Editorial Volume 11, Issue 1 pp 3—4

Figure 1. This figure describes the hypothesized relationship between systemic inflammation, neuroinflammation, and neurodegeneration. Inflammatory triggers, such as infection, chronic disease, and cellular aging can occur before or during middle adulthood. These events lead to increased pro-inflammatory signaling within the periphery, which can result in long-term perturbations in the balance between pro-inflammatory and anti-inflammatory networks. For some, these changes can lead to a state of chronic systemic inflammation that persists into older adulthood. By activating microglia and astrocytes, systemic inflammation can initiate or perpetuate a cytokine- and complement-mediated inflammatory response within the brain (i.e. neuroinflammation). Neuroinflammation has been shown to promote pathogenic brain changes, such as increased amyloid precursor protein processing, beta-amyloid oligomerization, tau phosphorylation, and small vessel disease. IL-1ß = interleukin 1 beta; IL-4 = interleukin 4; IL-6 = interleukin 6; IL-10 = interleukin 10; IL-13 = interleukin 13; TNF-α = tumor necrosis factor alpha.