This paper provides a multidisciplinary analysis of the relationship between beauty and addiction, with a focus on the emerging field of neuroaesthetics. Neuroaesthetics investigates the neural mechanisms that underlie aesthetic experiences and how the brain cognitively processes beauty. Since there is a biological foundation of this report, I will predominantly discuss neuroanatomy, neurological studies, and the overlap in neural circuitry between beauty and addiction. In addition, I will discuss the philosophical roots of beauty, as well as the environmental elements involved. Chapter 1 begins by explaining the history of beauty and its importance. I discuss the main constituents of beauty and differentiate between key terms involved in the beauty experience. In order to understand the link between beauty and addiction, it is essential to have a knowledgeable background on what beauty is. Next, I discuss the neurobiology of addiction. The main component of this chapter involves the mesolimbic and mesocortical reward pathways. I also describe neuroanatomical terms involved in addiction. The last chapter considers the implications of neuroaesthetics in various studies, which primarily involve the use of fMRIs. I discuss the sensory evaluations of beauty and the brain regions involved in the beauty experience. From this, I found that the experience of beauty activates these main brain regions: PFC, amygdala, striatum, NAcc, cingulate, VTA, and most remarkably, field A1 of the mOFC. By combining the neurological studies with studies of aesthetics, I reached the conclusion that there is an overlap in the neural pathways during the experience of beauty and during addiction. Although it is necessary for further research to be conducted to properly declare this, I discovered that the pursuit of beauty can lead to addictive behaviors, as the reward centers of the brain are activated by aesthetic experiences.

Alzheimer’s disease (AD) is an irreversible brain disorder that plagues millions of people with no current cure. Current clinical research is slowly advancing to more definitive treatments in hopes of reducing the effects of progressive cognitive and behavioral decline, but none so far can slow AD’s onset. A brain area known as the nucleus incertus (NI) was recently discovered to potentially impact AD because of its connections to brain targets that degenerate; however, the NI’s role is unknown. This goal of this experiment was to use a transgenic mouse model (APP/PS1) that expresses AD pathology slowly as found in humans, and to test the mice in a variety of cognitive and anxiety assessments. Mice of both sexes and two different ages were used, with the first being young adult before AD pathology manifests (around 3-4 months old), and the second being around the cusp of when AD pathology manifests (late adult, 8-10 months old). The mice were tested in a variety of cognitive tasks that included the novel object recognition (NOR), Morris water maze (MWM), and the object placement (OP), with the latter being the focus of my thesis. Anxiety measures were taken from the open field (OF) and elevated plus maze (EPM) with the visible platform (VP) used to ensure mice could perform on the rigorous MWM task. In the OP, we found an age effect, where the older mice were less likely to explore the moved object during the OP compared to the younger mice; motor ability was unlikely to explain this effect. We did not find any significant age by genotype effects. These findings indicate that cognitive impairment only just started to affect the older cohort, since OP impairment was found on one measure and not another. Other measures currently being quantified will be helpful in understanding this data, and to see whether learning, memory, and anxiety are affected.