Elena De Cecco

This study identifies PODXL as a suppressor of α-synuclein fibril uptake in neurons, highlighting its glycan-dependent surface properties and interaction with MME.

This study shows that Adgrd1 deficiency in mice leads to reduced nest-building, decreased exploratory behavior, and increased hippocampal vulnerability through molecular and circuit-level changes.

The paper identifies TFAP2C as a genetic interactor of hnRNP K, showing their roles in mTOR metabolic regulation and a causal link to prion propagation.

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.

The paper uses CRISPR screens to identify OXR1 and EMC4 as modifiers of α-synuclein aggregation in Parkinson's disease and related synucleinopathies.

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.

The paper constructs genome-wide CRISPR libraries for gene ablation, activation, and silencing with high efficacy and reports novel gene regulators and modifiers.

This study shows that neuronal hemoglobin overexpression in mice leads to dopaminergic neuron loss, cognitive deficits, and cleavage of α-synuclein.

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 the cellular prion protein facilitates tau amyloid uptake and reduces prion propagation in cultured cells.