Claire S. Durrant

This study establishes an adult-onset Drosophila model of tauopathy, revealing sex-specific effects on survival and behavior and identifying genetic modifiers of tau-induced dysfunction.

This study shows that FMRP depletion in human neurons causes cyclic-AMP-dependent hyperexcitability, which can be corrected by inhibiting phosphodiesterase 4D.

The paper tests for axon initial segment (AIS) structural plasticity in human, mouse, and rat cortical neurons across different conditions and finds no evidence of AIS length changes over short-term activity modulation.

This study uses live human brain slice cultures to show that physiological and pathological amyloid-beta have opposing effects on synapses, with physiological levels enhancing synaptic transcripts and pathological levels causing synaptic loss.

This study quantifies how GABAB receptor signalling contributes to circuit-level inhibition in rat and human cortical principal cells across the lifespan, revealing age and species differences.

This study shows that lowering glucose increases Aβ levels in mouse brain slices and human cells, likely via BACE1 activation, but not in hypoxia conditions.

The paper identifies transmembrane protein 97 as a synaptic receptor for amyloid beta in human Alzheimer's disease using advanced microscopy and drug intervention studies.

The paper shows Drosophila melanogaster resist trans-synaptic spread of human tau, suggesting they are not suitable for screening tau propagation modifiers.

This study shows that retaining proteins in the ER can rescue Aβ toxicity in Drosophila and mouse models, suggesting a potential therapeutic strategy for Alzheimer's disease.

The paper investigates whether tau assemblies behave like independently acting prion-like particles in mouse neural tissue and finds that seeding behavior only occurs at supra-physiological concentrations.

This study shows that BACE1 inhibition reduces excessive vascular sprouting in AD by restoring NOTCH3 signaling and normalizing endothelial filopodia formation.

This study develops an organotypic hippocampal slice culture model of neuroinflammation and shows that LPS-induced synaptophysin loss depends on microglia and IL1β.