This study investigates skeletal alterations in a triple transgenic 3xTg-AD mouse model of AD (3xTg-AD), which harbors mutations in β-amyloid precursor protein (βAPPSwe), presenilin-1 (PS1M146V), and tauP301L, and recapitulates key aspects of AD pathology, including age-dependent β-amyloid plaque accumulation and cognitive decline. The gene discussed is PSEN1; the disease is Mental deterioration.