Horia Pribiag

This study investigates Akap11 mutant mice to explore the neurobiological effects of AKAP11 loss, finding increased PKA activity and transcriptomic changes linked to schizophrenia and bipolar disorder.

This study shows that GPR34 maintains microglial homeostasis and limits disease-associated microglial responses in Alzheimer's disease models.

This study identifies AKAP11's role in regulating lipid metabolism and neuronal support in astrocytes, linking its dysfunction to schizophrenia and bipolar disorder risk.

The paper identifies two distinct GPe-PV neuron pathways in mice and shows they contribute to different Parkinsonian symptoms through differential electrophysiological responses to dopamine depletion.

This study shows that depolarizing GABAA transmission inhibits glutamatergic synapse formation in developing hippocampal neurons, with effects that persist after the transmission switches to hyperpolarizing.