User:Haylie Moehlenkamp/Sandbox1

Alzheimer's Disease is a neurodegenerative disease characterized by accumulation of extracellular plaques that cause interferences with memory retrieval. These plaques are made up of amyloid beta (Aβ) peptides which are products of the cleavage of human Amyloid Precursor Protein (hAPP) <ref name "Chang">doi:10.1002/iub.305</ref> <ref name "Shibuya">PMID:26669800</ref>. Within the cells, there is an accumulation of hyperphosphorylated tau <ref name "Chang">doi:10.1002/iub.305</ref> <ref name "Shibuya">PMID:26669800</ref>. Research has shown that the concentration of cholesterol within cells can affect the production of Aβ <ref name "Chang">doi:10.1002/iub.305</ref> <ref name "Shibuya">PMID:26669800</ref>. As the concentration of cholesterol in the endoplasmic reticulum of neurons increases, hAPP is downregulated <ref name "Chang">doi:10.1002/iub.305</ref> <ref name "Shibuya">PMID:26669800</ref>. Inhibition of ACAT1 would lead to higher concentrations of cholesterol in the cells, signaling downregulation of hAPP. Less hAPP available decreases the amount of Aβ peptides being produced and decreases the available Aβ peptides that could form the extracellular plaques associated with Alzheimer's Disease <ref name "Chang">doi:10.1002/iub.305</ref> <ref name "Shibuya">PMID:26669800</ref>