Dragomir Milovanović

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 investigates how synapsin-1 and actin form ordered nanoscale assemblies through phase separation, showing that actin scaffolds retain structural memory for condensate reformation.

This study shows that fluorescently tagged proteins in biomolecular condensates undergo crosslinking due to excitation-induced ROS, leading to condensate solidification and highlighting redox regulation of condensate properties.

The paper shows synaptic vesicles from mouse brains can sequester soluble tubulin in vitro, forming tubulin-rich regions.

The paper investigates how synapsin-SV condensates organize presynaptic actin through LLPS, revealing their role in SV clustering and actin polymerization in lamprey and mammalian synapses.

The paper shows that Intersectin-1 and Endophilin A1 form condensates near synaptic release sites to cluster replacement vesicles, enabling rapid replenishment of neurotransmitter release sites.

This study shows SynGAP forms condensates at low concentrations and recruits PSD95 and receptor oligomers, suggesting it initiates PSD formation.

The paper quantifies viscoelastic properties of synapsin condensates in live cells and identifies α-synuclein's role in regulating their material state.

This study shows that lipid packing and cholesterol content influence condensate-membrane interactions, with increased packing reducing condensate affinity.

This study identifies sequence-encoded molecular grammars in synapsin-1 IDRs that drive condensation and generate pH gradients relevant for synaptic function.

The paper shows RNA promotes synapsin phase separation, forming condensates that organize synaptic vesicles and enhance local translation.

This study investigates the role of synapsin isoforms in presynaptic plasticity at hippocampal mossy fiber boutons in male mice, finding decreased short-term and increased long-term plasticity upon synapsin deletion.

This study models aSyn assemblies in living cells and shows that Sph1-aSyn interactions influence inclusion formation, morphology, and localization, providing insights into protein aggregation and potential therapeutic strategies.

This study shows that spermidine reduces neuroinflammation and soluble amyloid beta in an Alzheimer's disease mouse model by targeting microglia and reducing inflammatory pathways.