In AD, saposins (e.g., Sap C) aberrantly accumulate in dystrophic neurites surrounding Aβ plaques, collaborating with loss of lysosomal hydrolases (e.g., CTSB/CTSD) to amplify pathology [15], and disrupted PSAP-progranulin interactions accelerate neurofibrillary tangle formation [108]. The gene discussed is GRN; the disease is Alzheimer disease.