Jordi Alberch

The paper shows that reduced IKZF1 and IKZF2 in immune cells of schizophrenic patients leads to impaired neural circuits and schizophrenia-like symptoms in mice and human cell models.

This study investigates how direct and indirect striatal pathways from DLS and DMS contribute to motor symptoms in HD mice, finding that these pathways are dysfunctional in HD.

This study shows that transient Yamanaka factor expression during development expands the neocortex and improves cognitive function in mice, while intermittent expression in adult neurons protects against Alzheimer's disease features.

This study investigates the role of the M2 cortex - superior colliculus circuit in Huntington's Disease, finding altered visual perception and behavioral responses in HD mice.

The paper shows that Egr1-dependent hippocampal neuronal ensembles limit motor learning in mice.

This study shows that RTP801 regulates synaptic transmission and motor learning by modulating synaptic plasticity in the motor cortex.

This study transplants HD patient-derived neurons into mice to observe in vivo degeneration and identifies mechanisms of disease propagation.

This study shows that optogenetic stimulation of fronto-striatal pathways in HD mice improves motor symptoms and synaptic plasticity.

This study shows that RTP801 mediates motor learning dysfunction in Huntington's disease by affecting synaptic plasticity, suggesting a therapeutic target through the RTP801/Akt/mTOR pathway.

This study identifies D1R-H3R heteromers as a therapeutic target for Huntington’s disease by showing their role in dopamine signaling and their modulation by H3R antagonists.