Enrico Glaab

This study identifies ZFHX4 as a key regulator of midbrain dopaminergic neuron differentiation by controlling cell cycle progression through the LIN28A-miR-9 axis.

The paper integrates metabolomic and transcriptomic data from ADPKD patients to identify metabolic reprogramming linked to cystogenesis and disease progression.

This study uses Boolean modeling on PD cohorts to show sex-specific miRNA dysregulation affects mitochondrial biogenesis, mitophagy, and autophagy in Parkinson's disease.

This study shows insulin resistance in midbrain organoids reduces metabolic efficiency and neural activity, contributing to Parkinson's disease pathology.

This study shows that PLCG2 downregulation impairs synaptic function and increases Alzheimer's disease-related markers in neurons.

This study shows SARS-CoV-2 infection causes gene expression changes and dopaminergic neuron loss in midbrain organoids over time.

The paper describes the development of a computational knowledge repository, the COVID-19 Disease Map, which curates SARS-CoV-2 virus-host interaction mechanisms and provides tools for their analysis and application.

The paper develops a pharmacophore model for SARS-CoV-2 3CLpro inhibitors and validates computationally screened compounds experimentally.

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

The paper develops genome-scale metabolic models of human dopaminergic neurons to study metabolic dysfunction in Parkinson's disease using exometabolomic and transcriptomic data.

This study uses a synuclein-transgenic mouse model to identify molecular changes in early Parkinson's disease before neurodegeneration occurs.

The paper predicts cellular positions in the Drosophila embryo using scRNA-seq data by benchmarking methods against spatially annotated genes.

The paper investigates the role of alpha-synuclein spreading and inclusions in Parkinson disease using a mouse model, finding that neurodegeneration and microgliosis occur independently of inclusions.