Inke Regina König

The paper validates a mitochondrial polygenic score for Parkinson's disease across diverse populations, finding strong associations in Europeans and Ashkenazi Jews but not in other ancestries.

The paper develops an improved polygenic score for idiopathic Parkinson's disease, showing higher discriminative performance and explaining variable penetrance in genetic forms of the disease.

The paper investigates FGF14 repeat interruptions in ataxia patients and unaffected individuals, finding that mosaic interruptions (mDRILS) correlate with age at onset and affect pathogenicity.

The paper examines how polygenic scores and lifestyle factors influence age at onset in Parkinson's disease, finding that lifestyle factors have a larger impact than genetic variants.

The paper introduces a new tree-based distance measure for random forests to identify representative trees, showing its effectiveness in capturing genetic interactions and replicating GWAS results.

This study examines how a mitochondrial polygenic score interacts with environmental factors to influence age at onset in LRRK2-PD and iPD, finding ethnic-specific effects and gene-environment interactions.

The paper identifies mitochondrial DNA heteroplasmy as a marker distinguishing disease manifestation in PINK1/PRKN mutation carriers.

This study explores associations between coffee, smoking, and aspirin use with age at onset and clinical severity in idiopathic Parkinson's disease using a large cohort.

This study uses Mendelian randomization to assess the causal relationship between glycemic and anthropometric traits and Parkinson's disease risk, finding protective effects of waist-hip ratio and suggestive associations with fasting glucose.

This study uses Mendelian randomization to investigate causal links between risky behaviors and Parkinson's disease in over a million participants, finding protective and risk associations for specific behaviors.

This study shows that a mutation in mt-Nd2, a mitochondrial complex I gene, reduces lifespan and increases glucose intolerance in mice by affecting tryptophan levels and aging pathways.