Aβ-Induced Proinflammatory Cytokine Release from Differentiated Human THP-1 Monocytes.

As noted in the introductory chapters of this book, neuritic plaques composed of accumulated amyloid β (Aβ) peptide are a hallmark pathological feature of the Alzheimer's disease (AD) brain. Compelling genetic data now implicate these plaques as key causative agents in AD onset, as all known mutations that lead to early onset familial AD (1-6) result in an increased production of the amyloidogenic Aβ1-42 isoform (7-11). Although it appears likely that the deposition of multimeric Aβ fibrils into plaques is a necessary step in AD onset, there is still uncertainty as to how Aβ and neuritic plaques might cause the neuropathology that leads to the dementia that is characteristic of this disease.