Neuroinflammation and microglial dysfunction are key contributors to the development of Alzheimer's disease (AD). Toll-like receptors (TLRs) are transmembrane proteins primarily involved in immune responses and expressed by several immune and non-immune cells within the central nervous system. Signaling of TLRs affects the core of AD changes, including synaptic plasticity, microglial activity, tau phosphorylation, and inflammatory responses. We reviewed the activity, expression, potential applications, and genetic polymorphisms of TLRs in AD. Activation of TLRs has shown both destructive and protective effects. Several genetic polymorphisms of TLRs have been also recognized as protective or risk factors for AD. We concluded that TLRs are one of the major components of AD pathogenesis, particularly in the early stages of the disease, which can provide novel therapeutic options.
Keywords: Alzheimer disease; Amyloid-beta; Inflammation; Microglia; Single nucleotide polymorphisms; Toll-like receptor.
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