Archival ReportValidating γ Oscillations and Delayed Auditory Responses as Translational Biomarkers of Autism
Section snippets
Subjects
The STG M100 latency findings for these subjects were previously reported (3). In this study, data were further analyzed to examine left- and right-hemisphere STG γ power and phase-locking. The MEG data collection and analysis procedures are briefly described in the following. Children with ASD (n = 25, age 10.20 ± 2.15) and typically developing children (TD) (n = 17, age 10.77 ± 1.98) participated. Subject inclusion, screening, and diagnostic assessment were performed as previously published (3
Human MEG
As reported, subjects with ASD showed an approximate 10% delay in the right hemisphere M100 response (Figure 2) [F(1,38) = 7.6, p < .009] (3). With a cutoff of 116 msec, M100 latency classified ASD subjects with a sensitivity of 75% and specificity of 81% (3). Building on these findings, transient γ-band power and phase-locking were calculated to assess neural oscillatory activity. The ASD subjects showed significantly reduced γ phase-locking across hemispheres (Figure 2) [F(1,43) = 5.2, p <
Discussion
This study characterizes two electrophysiological endophenotypes of autism in parallel human and mouse studies. Autistic subjects show delayed M100 STG responses and reduced γ-band phase-locking. In mice, prenatal VPA exposure causes selective behavioral alterations in domains affected in autism, including social and communicative functioning. The VPA model mirrors evoked-response latency delays and γ-band deficits identified in the clinical population. In mice, electrophysiological measures
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