Figure 2.

Inflammation mediates Aβ-induced BACE1 transcriptional activation. Aβ peptides are pro-inflammatory. They activate microglia and astrocytes that release inflammatory mediators. Those activate NF-κB, which is also activated by oxidative stress, ischemia or traumatic brain injury. Pathological activation of NF-κB activates BACE1 transcription, thus increasing Aβ peptides levels and feeding a vicious cycle. Aβ, amyloid peptide; BACE1, β-secretase βAPP cleaving enzyme 1; NF-κB, nuclear factor-κB.