Benjamin J. O’Callaghan

This study shows that glucose levels in neuronal culture media affect PINK1-dependent mitophagy in human iNeurons, with BrainPhys medium reducing mitophagy compared to N2B27.

This study shows that the SNCA A53T mutation increases vulnerability to ferroptosis in neurons and microglia, suggesting 15-LO inhibition as a potential therapeutic target for Parkinson's disease.

The paper identifies splicing dysregulation in Parkinson's disease linked to TDP-43 loss of function and shows its association with genetic mutations and cellular models.

The paper investigates how the 17q21.31 locus influences Parkinson's disease through KANSL1 activity, showing haplotype-specific effects on key biological processes.

This study generates hiPSC-derived myofibres with the m.3243A>G mutation to model mitochondrial disease, showing metabolic and physiological changes related to mutation load.

This study shows that KAT8 inhibition via MG149 blocks PINK1-dependent mitophagy initiation but promotes mitochondrial delivery to lysosomes without toxins.

The paper investigates the regulatory role of the NSL complex in Parkinson's disease by analyzing gene expression and regulatory networks in brain tissues.

The paper identifies KAT8 and KANSL1 as regulators of PINK1-mitophagy linked to Parkinson's disease risk, suggesting a novel pathway for therapeutic targeting.

This study shows that spinal cord dysfunction contributes to DYT1 dystonia by creating mouse models with dystonia-like symptoms.