Research

Parkinson’s disease (PD) is a neurodegenerative disease characterised by the loss of dopaminergic neuronal cells and the deposition of protein inclusions called Lewy bodies (LBs). LBs are not only composed of proteins but also lipid molecules and their main constituent in the pre-synaptic protein alpha-synuclein. αS is proposed to interact with membranes in the context of its proposed physiological function, i.e. synaptic plasticity, but this protein-lipid interaction can also lead to the co-assembly of αS and lipids into amyloid fibrils. Our research aims at understanding the molecular determinants responsible for the initiation of PD pathology in particular the role of lipids in this process.

Biophysics

Biophysical characterisation of protein-membrane interactions

We investigate the influence of the lipid composition on the thermodynamics of alpha-synuclein-membrane interactions as well as the kinetics of amyloid fibrils formation using a range of biophysical techniques including circular dichroism, microfluidic diffusion, calorimetry, fluorescence spectroscopy and electron microscopy.

See relevant publications: Nature Chemical Biology, PNAS, PCCP

Cell biology

Cellular Models of Parkinson’s disease

We model Parkinson’s disease and its risk factors (environmental and genetic) in fibroblasts and dopaminergic neuronal cell lines and we characterise their biochemical properties using enzymatic assays, Western Blot and qPCR analyses, bright field and fluorescence microscopy.

See relevant publications: Brain and BBA

Omics

Lipid changes associated with Parkinson’s disease

Increasing evidence points towards an interplay between changes in lipid levels and Parkinson’s disease. We investigate changes in lipid levels and properties associated with Parkinson’s disease using lipidomics analyses of patient-derived samples.

See relevant publications: Brain, bioRxiv