Craig A. Erickson

The paper analyzes EEG data from 4,812 individuals to identify shared and distinct neurophysiological signatures across psychiatric conditions and rare genetic variants.

This study finds reduced neural entrainment to word-level speech patterns in children with Fragile X Syndrome, indicating impaired statistical learning.

This study analyzes alpha oscillations in Fragile X syndrome, revealing sex-specific and region-specific abnormalities in burst characteristics that correlate with clinical symptoms.

This study investigates the role of ZMYND11 in neurodevelopment by analyzing its effects on cortical neural stem cells and splicing regulation in ASD risk factors.

The paper introduces ERSSP, an EEG analysis framework to study extralemniscal thalamocortical activity, validated in Fragile X Syndrome showing increased spatial power increases.

This study investigates neural correlates of auditory hypersensitivity in FXS using EEG source analysis, finding frontal cortex hyperactivation and gamma desynchrony linked to auditory processing issues.

The paper identifies a shared electrophysiological biomarker of Fragile X Syndrome in human and mouse models, showing slowed alpha oscillations linked to FMRP loss in excitatory neurons.

This study uses iPSC-derived neurons to show that FMRP deficiency in fragile X syndrome leads to m6A-mediated transcriptome dysregulation, causing synaptic dysfunction and suggesting therapeutic targets.

The paper shows that FXS mice show impaired performance on distractor tasks, linked to reduced modulation of VIP interneurons.

The paper uses latent class analysis to identify distinct behavioral subtypes in children with fragile X syndrome, revealing clinically meaningful groups with unique cognitive and behavioral profiles.

The paper identifies 60 new moderate risk genes for autism by integrating de novo and inherited variants across 42,607 cases and 236,000 controls.

The paper reports exome sequencing of 457 ASD families, identifying 10.4% with known ASD genes and 3.4% with possibly associated variants, and provides statistical support for 34 ASD risk genes using the TADA framework.

This study identifies parvalbumin neuron dysfunction in V1 as a mediator of impaired perceptual learning in Fragile X syndrome and shows that restoring PV neuron activity can reverse the deficit.