Suggesting that a significant proportion of our mixed-ancestry subjects may come from “low-starch” populations in which AMY1 copy number is evolving more neutrally, rather than undergoing positive selection. Whereas the specific fitness advantage conferred by upregulation of AMY1 gene copy number and high levels of salivary amylase is unknown, it is possible that the enzyme activity affects preference and intake of starchy foods through its influence on the oral sensory properties of such foods. For example, salivary amylase levels affect both creaminess and the release of flavor compounds from starch-thickened custards; these characteristics are likely to affect an individual’s liking of a food. Salivary amylase may also affect starch digestion and metabolism, as these factors are significantly affected by starch viscosity. Accordingly, when starch is delivered directly into the small intestine, skipping the oral “pre-digestion” by salivary amylase, significantly less digestion and glucose absorption occur. This latter hypothesis suggests that individuals who produce high levels of salivary amylase and rapidly break starch into smaller glucose polymers may experience increased glycemic load from a high starch meal. Further research will be needed to test this hypothesis. This research demonstrates that salivary amylase plays a significant role in the oral perception of starch viscosity when saliva is mixed into a food. Salivary amylase levels are under both environmental and genetic controls. Understanding the factors that underlie our perception of starchy foods will help us to learn how the changes that occur in such foods during oral manipulation impact our liking, preference, and ingestion of such foods. The (+)-JQ1 profound individual differences in salivary amylase levels and salivary activity, which are determined in part by our AMY1 gene copy numbers, may contribute significantly to individual differences in dietary starch intake and, consequently, to our overall nutritional status. Future research will examine whether differences in oral amylase levels directly impact our liking for and consumption of starchy foods. Genes implicated in the development of AD influence microtubule and actin filaments responsible for neuronal morphology. The presence of an apolipoprotein E4 allele, correlates with the simplification of dendritic branching patterns in the brains of AD patients. Consistent with this observation in human brains, the apolipoprotein E4 inhibits neurite outgrowth in cultured neuronal cells. Interestingly, amyloid precursor protein concentrates in lamellipodia where it is proposed to play a role in growth cone motility and neurite outgrowth. Upon acute neuronal injury, such as axotomy, the first critical steps that initiate regenerative response are microtubule polymerization and F-actin cytoskeleton rearrangement leading to the formation of a motile growth cone in a stable axonal segment. Actin cytoskeleton regulator CP is an a/b heterodimer that binds the barbed end of F-actin thus blocking the access of actin monomers to the fast growing end.