Jon-Ruben van Rhijn

This study uses human iPSC-derived neuronal networks to show that homeostatic plasticity involves network re-arrangement, increased excitability, and changes in gene expression related to extracellular matrix and cell communication.

This study shows that SETD1A loss-of-function mutations increase dendritic complexity and neuronal bursting in human neurons via a hyperactive cAMP/PKA pathway, which can be rescued by pharmacological intervention.

This study investigates the role of CDH13 in regulating GABAergic inhibition in human-derived neuronal networks and shows its impact on E/I balance.

This study shows that MAOA dysfunction in Brunner syndrome leads to increased NMDAR activity and neuronal network hyperactivity in dopaminergic neurons.

This study shows that EHMT1 deficiency in human neurons leads to NMDAR hyperfunction, causing neuronal network dysfunction in Kleefstra syndrome, and demonstrates pharmacological rescue of these phenotypes.

This study investigates MAOA dysfunction in Brunner Syndrome using iPSC-derived dopaminergic neurons, finding increased NMDA receptor expression and network activity.