Rachel Heon‐Roberts

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 that reduced NEU1 activity in neurological MPS leads to hypersialylation of brain glycoproteins, contributing to CNS pathology through disrupted synaptogenesis and behavior.

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.

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 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.