Abstract: The leading form of dementia worldwide, Alzheimer’s disease (AD) is a common neurodegenerative disorder. The underlying causes of AD are not well understood, and no current treatments are preventing the onset or delay progression of the disease. Currently, most investigation is directed towards the amyloid-beta (Aβ) and tau pathologies, yet there are many other underlying processes that have been implicated to contribute directly to AD progression. One such phenomenon is glutamatergic excitotoxicity, a loss of neuromodulatory balance inducing a hyper-excitable neuronal state, leading to cell death across several brain regions (Zhang et al., 2016; Bukke et al., 2020). Glutamate is the primary excitatory neurotransmitter in the brain and is involved in many critical signaling and metabolic functions but control of the glutamatergic system requires constant moderation to avoid excitotoxicity occurring (Bukke et al., 2020). As yet, glutamatergic signaling changes that contribute to this process, or result due to this process, have not been thoroughly investigated.