David J. A. Wyllie

This study shows astrocytes alter the transcriptomic and epigenetic landscape of developing cortical neurons, promoting intrinsic excitability and influencing disease-related pathways.

The paper introduces Gene Portals, a framework that integrates clinical, functional, and structural data for rare disease variant classification, demonstrating its utility across five gene-specific portals.

This study shows that reduced GluN2A expression in rat models decreases seizure-like activity in specific in vitro epilepsy models.

This study shows that neurodevelopmental processes in the cortex and thalamus can occur normally without microglia, using a genetically modified mouse model.

The paper examines flight-freeze response imbalances in Nlgn3-/y rats, finding hyperexcitability in periaqueductal grey neurons linked to altered fear behaviors.

This study investigates synaptic function in a Cdkl5 KO rat model of CDKL5 deficiency disorder, finding normal NMDA and AMPA receptor function but altered synaptic density and plasticity.

This study shows that loss of FMRP in a mouse model of Fragile X Syndrome leads to increased single-spine excitation and more multiply-innervated spines, contributing to circuit hyperexcitability.

The paper investigates the impact of a t(1;11) translocation on white matter integrity and oligodendrocyte-myelin function using DTI and cellular models.

The paper investigates how cellular and synaptic compensations in Fmr1-KO mice affect sensory processing in the barrel cortex, finding that despite compensatory mechanisms, sensory encoding precision is lost, leading to hypersensitivity.