Alison L. Hogan

SFPQ dysregulation promotes TDP-43 pathology through a pathogenic feedback loop

This study identifies SFPQ as a contributor to TDP-43 pathology through a bidirectional feedback loop, showing SFPQ dysregulation drives TDP-43 mislocalization and aggregation.

Human TDP-43 overexpression in zebrafish motor neurons triggers MND-like phenotypes through gain-of-function mechanism

This study uses zebrafish models to show that human TDP-43 overexpression in motor neurons causes MND-like phenotypes through gain-of-function mechanisms, with distinct effects based on TDP-43 variant.

The post-translational modification SUMO affects TDP-43 phase separation, compartmentalization, and aggregation in a zebrafish model

This study shows that SUMO modification affects TDP-43 phase separation and aggregation in zebrafish spinal neurons, linking post-translational changes to ALS pathology.

Flow cytometry allows rapid detection of protein aggregates in cell culture and zebrafish models of spinocerebellar ataxia-3

This study uses flow cytometry to detect and quantify protein aggregates in SCA3 models, showing early aggregation before movement impairment and responsiveness to autophagy modulators.

SFPQ intron retention, reduced expression and aggregate formation in central nervous system tissue are pathological features of amyotrophic lateral sclerosis

This study examines SFPQ dysregulation in ALS patients, finding increased intron retention, reduced mRNA expression in motor cortex, and cytoplasmic aggregates.

In Vivo Validation of Bimolecular Fluorescence Complementation (BiFC) to Investigate Aggregate Formation in Amyotrophic Lateral Sclerosis (ALS)

The paper validates and optimizes Bimolecular Fluorescence Complementation (BiFC) in zebrafish to study ALS-linked protein aggregate formation in vivo.