Britta Johanna Eickholt

The paper shows that alpha-synuclein phase separation can form Lewy body-like structures without pre-existing seeds, suggesting a new mechanism for neurodegeneration.

This study compares proteolytic pathway activity in neuronal compartments across aging in mice and C. elegans, revealing age-related differences in UPS and macroautophagy.

This study shows that LRRK2 regulates synaptic function by modulating actin cytoskeletal dynamics through BDNF signaling in neurons.

This study investigates how filaments deform biomolecular condensate droplets and identifies physical mechanisms governing their shapes.

The paper develops a workflow and tool to analyze the nanoscale organization of NET proteins, revealing periodic binding patterns resembling nucleosomes.

This study identifies PLPPR3 condensates as actin sinks that locally boost monomer concentrations, promoting actin polymerization and filopodia formation in neurons.

This paper develops a genetically encoded biosensor for dynamically monitoring PTEN activity in living cells and tissues with high spatial and temporal resolution.

The paper identifies phosphorylation sites in PLPPR3 and shows that phosphorylation at S351 regulates its interaction with BASP1, suggesting a role for the PLPPR3-BASP1 complex in synaptic signaling.

The paper investigates input sources to layer 1 of mouse somatosensory cortex using retrograde tracing and optogenetics, revealing local and long-range contributions and their interactions.

This study investigates the role of Pten T366 phosphorylation in cortical connectivity and behavior, finding that its disruption leads to cognitive deficits and sensory impairments in mice.

The paper introduces a GUI-based software for automated neuronal morphology analysis, achieving accurate classification of neurites and reproducing manual annotations on a benchmark dataset.

The paper identifies axonal PIP3 deficiency as a cause of CNS regeneration failure and shows that p110δ can restore regeneration by acting hyperactively.

This study shows Drebrin is essential for astrocyte scar formation after brain injury by regulating actin dynamics and RAB8 membrane trafficking.