Magdalini Polymenidou

This paper introduces a XL-MS workflow combining DDA and PRM for quantitative characterization of protein-RNA interactions, applied to TDP-43 and FOX1 complexes.

This study shows that the NTD of TDP-43 binds UG-rich RNA on monomers, while oligomerization is essential for repressing cryptic exons.

This study presents a one-step protocol to differentiate hiPSCs into functional astrocytes, enabling co-culture with neurons to support network development.

This paper introduces a microfluidic platform to study neurodegeneration in human neural circuits, identifying early electrophysiological biomarkers of disease progression.

The paper investigates factors determining TDP-43 seeding outcomes in FTLD-TDP, identifying TMEM106B fibrillar core and lysosomal escape as critical drivers.

The paper identifies BMP signaling as a regulator of prion uptake by screening for genetic modifiers in human cells and shows that modulating BMP components affects prion internalization.

This study shows that TDP-43 and Tau directly interact, promoting co-condensation but reducing Tau fibril formation and seeding.

The paper identifies Gpnmb as a marker of a phagocytic microglial state linked to neuronal loss in prion disease, showing its role in clearing apoptotic cells.

This study evaluates human-derived anti-poly-GA antibodies in cellular and animal models of C9ORF72 disease, showing mixed effects on poly-GA levels and disease progression.

The paper identifies Hnrnpk as a key regulator of prion propagation through a genome-wide RNAi screen using the QUIPPER assay, showing PSA's ability to reduce prion levels and toxicity in multiple models.

The paper develops a human iPSC-derived neural model to study TDP-43 pathology, identifying NPTX2 misregulation as a key factor in ALS/FTLD neurotoxicity.

This study shows that cytoplasmic FUS mislocalization in mice causes behavioral changes and inhibitory synaptic defects without widespread neuronal loss.

This paper shows that ASC controls AA amyloidosis by interacting with SAA and that anti-ASC antibodies reduce amyloid loads in mice.

This study shows LAG3 is not expressed in human and mouse neurons and does not worsen α-synuclein pathology in vitro or in vivo.

This study shows that synaptic accumulation of FUS in ALS-FUS mice leads to age-dependent misregulation of inhibitory synapses, suggesting a role in early neurodegeneration.