults on the autism spectrum compared to their neurotypical peers, possibly indicating accelerated aging. However, given limited prior research, additional longitudinal analyses will be necessary to determine if the results presented truly reflect accelerated aging or arise from lifelong persistent differences in brain function.
