Development of Aβ and anti-Aβ dynamics models for Alzheimer’s disease

Abstract

Alzheimer’s disease is one of the most prevalent types of dementia worldwide. It is caused by the accumulation of amyloid-beta (Aβ) plaques in the brain, disrupting communication pathways and memory. Microglia and astrocytes act as the immune system of the brain, clearing Aβ plaque deposits. However, these cells can lose effectiveness when Aβ plaque accumulation exceeds normal limits, leading to inflammation induced by proinflammatory cytokines. One type of treatment involves anti-Aβ drug therapy. Anti-Aβ drugs are believed to have the ability to reduce Aβ plaque deposits effectively. The mechanism of Aβ plaque accumulation can be explained by ordinary differential equations describing the growth of Aβ monomers. In this study, we aimed to develop a new mathematical model to elucidate the role of the immune system and drug therapy in reducing Aβ plaque deposits. Based on the simulation results, we conclude that the use of anti-Aβ drug therapy can decrease the concentration of Aβ plaque deposits, and the effective treatment duration for Alzheimer’s patients is estimated to be approximately 4 months starting from the time the drug was first administered.

Keywords

• alzheimer
• amyloid-beta (aβ)
• drug therapy
• immune system
• ordinary differential equation
• 34a12
• 92-08
• 92-10