Monica Frega

This study compares three metabolic stress models on human-derived neuronal networks, showing distinct effects on activity and viability, with limited recovery after reoxygenation.

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 examines sex differences in neuronal response to hypoxia, finding that estrogen modulates network activity but does not provide long-term neuroprotection.

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 models mTORopathy-related epilepsy in cultured murine hippocampal neurons using a multi-electrode array to identify network activity phenotypes and test drug treatments.

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 investigates SCN1A mutations in excitatory neuronal networks derived from patient hiPSCs, revealing mutation-specific phenotypes that correlate with clinical outcomes and drug responses.

The paper benchmarks MEA recordings from healthy hiPSC-derived neuronal networks to establish standards for experimental design and analysis, showing MEAs are robust for disease-phenotyping and drug discovery.

This study shows that KANSL1 deficiency leads to oxidative stress-induced autophagy, causing synaptic dysfunction and neuronal network impairments in neurons.

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 investigates how KMT2D mutations in Kabuki Syndrome disrupt neuronal function through chromatin and transcriptional changes, independent of H3K4me1.

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 mitochondrial dysfunction in human neurons, caused by high heteroplasmy of the m.3243A>G variant, leads to impaired neural development, reduced synaptic connectivity, and decreased network activity.

The paper investigates how mutations in distinct genes causing intellectual disability and autism affect neuronal network development, finding shared effects on excitability and synaptic function.

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.