OPTIMIZATION OF DROSOPHILA LEARNING ASSAYS TO EVALUATE ALZHEIMER’S DISEASE MODEL

Abstract

Alzheimer’s disease (AD) is the most prevalent form of dementia and is characterized by the formation of plaques and neurofibrillary tangles. Approximately two thirds of people over 65 years old and older with Alzheimer’s disease are women (14). Plaques are typically formed by the accumulation of amyloid beta while neurofibrillary tangles are largely the accumulation of hyperphosphorylated tau(1,3, 4). Research studies suggest that Aβ influences tau pathology and vice versa. Current studies have been unable to improve cognitive decline by targeting amyloid beta plaques(24). Neuroimaging studies have shown cognitively normal people with similar deposition of amyloid beta plaques and tau tangles suggesting there are other factors contributing to cognitive decline (1, 4). Thus far many clinical studies have been conducted using various strategies to target amyloid beta based on the amyloid beta hypothesis, which proposes that amyloid beta pathology is the driving force behind Alzheimer’s disease. However recent attempts at targeting amyloid beta plaques in clinical trials had no significant effects on cognitive decline (24). We investigated how altering gene expression of Alzheimer’s disease associated genes in flies affects memory. Preliminary data does suggest that targeting gene expression of significantly altered genes within the progression of Alzheimer’s disease can improve memory function in flies but further testing is required.