Clemens R. Scherzer

The paper fine-maps PD GWAS signals across cell types, revealing convergent glial-neuronal risk genes and a shared vesiculopathy network.

This paper develops computational tools for allelic imbalance analysis using single-nucleus RNA-seq and demonstrates their application in a Parkinson's disease cohort.

This study integrates long-read WGS and single-nucleus RNA-seq to identify structural variants affecting gene expression in Parkinson's disease with cell type resolution.

This study integrates multi-omics data from Drosophila and human Alzheimer's disease models to identify pathways involved in neurodegeneration.

This study identifies 1,111 PD-associated RNAs in blood and develops a multi-omics model with AUC 0.89 for PD diagnosis, offering insights into pathobiology and potential clinical applications.

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 circRNAs specific to dopamine and pyramidal neurons and links them to neuropsychiatric diseases.

The paper uses proteomics and machine learning to identify potential biomarkers in cerebrospinal fluid for Parkinson's disease, showing altered protein levels and neuroinflammation signatures.

The paper introduces powerEQTL, an R package and web tool for calculating sample size and power for bulk and single-cell eQTL analysis.

This study investigates how parkin's redox state and insolubility in human midbrain relate to oxidative stress and dopamine metabolism, showing that parkin's cysteine modifications affect H2O2 levels and neuroprotection.

The paper identifies pathway-specific polygenic risk factors and transcriptomic networks associated with Parkinson disease using large-scale genetic and expression data.

This study identifies oxidative modifications of parkin in adult human brain that confer neuroprotection by reducing H2O2, conjugating dopamine radicals, and forming neuromelanin.

This study identifies two genome-wide significant variants associated with Parkinson's disease progression and replicates known risk variants' effects on motor and cognitive decline.