Oliver Brüstle

This study uses human oligodendrocyte spheroids to model leukodystrophies and identifies disease-specific transcriptional changes and lineage-specific vulnerabilities.

This study converts human blood cells into induced neural stem cells, showing prolonged epigenetic de-aging and delayed acquisition of neural stem cell identity over time.

This study demonstrates the generation of functional human sensory neurons from iPSCs using NBI factors, showing their electrophysiological properties and disease relevance.

The paper develops an imaging and analysis framework to map human microglial activation states using handcrafted and deep learning features, showing deep learning features achieve high classification accuracy and correlate with biological states.

This study shows JAK inhibitors block RA synovial fluid-induced sensory neuron activation by inhibiting STAT3 phosphorylation and pain gene expression.

The paper investigates the effects of inflammatory soup on sensory neuron excitability using human and mouse models, finding minimal changes and suggesting that in vitro modeling of peripheral sensitization is complex.

The paper develops a technique to image human brain organoids at mesoscopic and super-resolution scales, revealing cellular and synaptic structures during development.

This study identifies how GDAP1 loss of function disrupts actin signaling, leading to mitochondrial tubularity and metabolic changes in CMT4A.

The paper uses machine learning to classify Parkinson's disease patient-derived midbrain dopaminergic neurons based on multiple image-based phenotypes and identifies treatable targets.

This study identifies nutrient signaling pathways that regulate amyloid clearance and synaptic loss in Alzheimer's disease, showing both protective and harmful effects.

This paper shows anthrax toxin can target and modulate pain by acting on nociceptive neurons through ANTXR2, with potential for new pain therapeutics.

This study identifies Reelin's role in promoting fast, laterally-directed migration of midbrain dopaminergic neurons through stabilization of leading processes and induction of bipolar morphology.