Douglas W. Allan

This study shows that human Tau isoforms have context-dependent toxicity in a Drosophila model, with variations in expression timing, tissue type, and neuronal identity affecting degeneration outcomes.

This paper describes using Drosophila wing discs to study Tau-mediated disease mechanisms and screen for neuroprotective drugs, showing that human Tau causes cell death and that NAP reduces toxicity.

The paper develops a yeast growth assay to assess the functional impact of ALDH5A1 variants linked to autism spectrum disorder, showing they range from loss of function to normal activity.

The paper assesses nine MECP2 variants in ASD using yeast and Drosophila assays, finding four as loss of function and five as functional, highlighting non-methyl DNA-binding roles.

This study shows that Tau aggregation, not phosphorylation, is critical for neurotoxicity in Drosophila, suggesting that targeting aggregation may be more effective than targeting phosphorylation in tauopathies.

This study shows that Fasciclin 3 is required for the maintenance of adult olfactory interneurons in Drosophila, as its knockdown leads to neuronal death and reduced adult survival.

The paper uses Drosophila to functionally assess human EED variants, showing that pathogenic variants cause loss of function while benign variants function normally.

The paper identifies fourteen guidance genes essential for adult Drosophila nervous system survival and motility through RNAi screening, highlighting the role of Semaphorins and Plexins in motoneuron survival.

The paper evaluates 106 PTEN variants using 18 assays across 5 models to identify molecular mechanisms of dysfunction, finding that stability and domain-specific assays are critical for accurate impact assessment.