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Figure 1 | Journal of Neuroinflammation

Figure 1

From: Down’s syndrome, neuroinflammation, and Alzheimer neuropathogenesis

Figure 1

Schematic highlighting the importance of inflammation-associated genes in the promotion of Alzheimer neuropathogenesis in trisomy 21. Chromosome 21 genes triplicated in trisomy 21 activate microglia with overexpression and release of proinflammatory cytokines, especially IL-1β, which, in turn, induces further increases in precursor protein for β-amyloid (APP), favoring β-amyloid (Aβ) plaque deposition, and in mitogen-activated protein kinase (MAPK)-p38-dependent phosphorylation and production of phosphorylated tau, favoring neurofibrillary tangle formation, and through nuclear factor κB (NFκB) activity such changes sustain neuroinflammatory responses and consequent neuropathological change.

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