Angela S. Laird

Gut transit and gut microbiome changes occur prior to the onset of motor impairment in a mouse model of Machado-Joseph disease

This study shows that gut microbiome changes and colonic dysfunction occur before motor impairments in MJD mice, suggesting inflammation and endocrine factors may link gut and brain in disease progression.

Mitochondrial dysfunction in Machado Joseph disease: insights from a multi-model system

This study investigates mitochondrial dysfunction in Machado Joseph disease using multiple models, finding impaired oxidative phosphorylation and altered mitochondrial morphology in mice and zebrafish.

Treatment with sodium butyrate induces autophagy resulting in therapeutic benefits for spinocerebellar ataxia type 3

This study shows that sodium butyrate improves symptoms of SCA3 by enhancing autophagy through PKA/AMPK signaling in both cell and zebrafish models.

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.

Protein disulphide isomerase (PDI) is protective against several types of DNA damage, including that induced by amyotrophic lateral sclerosis-associated mutant TDP-43 in neuronal cells/ in vitro models

This study shows PDI protects neuronal cells from DNA damage caused by etoposide, H2O2, or mutant TDP-43, and localizes to DNA damage sites in the nucleus.

Sodium valproate increases activity of the sirtuin pathway resulting in beneficialeffects for spinocerebellar ataxia-3 in vivo

The paper shows sodium valproate activates the sirtuin pathway, improving movement in a zebrafish model of spinocerebellar ataxia-3.

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.

Accelerated loss of hypoxia response in zebrafish with familial Alzheimer's disease-like mutation of Presenilin 1.

This study shows that zebrafish with PSEN1 mutations exhibit accelerated hypoxia response loss with age, suggesting a link between PSEN1 dysfunction and Alzheimer's disease pathogenesis.