In Alzheimer’s disease, biomarkers like phosphorylation of tau at the 217th amino acid (pTau-217) highlight the role of post-translational modifications in distinguishing Alzheimer’s disease from other tauopathies, while N-terminal tau, linked to truncation, illustrates how targeting specific protein regions reflects disease mechanisms.18-21,29,30 The Aβ42/40 ratio further exemplifies this, capturing the differential cleavage of amyloid precursor protein to produce aggregation-prone Aβ42, whose reduction in biofluids serves as a key marker of amyloid pathology. This evidence concerns the gene APP and early-onset autosomal dominant Alzheimer disease.