Abstract
Alzheimer’s and other neurological diseases are a rapidly growing epidemic. Alzheimer’s is most common in older adults and is a progressive neurological disease that degrades the neuron structure of the brain. The two main perpetrators associated with brain degradation are amyloid-beta peptides and hyperphosphorylated Tau proteins. Both impede the ability of the brain’s neuronal pathways to function properly and lead to symptoms such as dementia, mood change, and others that are associated with Alzheimer's disease. The current focus of medical treatment is the management of symptoms and therapeutic techniques that may reduce their severity. Nicotine presents a possible therapeutic approach to the treatment of these damaging diseases and may allow for the management of the disease symptoms for patients. Nicotine is a naturally occurring chemical and has been used by ancient civilizations to the present day. Our study aimed to assess the effects of nicotine on the expression of amyloid-beta peptides and the Tau protein. We used Drosophila melanogaster as the model organism due to its ability to express both the amyloid-beta and Tau proteins in its eye, which allowed us to quantify the effects of the proteins. Drosophila have eyes that develop similarly to human neurons, and thus made our study more analogous to human brain development. To observe the effect that nicotine would have on the protein expression in the eye, we created a food medium containing three different concentrations of nicotine: 0.0 mg/mL, 0.2 mg/mL, and 0.4 mg/mL. Drosophila hybrids were created that contained either the AB42 gene to express amyloid-beta peptide, the Tau or TauSIIA gene to express Tau protein, or the W118 or TauS2A gene, which acted as controls for the study. Specimens were collected and underwent an eye examination, looking at the eye shape, color, size, and texture. Each sample mean was collected, and the average of these means was compared to the average of the other treatment groups. Across all three levels of nicotine exposure and all five genetic crosses, the means showed no statistically significant differences. We concluded that nicotine, in the concentrations that we used, did not affect amyloid-beta peptide or Tau protein accumulation on the neurons.