Over the last decades, two neuropathologies have been studied and characterized in the brain of AD patients. First, the formation of amyloid plaques involved in the amyloid-β (Aβ) aggregation and deposition, and second, the formation of neurofibrillary tangles (NFTs) due to tau protein hyperphosphorylation and aggregation; in addition the loss of connections among neurons in the brain is also involved . Neurodegeneration induced by abnormal deposits of Aβ and NFTs is estimated to begin around 10-20 years before the cognitive function deterioration is manifested . Other hypotheses involve different processes and conditions in AD development, such as oxidative stress, neuroinflammation , vascular risk factors, cholesterol disorders, glucose hypometabolism, insulin signaling, bacteria-derived metabolites, among others . Therefore, multiple targets are involved in AD, thus this pathology is, in fact, a complex disease -multifactorial in nature -whose edges should be studied from a systems pharmacology level. Therefore, therapeutic alternatives that simultaneously modulate multiple key factors in this pathology can be proposed by globally studying its pathophysiological state .