Brent James Ryan

The paper uses patient-derived iPSC-dopamine neurons to screen compounds and identifies the FASN-SREBP1 axis as a potential therapeutic target for Parkinson's disease.

This study shows simvastatin reduces PD-related phenotypes in iPSC-derived neurons by inhibiting RhoA, with RhoA activity varying across PD subtypes.

This study identifies phosphorylated ubiquitin (pS65Ub) as a signaling molecule that mediates mitochondrial-to-nuclear communication by modulating histone ubiquitination and gene expression in Parkinson's disease.

This study shows LUBAC activates AMPK and OTULIN restricts it, affecting metabolic responses to energy stress in cells, mice, and flies.

The paper examines TFEB and TFE3 expression and function in brain cells, showing TFEB is restricted to glia while TFE3 is widespread, with distinct roles in mitochondrial and lysosomal biogenesis in neurons.

The paper identifies chromatin modifications and regulatory elements that enable long-term transcriptional memory of IFNγ exposure in immune cells.

This study shows USP30 inhibition improves mitochondrial health through both PINK1-dependent and independent mechanisms, enhancing mitophagy and mitochondrial efficiency in neurons.

This study uses proteomic techniques to show that PGRN deficiency impairs lysosomal function and proteostasis in neurons by altering pH, enzyme levels, and protein turnover.

This study uses a novel proteomics platform to identify PTM dysregulation in GBA-N370S PD neurons, revealing impaired neuritogenesis and a role for tau.

This study identifies altered mitochondrial and energy metabolism in PARK2 mutant human iPSC-derived dopaminergic neurons through metabolomic analysis.

This study investigates lysosomal alterations in PARK2 knockout dopaminergic neurons derived from iPSCs, revealing links between parkin deficiency and lysosomal dysfunction in Parkinson's disease.