Marius Wernig

The paper maps age-related changes in the N-glycoproteome across multiple tissues in mice, showing how glycosylation affects autoantibody binding to MOG in the brain.

The paper uses human iPSC-derived neurons to study WNV effects, identifying strain-specific neuroattenuation and pathogenic signatures not seen in conventional cell lines.

This study shows that deleting neuroligins from astrocytes does not affect synapse numbers or astrocyte structure in mice or human neuron co-cultures.

This paper introduces a mechanically-mediated low-pressure poration method for efficient, cargo-agnostic intracellular delivery with high throughput and clinical scalability.

The paper introduces Plate-C, a high-throughput method for whole-genome 3D architecture profiling, and identifies modulators of DNA structure across multiple biological pathways and cell types.

The paper identifies strategies to prevent transgene silencing during human pluripotent stem cell differentiation and introduces a robust vector construct.

The paper creates a cell-type-specific lysosome protein atlas in the brain, identifies SLC45A1 as a neuron-specific lysosomal protein, and shows its role in lysosomal function and neurodegeneration.

This study uses heterochronic myeloid cell replacement to show that the local brain environment, not intrinsic factors, drives microglia aging.

The paper develops human tri-lineage brain microtissues composed of neurons, astrocytes, and microglia, showing they recapitulate cell-cell interactions and pathological processes.

The paper identifies CD72 as a regulator of microglial tiling through proteomic profiling and functional assays.

RAPIDASH enriches ribosome-associated proteins from diverse samples, revealing their roles in neurodevelopment and immune response.

This study shows that inhibiting IDO1 restores hippocampal glucose metabolism and rescues cognition in Alzheimer's disease models.

This study identifies a neuroprotective myeloid state in MS and EAE models, showing that HCT enhances this state, leading to clinical improvement and reduced demyelination.

This study identifies a synaptic mechanism linking collagen VI to motor control through cannabinoid receptor interaction and shows that CB1R agonists can improve motor performance in a dystonia mouse model.

This paper develops a method to generate neuronal cells from adult fibroblasts and uses it to study gene expression and epigenetic changes in 22q11.2 deletion syndrome.

This study validates that heterozygous NRXN1 deletions impair neurotransmitter release in human neurons across multiple labs, suggesting a human-specific synaptic dysfunction relevant for schizophrenia drug discovery.

The paper shows that co-expressing NGN2 with EMX1 generates homogeneous glutamatergic neurons from human pluripotent stem cells, with altered transcriptional output and chromatin binding compared to NGN2 alone.

The paper introduces LS-SOFI, a method combining light-sheet fluorescence microscopy and super-resolution optical fluctuation imaging for fast nanoscale-resolution imaging in 3D tissues.

The paper shows ApoE variants differentially affect neuronal signaling and synaptogenesis, mirroring their impact on Alzheimer’s disease risk.

This study develops a CRISPR/Cas9 method to reversibly disrupt specific transcription factor-DNA interactions and assess their functional impact on gene expression and cell division.

This study examines DNA methylation changes during fibroblast-to-neuron reprogramming, identifying key factors and mechanisms involved in epigenomic remodeling.

The paper identifies lnc-NR2F1 as a pro-neurogenic lncRNA mutated in neurodevelopmental disorders through genetic and functional studies.

This study shows that old fibroblasts secrete inflammatory cytokines, leading to variability in reprogramming efficiency and affecting wound healing in older individuals.

The paper identifies TFAP2C and p63 as key regulators of epidermal lineage commitment and shows TFAP2C initiates differentiation while p63 drives maturation through chromatin dynamics.