Our group, Translational Disease Models and Neurodegeneration, studies how tau and α-synuclein aggregates form, spread, and disrupt neural systems in Parkinson’s disease, Alzheimer’s disease, and frontotemporal dementias. We focus on the structural and mechanistic steps that turn normal proteins into disease-driving assemblies, and how specific mutations alter their behaviour, stability, and ability to propagate.

We develop targeted strategies that directly engage these processes, including peptide inhibitors that block the α-synuclein NAC region and compounds that interfere with the VQIVYK motif of tau. Alongside these protein-directed approaches, we investigate Bruton’s tyrosine kinase (BTK) as a modulator of neuroinflammation and test BTK inhibitors and BTK-oriented PROTACs to understand how kinase signalling shapes disease progression.

A significant aspect of our work involves linking therapeutic discovery to biomarker development. We refine and apply seed amplification assays (RT-QuIC and IP/RT-QuIC) to detect and functionally characterise pathological tau and α-synuclein seeds in patient samples, and we use these assays to evaluate the impact of candidate inhibitors under clinically relevant conditions.

Our research uses a broad experimental toolbox, including iPSC-derived neurons and glia, 3D neural cultures, organoids, and microfluidic co-culture systems. Across these platforms, our goal is clear: to translate mechanistic insights into therapies and biomarkers that meaningfully advance the early detection and treatment of neurodegenerative diseases.