The Use of Mus Musculus Model to Evaluate Pharmacological Mechanisms of Curcumin in Alzheimer's disease

Alzheimer’s disease (AD) is a progressive neurodegenerative disease that is the primary cause of dementia in late adulthood. With the increasing global population and life expectancy, the incidence of AD is also rapidly rising. Currently, available drugs for AD cannot prevent disease progression but can only treat its symptoms, accompanied by severe side effects and high costs. Therefore, curcumin is expected to be an alternative treatment for AD. The aim of this study was to investigate the pharmacological pathway of curcumin’s mechanisms of action on AD using mice as animal models. A search was conducted on four databases using the keywords "curcumin", "Mus musculus", and "Alzheimer's disease". Curcumin possesses multiple mechanisms of action, namely: (1) as an antioxidant agent by increasing antioxidant enzyme activity and decreasing the number of reactive oxygen species (ROS); (2) an anti-inflammatory agent characterized by a decrease in neuroinflammatory cytokines and inhibits endoplasmic reticulum stress; (3) inhibition of amyloid beta and tau hyperphosphorylation, resulting in a decrease in Aβ deposit and tau expression, as well as increased expression of beta-site APP cleaving enzyme-1 (BACE-1) and amyloid beta degrading enzyme; (4) Reducing the activated microglial cell population and decreasing ionized calcium binding adaptor-1 molecule (Iba-1) and glial fibrillary acidic protein (GFAP); (5) regulating important molecules in insulin signaling pathways and glucose metabolism; (6) Inhibition of activity of acetylcholinesterase (AChE) enzyme..