Hansruedi Mathys

The paper identifies functionally distinct subtypes within Grpr+ neurons in the dorsal horn that mediate itch and mechanical allodynia, demonstrating the utility of genomic enhancer-based strategies for modality-specific targeting.

The paper introduces causarray, a causal inference framework for analyzing genomic data under unmeasured confounders, and applies it to identify causal effects in autism and Alzheimer's disease studies.

The paper shows that enhancing oligodendrocyte function in a mouse model of Alzheimer's Disease reduces neuronal damage and slows disease progression.

The paper develops a platform combining machine learning and multiplexed in situ screening to identify enhancers with cell-type and behavioral specificity for neural circuit engineering.

This study identifies molecular and cellular signatures of cognitive resilience in Alzheimer's disease by integrating multi-omics data from brain tissues.

The paper links chronic pain genetic variants to dorsal horn neuron subtypes using multi-species single-cell and spatial transcriptomic analyses.

This study identifies ABCA7 loss-of-function variants' impact on phosphatidylcholine metabolism in human neurons and shows CDP-choline can reverse these effects.

The paper introduces MorphOMICs, a topological data analysis method to identify sex- and region-dependent microglial morphological phenotypes across development and neurodegeneration.

This study analyzes somatic mosaicism in Alzheimer's Dementia using single-cell data, finding increased mutational burden in specific cell types and genes associated with disease processes.

The paper identifies cell-type-specific molecular changes in cerebrovascular cells across brain regions in Alzheimer's Disease, linking them to genetic variants and potential therapeutic targets.

The paper uses single-cell transcriptomics to analyze the hippocampus and entorhinal cortex in Alzheimer's disease, identifying stage-specific molecular changes across cell types.

The paper deconvolves 3,387 post-mortem brain samples using SPLITR to identify cell-type-specific eQTLs and genetic effects in mental disorders.

This study identifies R47H-TREM2 mutation-induced proinflammatory microglial states in human AD and tauopathy mice, showing Akt pathway involvement and potential therapeutic targets.