Rejko Krüger

The paper generates iPSCs from a Parkinson's patient with a RAB32 mutation and confirms their pluripotency and differentiation potential.

This study investigates how SNCA triplication affects neuronal extracellular vesicle biology and microglial activation in Parkinson's disease using iPSC-derived models.

This study identifies ZFHX4 as a key regulator of midbrain dopaminergic neuron differentiation by controlling cell cycle progression through the LIN28A-miR-9 axis.

The paper identifies Parkinson's disease-associated regulatory variants in human dopaminergic neurons and shows they modulate SCARB2 and BAG3 expression.

This study identifies genetic associations between lysosomal genes and Parkinson's disease risk across diverse populations using GWAS and whole genome sequencing data.

This study shows that DJ-1 mutations impair astrocytic dopamine metabolism, leading to disrupted detoxification and potential contribution to Parkinson's disease pathogenesis.

The paper assesses the frequency of dystonia-linked pathogenic variants in Parkinson's disease patients and finds they are present in 0.57% of cases, with GCH1 being the most common gene affected.

This study uses Boolean modeling on PD cohorts to show sex-specific miRNA dysregulation affects mitochondrial biogenesis, mitophagy, and autophagy in Parkinson's disease.

The paper identifies compounds that restore morphology in Parkinson's disease neurons by targeting mitochondrial uncoupling.

This paper investigates the role of alpha-synuclein in lipid regulation at MAM domains in synucleinopathies, showing disease-specific lipid alterations and Syn's impact on phosphatidylserine metabolism.

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.

This study shows that a Miro1 mutation causes mitochondrial dysfunction and dopaminergic neuron loss in both cell models and mice, supporting its role in Parkinson's disease.

This study shows that GBA1 variants increase Parkinson's disease risk, with severe variants having higher risk than risk variants, and polygenic scores further increase this risk.

This study shows DJ-1 affects metabolism and immune response differently in Parkinson's disease and glioblastoma cells, with antioxidant treatment rescuing PD-related phenotypes.

The paper shows that CISD1 dimerization in PINK1 mutants disrupts iron-sulfur cluster coordination, leading to Parkinson's disease-like phenotypes, and suggests CISD1 as a therapeutic target.

This study shows insulin resistance in midbrain organoids reduces metabolic efficiency and neural activity, contributing to Parkinson's disease pathology.

The paper shows that Park7 deletion causes sex-specific transcriptome changes in male mouse midbrain astrocytes via the NRF2-CYP1B1 axis, affecting oxidative stress and EMT processes.

This study identifies how GDAP1 loss of function disrupts actin signaling, leading to mitochondrial tubularity and metabolic changes in CMT4A.

This study uses patient-specific midbrain organoids with SNCA triplication to show synaptic decline precedes dopaminergic neuron loss in Parkinson's disease.

The paper analyzes sncRNA-seq data from the PPMI cohort to identify miRNAs associated with Parkinson's disease progression and systemic inflammation.

The paper analyzes mitochondria-mitochondria interaction networks in Parkinson's disease and finds altered topological patterns that correlate with clinical scores and can distinguish patients from controls.

This study shows that the A30P alpha-synuclein mutation in Parkinson's disease neurons reduces branching and function, with mitochondrial dysfunction and susceptibility to Rotenone.

This paper identifies five new genetic risk loci for Lewy body dementia through whole-genome sequencing and shows shared risk profiles with Alzheimer’s and Parkinson’s disease.

This study shows that HP-β-CD treatment improves dopaminergic differentiation in PD patient-derived midbrain organoids by enhancing mitophagy.

This study identifies PINK1's role in regulating mitochondrial function, lipid metabolism, and dopamine homeostasis in dopaminergic neurons, showing that cholesterol depletion can reverse PINK1-related phenotypes.