The idea that microglial activation states could impact Alzheimer’s disease has recently gained momentum. Alzheimer’s disease is the most common form of dementia and is characterized by the presence of neurofibrillar tangles of hyperphosphorylated Tau and extracellular deposits of the peptide amyloid β (Aβ), forming neuritic plaques. Another key feature of Alzheimer’s disease is the presence of prominent neuroinflammation [113]. Interestingly, Aβ itself has been shown to have proinflammatory properties when injected into the CNS [114,115]. Amyloid β can bind to several innate immune receptors present on microglia, such as TRL2 [114], TRL4 [116], TLR6 [116], and CD14 [117], all of which can lead to activation when triggered. To that end, microglia surrounding Aβ plaques show elevated production of inflammatory factors [118]. The inflammatory nature of amyloid has been recognized as a potential mechanism of disease progression. Amyloid β is generated from a parent protein called the amyloid precursor protein (APP), which is cleaved in two steps by the enzymes β then γ secretase, leading to release of the Aβ fragment [119]. This is a normal physiological process that is
