Pathological features of Alzheimer‘s disease (AD) include the formation of senile plaques due to extracellular amyloid-β (Aβ) accumulation and the formation of neurofibrillary tangles due to intra-neuronal accumulation of hyperphosphorylated tau. The Vacuolar Protein Sorting (VPS) 35/26/29 complex proteins are significant components of retromers associated with intracellular vesicular trafficking. It has been suggested that retromer components are involved in the pathogenesis of neurodegenerative diseases, but the details remain unknown. In this study, our objective was to investigate the expression changes of retromer components during the pathogenesis of AD using a model mice. We employed App-NL-GF knock-in mice as AD model mice, including 3-month-old and 6-month-old males. Cognitive function in the mice was assessed through the Y-maze test and the fear conditioning test. The amount of Aβ was measured via immunohistochemical staining and ELISA. Changes in the expression of each VPS were analyzed using the western blot method. The behavioral test results indicated no cognitive decline in the 3-month-old AD model mice but did show cognitive decline in the 6-month-old AD model mice. However, both 3-month-old and 6-month-old AD model mice exhibited Aβ accumulation and a reduction in certain VPS proteins. Therefore, the decreased expression of VPS proteins occurring before cognitive decline may represent a potential molecular target for AD disease-modifying drugs, with potential therapeutic applications such as retromer stabilizers.