Nicholas Christiansen

This study investigates microscale and mesoscale changes in ALS motor neuron networks using in vitro models, showing increased network centralisation and rich-club connectivity as compensatory mechanisms.

This study shows that blocking potassium channels with TEA improves synaptic stability and restores network function in ALS motor neuron networks.

This study identifies early synaptic dysfunction in ALS patient-derived motor neurons as a mechanism contributing to network-wide structural and functional compensation and vulnerability to neurodegeneration.

This study uses spatial network models to show that wiring cost and spatial clustering influence network topology, with long-range connections improving global communication and resilience to pruning.

The paper shows ALS patient-derived motor neuron networks develop cytopathology and form efficient networks with functional impairments and heightened vulnerability to perturbation.

This study inhibits excitatory synaptic transmission in vitro neural networks and finds increased burstiness and synchrony over time, suggesting E/I balance is critical for normal bursting dynamics.