Erika L. F. Holzbaur

This study shows STMN2 regulates microtubule dynamics and axonal resilience in human motor neurons, linking cytoskeletal homeostasis to ALS pathology.

This study investigates how pathogenic KIF1A variants affect axonal trafficking and synaptic development in human neurons using gene-edited iPSCs.

This paper determines the cryo-EM structure of the PI3KC3-C2 complex with Rubicon's PIKBD domain, revealing how Rubicon selectively inhibits PI3KC3-C2 to regulate endolysosome maturation and mitophagy.

This study shows that KIF1A mutations impair autophagy in human neurons by disrupting ATG9 trafficking and lysosomal function, contributing to KAND pathogenesis.

This study shows that PPM1H knockout disrupts axonal autophagy and increases alpha-synuclein aggregation in neurons, linking LRRK2 hyperactivity to Parkinson disease pathology.

This study shows that mitochondrial damage in astrocytes triggers inflammatory responses via PINK1/Parkin-dependent mitophagy, leading to cytokine release and neuroinflammation in Parkinson's disease.

The paper identifies a novel stress response pathway, MitoSR, triggered by mitochondrial damage that enhances mitophagy by degrading negative regulators in neurons.

The paper shows that neurons with Parkinson's disease-associated LRRK2 mutations increase secretion of autophagosomes and exosomes to manage cellular waste and communication, potentially delaying disease onset but contributing to neuroinflammation.

This study examines how aging affects autophagosome formation and maturation in murine neurons, finding reduced formation but increased maturation in aged neurons.

The paper shows that LRRK2 mutations disrupt autophagosome transport in neurons by creating a tug-of-war between dynein and kinesin motors, contributing to Parkinson's disease pathogenesis.

The paper identifies and characterizes a reference iPSC line, KOLF2.1J, for standardized use in collaborative studies across multiple differentiation protocols and assays.

The paper uses proteomics to compare autophagy cargos in two Parkinson disease mouse models, finding distinct adaptive pathways in PINK1 and LRRK2 models.

This study shows that WIPI2B expression counteracts age-related decline in autophagosome biogenesis in neurons, suggesting it as a therapeutic target for age-associated neurodegeneration.