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DTPs exhibit marked transcriptional heterogeneity, enabling their survival under therapeutic stress via dedifferentiation or EMT
mutations in -secretase components Presenilin 1 (PSEN1) and Presenilin 2 (PSEN2) are linked to familial forms of AD (fAD), with PSEN1 mutations reducing Notch signaling and disrupting neurogenesis [42]
p = 0.0018) (Fig
