More than 55 million people worldwide currently suffer from dementia. Among them, Alzheimer’s disease (AD) is the most common, and it is believed that aggregates of amyloid β (Aβ) peptides begin accumulating in the brain parenchyma and vasculature over 20 years before symptom onset (Fig. 59.1). Subsequently, neurofibrillary tangles composed of tau aggregates accumulate in the neurons, exhibiting neurotoxicity and leading to neuronal death. For this reason, Aβ and tau aggregates have long been considered therapeutic targets.