Lorenz Studer

This paper shows that timed WNT pulses can specify distinct neural domains in human pluripotent stem cells, enabling the generation of specific neuron and progenitor types.

This study shows EHMT1's functional rewiring during human cortical neurogenesis, revealing its shift from restraining pluripotency to supporting neuronal programs and its resilience to prolonged depletion.

This study develops a method to derive and maintain specific subtypes of human midbrain dopaminergic neurons in vitro, revealing their functional and molecular characteristics and potential vulnerability in disease.

This paper presents a protocol to rapidly generate human oligodendrocytes from pluripotent stem cells using BMP and Notch signaling inhibition, achieving high purity and functional myelination.

NERINE tests gene network hypotheses with rare variant associations, identifying a subnetwork linked to Parkinson's disease.

The paper benchmarks dopaminergic stem cell models and cell therapy candidates using a human brain atlas to identify off-target populations and lineage plasticity.

The paper introduces scJLIM, a cluster-free method for single-cell colocalization testing, improving power to link GWAS loci with gene expression changes in specific cell types.

This study investigates the role of ZMYND11 in neurodevelopment by analyzing its effects on cortical neural stem cells and splicing regulation in ASD risk factors.

This study develops a CRISPRa-based method to rapidly verify gene editing in human pluripotent stem cells without differentiation.

This study identifies 3D regulatory hubs in glioblastoma stem cells and shows their role in oncogenic programs through computational and experimental analysis.

This study improves the yield and subtype identity of hPSC-derived midbrain dopamine neurons through optimized WNT and FGF18 signaling modulation, enhancing their functional and transcriptional similarity to primary neurons.

The paper develops a cortical assembloid system to study human PVALB+ interneuron development and identifies schizophrenia-associated defects in their migration and molecular profiles.

Genipin rescues developmental and degenerative defects in familial dysautonomia and enhances neuron regeneration after injury.

The paper demonstrates the feasibility of identifying biologically active DNA aptamers that modulate the activity of human SH-SY5Y neuroblastoma cells.

The paper identifies p53-mediated apoptosis and TNF-NFkB signaling as key factors limiting survival of grafted dopamine neurons and shows that adalimumab treatment improves their engraftment and function in a PD mouse model.

This study generates human cerebral organoids with a structured outer subventricular zone by activating the STAT3 pathway with LIF, mimicking in vivo oRG development and enhancing neuronal maturation.

The paper identifies a shared genetic risk module involving PSEN2 and actin regulation across alpha-synucleinopathies, linking them to Alzheimer's disease mechanisms.

This study identifies a gene regulatory pathway involving SATB1, MIR22HG, and GBA that leads to glucocerebroside accumulation and cellular senescence in dopaminergic neurons, contributing to Parkinson's Disease and aging.

Chromatin regulators including EZH2, EHMT1/2, and DOT1L establish an epigenetic barrier in human neural progenitors that poises maturation genes and sets the protracted pace of cortical neuron maturation.

This study identifies a drug cocktail that accelerates maturation of hPSC-derived neurons and other cell types through pharmacological intervention.

This study derives Schwann cells from human pluripotent stem cells to model diabetic peripheral neuropathy and identify a drug candidate that rescues sensory function and prevents myelin damage.

This study shows that loss of SATB1 in dopaminergic neurons leads to cellular senescence through p21 activation, suggesting a role for senescence in Parkinson's disease pathology.

The paper identifies a subclass of sporadic ALS patients with metabolic defects in trans-sulfuration, characterized by increased cysteine and glutathione synthesis and distinct metabolic responses.

The paper identifies a distinct metabolomic subtype in sporadic ALS patients through metabolite profiling and multi-omics integration, showing increased cysteine metabolism and potential therapeutic targets.