Giovanni Cuda

ClonoDynamics distinguishes estimator-induced patterns from true longitudinal variation in T cell receptor repertoires using replicate-resolved analysis.

This study establishes an in vitro model of SORD deficiency using iPSCs and identifies mitochondrial dysfunction and oxidative stress as key mechanisms, suggesting AR inhibition as a therapeutic target for CMT2/SORD and diabetic neuropathies.

The paper identifies TGF-β-driven extracellular matrix remodeling in vascular leptomeningeal-like cells as a driver of neurodegeneration in PSP-RS, showing therapeutic potential through pharmacological inhibition.

The paper introduces a novel iPSC-derived mosaic midbrain organoid system to model PSP-RS and demonstrates its ability to recapitulate key pathological features of the disease.

This study shows that ZZZ3 supports human ESC proliferation by enhancing mTOR/ribosome pathway activity and preventing nucleolar stress.

The paper shows that 3UTR cleavage occurs in sympathetic neuron axons, mediated by Ago2 and HuD, and regulates local protein synthesis and generates new 3UTR RNA fragments.