Alexandra G. Beilina

The paper integrates cell-specific gene expression and chromatin accessibility to identify neurodegenerative disease risk loci specific to microglia.

This study shows that DJ-1 deficiency impairs autophagosome-lysosome fusion and lysosomal degradation, leading to autophagic substrate accumulation through ROS-dependent modulation of the AMPK/mTORC1 axis in Parkinson's disease.

The paper shows that inflammatory signaling affects LRRK2 regulation differently in human and mouse models, highlighting species-specific regulatory mechanisms.

The paper generates and characterizes a custom genome assembly for the KOLF2.1J iPSC line to improve genomic analysis accuracy compared to standard references.

The paper identifies JIP4 and RILPL1 as opposing motor adaptors regulating lysosomal tubulation through differential microtubule transport.

The paper presents the cryo-EM structure of the LRRK2:14-3-32 complex, showing how 14-3-3 binding inhibits LRRK2 activity and how PD mutations disrupt this interaction.

This study shows that triglyceride metabolism is essential for microglial activation and disease states in APOE4 microglia, with implications for modulating immune responses.

The paper profiles HLA immunopeptidomes and interactomes in microglia, identifying disease-associated epitopes and their interactions.

The paper shows that DNA methylation is reset in iPSCs compared to donor PBMCs, with unique methylation sites influenced by genetics in each cell type.

The paper presents a multi-layered molecular dataset from iPSC-derived dopaminergic neurons to model Parkinson's disease genetic risk and provides a data browser for accessing these resources.

The paper shows that a non-coding genetic variant affects LRRK2 expression specifically through microglia, highlighting the importance of cell type in understanding non-coding variation's role in Parkinson's disease.

This study identifies Auxilin mutations as a cause of Parkinson's disease by showing they impair clathrin-mediated trafficking at the Golgi and synapse, leading to neuropathological lesions.

The paper identifies LRRK2 as a regulator of clathrin-mediated endocytosis and links clathrin-trafficking pathways to Parkinson's disease risk.