Cellular and Molecular Mediators of Neuroinflammation in Alzheimer Disease

Abstract

Alzheimer disease (AD) is a neurodegenerative disorder characterized by the loss of neuronal cells and the progressive decline of cognitive function. The major pathological culprit of AD is aggregation of amyloid-beta (A beta) and hyperphosphorylation of tau, eventually leading to progressive neuronal cell death and brain atrophy. However, the detailed molecular and cellular mechanisms underlying AD development as a result of neuronal cell death are little known. Although several hypotheses have been proposed regarding the development of AD, increasingly many studies suggest that the pathological progress of AD is not restricted to neuronal components such as A beta and tau, but is also closely related to inflammatory responses in the brain. Abnormalities of A beta and tau cause activity of pattern recognition receptors on the brain's immune cells, including microglia and astrocytes, and trigger the innate immune system by releasing inflammatory mediators in the pathogenesis of AD. In this review, we present a basic overview of the current knowledge regarding inflammation and molecular mediators in the pathological progress of AD.