Clinton P. Turner

This study examines the immunophenotypic and ubiquitination diversity of Huntingtin inclusion bodies in Huntington's disease cerebral cortex, revealing heterogeneity in composition and degradation pathways.

This study shows that microglial morphology changes before immunophenotype shifts in ALS, driven by TDP-43 aggregation, suggesting morphological changes may trigger immunological responses.

This study identifies huntingtin as an RNA-binding protein that interacts with G-rich RNA sequences, including those in the NEAT1 paraspeckle lncRNA.

This study examines microglial activation and TDP-43 pathology in ALS brains, finding increased CD68 and L-ferritin expression in human and mouse models linked to pTDP-43 aggregation.

The paper compares ubiquilin 2 and TDP-43 aggregate distribution in UBQLN2-linked and sporadic ALS/FTD cases across the CNS.

The paper investigates the roles of canonical and alternative RPA in CAG repeat diseases, finding that Alt-RPA antagonizes RPA's suppression of CAG expansions, contributing to disease pathogenesis.

The paper identifies a hippocampal protein aggregation signature that distinguishes pathogenic from wildtype UBQLN2 in ALS/FTD cases.

The paper examines whether blood-spinal cord barrier breakdown correlates with motor neuron loss and TDP-43 proteinopathy in ALS, finding they have distinct regional patterns.

The paper identifies cardiac glycosides as regulators of neuroinflammatory pathways in brain-barrier tissues using in vitro and ex vivo human models.

This study identifies hotspot KRAS mutations as enriched in early brain metastases of melanoma, associated with worse survival and clonal origin, suggesting potential for risk stratification.