According to recent research, depression may be a significant risk factor for Alzheimer's disease (AD) and cognitive impairment. AD and depression in later life are strongly correlated. Patients with mild cognitive impairment (MCI) and a history of depression have been shown to have an accelerated age of AD onset; women seem to be more susceptible to this condition. Furthermore, compared to MCI patients without depression, those with MCI who exhibit depressive symptoms have a higher burden of amyloid-beta (Aβ), the primary toxic protein linked to Alzheimer's pathology, and a higher risk of developing AD compared to non-depressed MCI patients. The induction of Alzheimer's pathology due to a depressive process has not been investigated under experimental conditions to mimic late-life depression as a risk factor for AD, despite the fact that some transgenic models of AD have been reported to develop signs similar to depression in advanced stages. By subjecting APP transgenic mice to unpredictable mild chronic stress (CUMS), this study aims to ascertain whether depression is a cause of AD development rather than a result. Our study's findings suggest that CUMS induction in transgenic animals causes phenotypic alterations associated with depression. According to behavioral and histological research, depression-like induction may exacerbate AD pathology. The results of this project may offer proof of depression's role as an AD risk factor, its mechanisms of action, its application as an early biomarker, and the development of novel AD treatments.