Abstract: Alzheimer ’s disease (AD) is a progressive neurodegenerative disease characterized by memory loss and cognitive decline. Beyond the accumulation of amyloid-beta (Aβ) plaques and tau neurofibrillary tangles, the hallmark pathologies of AD, glutamatergic dysregulation, and excitotoxicity are key contributors to disease progression. Given that glutamate is the main excitatory neurotransmitter and has a central role in the regulation of synaptic plasticity, memory, and learning, any disturbance in glutamate signaling can disrupt normal brain function. The medial temporal lobe and superior temporal gyrus (STG) are severely impacted in AD, and the remodeling of glutamate receptors and transporters has been extensively examined as mechanisms linked to neuronal network dysfunction.