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Ataxia-telangiectasia (A-T) is a neurodegenerative disorder caused by ATM mutations, leading to progressive Purkinje neuron loss. While ATM regulates the DNA damage response, mechanisms of cell degeneration remain unclear. Using cerebella, hiPS cells, and cerebellar organoids from A-T patients, we show that Purkinje cells shift from a soft, low-viscosity state to hyperstiffness with nuclear deformation and chromatin hypermethylation. Proteomics reveal dysregulated mechanotransduction, chromatin remodelling, and loss of calcium channels. Epigenetic inhibition restores nuclear structure and ITPR1 levels. These findings identify A-T as a “mechano-disease” and suggest that targeting nuclear mechanics could offer new therapeutic avenues
