The Effects of Copper and Zinc on PSN gene expression in a Drosophila Alzheimer's Model

Abstract

Based on the current trajectory of Alzheimer's disease, the number of Americans affected are said to increase by 13.5 million people, approximately 16% of the elderly population, by the year 2050. [1] Alzheimer's disease is characterized by the presence of amyloid‐β plaques and neurofibrillary tangles resulting in loss of cognition, memory, behavior, and locomotion.[2] Amyloid‐β plaques are proteolytic fragments of the amyloid precursor protein (APP), which is a resultant of processing through the amyloidogenic pathway. [2,3,4] It is believed that elevated consumption of copper or zinc will increase or decrease the toxicity of amyloid‐β in the brain respectively due to its interactions with presenilin, a component of the γ‐secretase complex responsible for the cleavage of APP.[2,3,4] In order to begin mapping out the amyloidogenic pathway, levels of the PSN gene, the Drosophila melanogaster ortholog responsible for coding for the presenilin protein. In order to begin mapping out the amyloidogenic pathway, levels of the PSN gene will be quantified over various time points and under different dietary conditions. It is hypothesized that increased copper consumption will upregulate the expression of PSN, promoting the amyloidogenic cleavage of APP, therefore speeding up the progression of the disease, while zinc will have an opposite effect and potentially break down amyloid‐β aggregates. The proposed experiments will ultimately develop a more efficient model of Alzheimer's disease in Drosophila melanogaster by monitoring physical and genetic effects of dietary changes.Support or Funding InformationThis work was supported by funds from the Department of Sciences at Wentworth Institute of Technology.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.