Erwan Bézard

This study identifies shared and distinct lipid profile changes in amygdala from sporadic and GBA-associated Parkinson's Disease, linking lipid metabolism to alpha-synuclein and glucocerebrosidase activity.

This study identifies WDR44 as a driver of de novo α-synuclein aggregation at the lysosomal membrane, linking early aggregation events to neuronal dysfunction in Parkinson's Disease.

This study uses UPLC-MS to analyze amino acid profiles in post-mortem brain tissue from PD and AD patients, revealing region-specific metabolic changes.

This study shows synthetic alpha-synuclein fibrils can replicate in mice, causing MSA-like pathology and forming glial cytoplasmic inclusions.

This study investigates amyloid plaque penetrability and extracellular space rheology in an AD mouse model using imaging techniques, finding heterogeneous diffusivity and dysregulated extracellular matrix around plaques.

This study identifies a subset of dorsal raphe dopamine neurons (DRNVIP) critical for regulating threat assessment and defensive behaviors through feedback loops with the central extended amygdala.

This study identifies interhemispheric Insula neurons in mice and shows their role in social and anxiety processing through electrophysiology and circuit manipulation.

The paper compares aggregated alpha-synuclein in Parkinson's disease and multiple system atrophy brains to determine their proteomic composition and potential cross-seeding mechanisms.

This study shows that amyloid beta oligomers impair autophagy in neurons via the primary cilium, with age-dependent effects mediated by Akt and p75NTR.

Stealth α-synuclein fibrils escape ThT detection, outcompete visible polymorphs, and spread neurodegeneratively in vivo.

The paper uses machine learning to identify neurodegeneration signatures in non-human primates caused by patient-derived α-synuclein structures, showing that small aggregates are as toxic as larger fibrils.

The paper validates DREADD-based inhibition of pallidal neurons in non-human primates using electrophysiological recordings and histochemical analysis.

This study shows that enhancing sonic hedgehog signaling reduces L-Dopa-induced dyskinesia in Parkinson's models by targeting dopamine neurons and cholinergic interneurons.