The dense-core plaques of Alzheimer's disease are granulomas

Dense-core plaques, whose centers contain highly polymerized and compacted aggregates of amyloid beta peptides, are one of the two defining histopathological features of Alzheimer's disease. Recent findings indicate that these plaques do not form spontaneously but are instead constructed by microglia, the tissue macrophages of the central nervous system. We discuss cellular, structural, functional, and gene expression criteria by which the microglial assembly of dense-core plaques in the Alzheimer's brain parallels the construction of granulomas by macrophages in other settings. We compare the genesis of these plaques to the macrophage assembly of mycobacterial granulomas, the defining histopathological features of tuberculosis. We suggest that if dense-core plaques are indeed granulomas, their simple disassembly may be contraindicated as an Alzheimer's therapy. Microglia, the tissue macrophages of the central nervous system, use phagocytosis of loosely organized amyloid beta (A beta) to construct dense-core plaques, one of the defining histopathological features of Alzheimer's disease. The biology of this process parallels macrophage construction of granulomas in tuberculosis and other settings.

Automated summary

Dense-core plaques, a defining histopathological feature of Alzheimer's disease, are constructed by microglia in the central nervous system rather than forming spontaneously. The process parallels macrophage construction of granulomas in tuberculosis and other settings.