Microglia - a vital marker in early Alzheimer’s disease

Abstract

Alzheimer’s disease (AD) is a neurodegenerative disease characterized by memory impairment. The extremely complex etiology of Alzheimer’s disease presents substantial difficulties for clinical diagnosis and treatment. The pathophysiology of Alzheimer’s disease is currently explained by the amyloid-β (Aβ) hypothesis and the tau tangling theory. The therapeutic effectiveness of A and tau targeting, however, is yet insufficient. Growing interest has been shown in the pathogenic function of microglia as a potential new etiological component. Microglia are immunological cells in the central nervous system.There is a growing consensus that neuroinflammation and microglia-induced processes in Alzheimer’s disease are strongly related. Additionally, under pathological settings, aberrant microglial phagocytic function may contribute to synapse loss, which in turn causes a reduction in cognitive capacity. Several individual genes, enzymes, signaling molecules, regulators, and targets in microglia are noteworthy. Targeting these diseased microglial targets has the potential to both shed light on the real mechanisms by which microglia cause Alzheimer’s disease and suggest new avenues for future treatments for the condition.