Abstract: Alzheimer ’s disease (AD) is an age-related neurodegenerative disease that involves a progressive decline in memory, thinking, and learning. AD has been studied rigorously for more than 50 years yet there is a marked lack of progress in pharmacological treatment. The challenges to developing AD therapeutics are rooted in the disease being ill-defined in terms of diagnosis, progression, and etiology. The neuropathological hallmarks of AD are extracellular amyloid-β (Aβ) plaques and intracellular neurofibrillary tangles of hyperphosphorylated tau. Generally, Aβ plaques disrupt neuronal connectivity, while neurofibrillary tangles interfere with intracellular function (Zhang et al., 2023). Therefore, developing innovative strategies to slow the formation or enhance the clearance of these toxic proteins has shown promise in disease-modifying approaches for AD.