Evaluating the Role of Microglial Cells in Clearance of Aβ from Alzheimer's Brain

Ever increasing incidence of Alzheimer's diseases (AD) has been reported all over the globe, and practically no drug is currently available for its treatment. In the past 15 years, not a single drug came out of clinical trials. The researchers have yet to discover a drug that could specifically target AD; in fact, the drugs that are about to launch in the global market either belong to natural compounds or are already approved drugs targeting other diseases. So, we need to shift our focus on finding novel targets which are more specific and could either detect or inhibit the disease progression at a very early stage. Microglia are the only resident innate immune cells of the brain that are originated from erythromyeloid progenitors. They migrate to the brain during early embryonic development, although their number is less (∼5 to 10%), but they could act as guardians of the brain. It has been shown that the extracellular deposits of Aβ are continuously phagocytosed by microglia in healthy individuals, but this ability would decrease with age and lead to development of AD. In this review, we have explored the possibility of whether microglial cells could be utilized as an early predictor of the AD progression. Here, we discuss the innate immune response of microglial cells, the factors affecting microglia response, microglial receptors to which Aβ could bind, and microglial phenotype markers. Last, we conclude with a list of available AD therapeutics along with their mechanism.