Abstract: Dementia refers to a variety of conditions that affect the normal function of the brain, leading to symptoms like memory loss, issues with problem solving, difficulty in processing thoughts and disordered language (McKhann et al., 2011). AD serves as one of the major causes of dementia as it is responsible for ~80% of its cases according to the Alzheimer’s Association. AD affects the ability of neurons, the major information transmitting cells of both the peripheral and central nervous system, to send and receive signals through the body, leading to the aforementioned symptoms associated with dementia. The biological hallmarks of AD include the presence of amyloid beta (Aβ) plaques as well as neurofibrillary tangles containing a protein called tau (Lane et al., 2018). These proteins disrupt the normal function of neurons through a variety of mechanisms. In particular, AD first results in a loss of a specific neuronal subtype – the cholinergic neurons found in the basal forebrain - by reducing the expression levels of choline acetyltransferase. This enzyme breaks down acetylcholine, a neurotransmitter expressed in the neuromuscular junction, resulting in the loss of normal brain function. This loss of acetylcholine in AD patients was first noted in the late 1970s, and is now known to correlate with reduced cortical choline acetyltransferase, the enzyme responsible for synthesizing acetycholine from choline, which in turn correlates with neuritic plaque numbers and reduced Mini-Mental State Exam scores (Gauthier, 2002). Currently available pharmacological treatments for AD focus on inhibiting the loss of choline acetyltransferase, but do not represent a longterm cure.