Ariana P. Gatt

This study identifies TDP-43 dysfunction as a cause of cryptic circular RNA formation in ALS/FTD, showing their association with disease-relevant protein loss and potential as biomarkers.

The paper shows that increased HCN1 activity in excitatory neurons causes excessive network bursting in Dravet syndrome, suggesting HCN1 as a therapeutic target.

This study investigates the hnRNP network's role in FTLD-TDP subtypes using single-nuclei RNA-sequencing and immunohistochemistry, finding glial-specific RNA processing changes associated with different pathological subtypes.

This study identifies cryptic epitopes from de novo proteins caused by TDP-43 pathology as targets of CD8+ T cell activation in ALS and IBM.

This study shows that TDP-43G298S mutations in human iPSC-derived motor neurons alter axon initial segment structure and neuronal excitability at different developmental stages.

This study investigates how amisulpride interacts with GLUT1 at the blood-brain barrier and how Alzheimer's disease affects this transport mechanism.

The paper shows that ALS/FTD risk variants in UNC13A increase sensitivity to TDP-43 depletion by promoting cryptic exon inclusion and protein loss.

The paper identifies 19 compounds from the CMAP library that show significant inverse correlation with Alzheimer's disease transcriptome signatures and pass in vitro screening assays.