Cláudia Saraiva

This study uses iPSC-derived neurons and midbrain organoids with SNCA triplication to show autophagy defects correlate with -Synuclein pathology and neuronal loss in Parkinson's disease.

This study creates vascularized midbrain organoids to model Parkinson's disease, showing increased neuroinflammation and dopaminergic neuron vulnerability in patient-derived assembloids.

The paper integrates multi-modal data to identify shared molecular dysregulation across Parkinson's disease variants, finding common transcriptomic features in glial cells and potential involvement of ROBO signalling.

This study shows that a Miro1 mutation causes mitochondrial dysfunction and dopaminergic neuron loss in both cell models and mice, supporting its role in Parkinson's disease.

This paper introduces midbrain-striatum assembloids with inducible aging to model early Parkinson's disease phenotypes and nigrostriatal connectivity.

This study integrates human iPSC-derived microglia into midbrain organoids, enhancing neuronal maturation and functionality through effects on synaptic remodeling and excitability.

This study uses patient-specific midbrain organoids with SNCA triplication to show synaptic decline precedes dopaminergic neuron loss in Parkinson's disease.