Jan H.J. Hoeijmakers

The paper analyzes RNA-seq data from Parkinson's Disease patients and controls to find increased somatic mutations in PD, with some clonal mutations being protective.

The paper develops a mathematical model to describe transcription loss due to accumulated DNA damage and analyzes its asymptotic behavior and first hitting time using mice data.

This study shows that DNA mismatch repair-deficient mouse fibroblasts can tolerate high mutation burdens in vitro without significant growth effects, revealing mutation-driven population changes and negative selection.

The paper examines the association between clonal hematopoiesis and Parkinson's disease using whole exome sequencing data from controls and patients.

This study uses single-nuclei multi-omics analysis to identify molecular and cellular changes in human ovarian ageing and links genetic variants to age at natural menopause.

The paper shows that NER deficiency increases Signature 8 mutations in specific tissues and suggests this could be a biomarker for NER-deficiency in cancer.