Back

Cardiac glycosides restore autophagy flux in an iPSC-derived neuronal model of WDR45 deficiency

Papandreou, A.; Singh, N.; Gianfrancesco, L.; Budinger, D.; Barwick, K.; Agrotis, A.; Luft, C.; Shao, Y.; Lenaerts, A.-S.; Gregory, A.; Jeong, S. Y.; Hogarth, P.; Hayflick, S.; Barral, S.; Kriston-Vizi, J.; Gissen, P.; Kurian, M. A. A.; Ketteler, R.

2023-09-13 cell biology
10.1101/2023.09.13.556416 bioRxiv
Show abstract

Beta-Propeller Protein-Associated Neurodegeneration (BPAN) is one of the commonest forms of Neurodegeneration with Brain Iron Accumulation, caused by mutations in the gene encoding the autophagy-related protein, WDR45. The mechanisms linking autophagy, iron overload and neurodegeneration in BPAN are poorly understood and, as a result, there are currently no disease-modifying treatments for this progressive disorder. We have developed a patient-derived, induced pluripotent stem cell (iPSC)-based midbrain dopaminergic neuronal cell model of BPAN (3 patient, 2 age-matched controls and 2 isogenic control lines) which shows defective autophagy and aberrant gene expression in key neurodegenerative, neurodevelopmental and collagen pathways. A high content imaging-based medium-throughput blinded drug screen using the FDA-approved Prestwick library identified 5 cardiac glycosides that both corrected disease-related defective autophagosome formation and restored BPAN-specific gene expression profiles. Our findings have clear translational potential and emphasise the utility of iPSC-based modelling in elucidating disease pathophysiology and identifying targeted therapeutics for early-onset monogenic disorders.

Matching journals

The top 12 journals account for 50% of the predicted probability mass.

50% of probability mass above

"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.