Jens Christian Schwamborn

This paper develops a lab-on-a-chip system integrating a human BBB model with neural organoids to study BBB function and nanoparticle transport, showing BBB integrity and nanoparticle entry into neural tissue.

The paper introduces scGENet, a framework to generate interpretable gene networks from single-cell foundation models, revealing conserved neurogenic dysfunction in Parkinson's disease.

This study uses electrophysiological recordings from midbrain organoids to cluster action potential waveforms and identifies three categories, one potentially from dopaminergic neurons.

This study uses human iPSC-derived cells to model replicative senescence in neural progenitors and shows it induces astrocyte senescence in 2D cultures and midbrain organoids, linking it to Parkinson's disease.

This study shows that human midbrain organoids remain viable and show adaptive responses under microgravity and nutrient limitation on the ISS.

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.

This study shows that patient-derived microglia in midbrain organoids induce endogenous alpha-synuclein pathology without exogenous seeding.

This study evaluates the reproducibility of midbrain organoid data from healthy individuals and GBA-N370S PD patients across batches and time points, showing consistent transcriptomic and metabolic signatures.

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.

The paper assesses mitochondrial DNA and neurofilament light chain levels in midbrain assembloids to identify Parkinson's disease phenotypes and potential biomarkers.

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 study shows DJ-1 affects metabolism and immune response differently in Parkinson's disease and glioblastoma cells, with antioxidant treatment rescuing PD-related phenotypes.

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

This study shows that CLN3 deficiency in zebrafish leads to metabolic changes, including GPD accumulation and BMP reduction, and confirms these findings in human stem cell models.

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

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

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.

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 investigates neuronal activity in LRRK2-G2019S mutant neurons and finds increased spontaneous calcium transients and shorter inter-spike intervals.

This study compares single-cell transcriptomes of human brainstem and midbrain organoids, identifying unique cell types and similarities with fetal midbrain data.

The paper uses single-cell RNA-sequencing to identify multiple neuronal cell types in human midbrain organoids, including dopaminergic, GABAergic, and glutamatergic neurons.

This study shows that HP-β-CD treatment improves dopaminergic differentiation in PD patient-derived midbrain organoids by enhancing mitophagy.

This study transplants Parkinson's patient iPSC-derived neurons into mice, finding increased alpha-Synuclein levels but no spreading in the mouse brain.

This paper introduces a novel method to generate midbrain-specific human organoids from neuroepithelial stem cells, which exhibit dopaminergic neurons, synaptic connections, and myelination, making them suitable for Parkinson's disease research.