Abstract: Alzheimer’s disease (AD) is one of the major forms of dementia, accounting for 60 to 80% of the cases of dementia, affecting approximately 50 million people worldwide, which is why it has become an object of great interest in both the medical and social fields (Source: Alzheimer’s Association). One of the main histopathological hallmarks of AD is the formation and accumulation of senile plaques in the brain parenchyma, mainly composed by fibrillar aggregates of the amyloid β (Aβ) peptide. This peptide is generated by the cleavage of the membrane protein named amyloid β precursor protein, and its secretion in the extracellular space leads to its aggregation into amyloid fibrils. Various intermediates of this process of aggregation have been identified, and it was found that prefibrillar, soluble oligomeric forms of Aβ are more likely to be the pathological species (Benilova et al., 2012).