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Because inflammation and serotonin signaling have been implicated in both Alzheimer disease (AD) and depression, which frequently accompanies AD, Brazilian investigators examined the relationships among amyloid-β oligomers (AβOs), the proinflammatory cytokine tumor necrosis factor-α (TNF-α), and serotonin levels in a mouse model of AD.
Intracerebroventricular administration of AβO induced depressive behavior via toll-like receptor 4–dependent (TLR4–dependent) activation of microglia, leading to excessive activity of TNF-α, but not some other proinflammatory cytokines. At the same time, AβO reduced brain serotonin levels, which in turn increased TNF-α levels. In addition, serotonin injection reduced AβO -induced microglial activation and TNF-…