J. Robin Highley

Two functionally distinct amyloid-β intermediates link aggregation pathways to pathology in Alzheimer's disease

This study identifies two distinct amyloid-β intermediates that drive Alzheimer's pathology and shows their suppression reduces plaque burden and improves cognition in mice.

STMN2 protein depletion via translation deficits and stress granules and its compensation in ALS

This study identifies TDP-43-independent mechanisms of STMN2 depletion in ALS, showing acute stress causes proteasomal degradation and translational repression, while chronic stress leads to reduced protein levels, with mRNA upregulation as a compensatory mechanism in some subtypes.

Secondary nucleation of α-Synuclein drives Mitochondria dysfunctions and Lewy body formation in Parkinson's Disease

This study identifies secondary nucleation of α-Synuclein as the key mechanism driving mitochondrial dysfunction and Lewy body formation in Parkinson's Disease.

Molecular determinants of protein pathogenicity at the single-aggregate level

This study investigates how variations in protein aggregate size, composition, and mutations affect biological functions in Alzheimer's and Parkinson's diseases.

GRASPS: a simple-to-operate translatome technology reveals omics-hidden disease-associated pathways in TDP-43-related amyotrophic lateral sclerosis

GRASPS identifies more differentially expressed transcripts with higher fold changes and significance in TDP-43 ALS models, revealing previously missed disease pathways.