Christoph Erbacher

This study models Fabry disease in human sensory neurons and finds axon guidance deficits and reduced neurite length due to Gb3 accumulation, with partial rescue by AGAL enzyme supplementation.

The paper isolates nerve terminals from NaV1.9 knockout mice and performs proteomic analysis to identify dysregulated pathways in neuropathic pain signaling.

The paper investigates the interaction between human keratinocytes and nerve fibers at the neuro-cutaneous unit using advanced imaging techniques and a co-culture system.

This study creates a neuronal in vitro model of Fabry disease to investigate small fibre neuropathy mechanisms, finding Gb3 accumulation, altered ion channel function, and mitochondrial trafficking issues.