PRNP and Alzheimer disease: Moreover, the artificial modification by collagenase observed here would induce the release of the N‐terminal part of PrPC, which typically interacts with diverse ligands, potentially modulating their functions (Shafiq et al., 2022), such as synaptic receptors in epilepsy (Carulla et al., 2011), toxic Amyloid‐β oligomers in AD (Falker et al., 2016; Halipi et al., 2024; Laurén et al., 2009; Resenberger et al., 2011), α‐synuclein in PD models (Urrea et al., 2018) or the pathogenic misfolded isoform of PrP (PrPSc) in PrD (Turnbaugh et al., 2011).