Nina Doorn

This study investigates how weak electric fields from deep brain stimulation (DBS) can modulate cortical neuron spike timing through computational models.

The paper identifies burst suppression as a default brain state linked to loss of network complexity, distinguishing between two forms with different clinical implications.

This study uses simulation-based inference to automatically identify molecular mechanisms from patient-derived neuronal network activity measured by MEA.

This study characterizes a human neuronal model of CACNA1A haploinsufficiency, revealing synaptic deficits and increased intrinsic excitability linked to reduced potassium channel function.

The paper investigates fragmented network bursts in patient-derived neurons using a biophysically detailed model and experimental validation, identifying short-term synaptic depression as a key mechanism.

This study investigates the role of the thalamus in resting-state functional connectivity using computational models, finding that its noisy inputs, not structural connectivity, drive cortical activity and enhance synchrony.