Compared to regions without aggregated amyloid, markers of cellular senescence (p16, p21), neuronal death (cleaved Casp3, TUNEL), inflammation (GFAP, Iba1), and endosomal–lysosomal dysfunction (Rab5, LAMP1) were all colocalized with amyloid plaques (Figure 1a, Figure S1 A‐D). This evidence concerns the gene RAB5A and amyloidosis.