Alzheimer disease (AD) is the most prevalent cause of dementia in humans, and the symptoms are commonly manifested after the seventh decade of life. Numerous pathological changes have been described in the postmortem brains of AD patients, including senile plaques, neurofibrillary tangles, neuroinflammation, synapse loss, and neuronal death. Reactive astrocytes surrounding senile plaques seem to be responsible for the ongoing inflammatory process in the disease through the release of cytokines and other toxic products. However, little is known about the regulation of these cells in the AD brain. Here we discuss the potential translational impact of the recent findings of Carrero and colleagues, published in Experimental Neurology, that shows the underlying molecular mechanism of astrocyte activation in response to β-amyloid (Aβ). Likewise, the relevance of pro-inflammatory mediators tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), cyclooxygenase-2 (COX-2) and nuclear factor-κB (NF-κB), as integral players in disease progression will be discussed.
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