:
Alzheimer’s disease (AD) is a chronic neurodegenerative disease characterized by the formation
of intracellular neurofibrillary tangles (NFTs) and extracellular amyloid plaques. Growing
evidence has suggested that AD pathogenesis is not only limited to the neuronal compartment
but also strongly interacts with immunological processes in the brain. On the other hand,
aggregated and misfolded proteins can bind with pattern recognition receptors located on
astroglia and microglia and can in turn induce an innate immune response, characterized by the
release of inflammatory mediators, ultimately playing a role in both the severity and the
progression of the disease. It has been reported by genome-wide analysis that several genes
which elevate the risk for sporadic AD encode for factors controlling the inflammatory response
and glial clearance of misfolded proteins. Obesity and systemic inflammation are examples of
external factors which may interfere with the immunological mechanisms of the brain and can
induce disease progression. In this review, we discussed the mechanisms and essential role of
inflammatory signaling pathways in AD pathogenesis. Indeed, interfering with immune
processes and modulation of risk factors may lead to future therapeutic or preventive AD
approaches.