This perspective by Youtong Huang and I argues that the dense-core plaques of Alzheimer's disease are in fact granulomas constructed by microglia. We highlight structural, functional, and transcriptomic correspondences between dense-core plaques and the granulomas constructed by macrophages in other settings, including tuberculosis.
Dietmar Thal Katholieke Universiteit Leuven, Department of Imaging and Pathology, Laboratory of Neuropathology
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In this interesting paper, Greg Lemke uses the somewhat provocative term granuloma to highlight the reactive/resorptive nature of the glial cell response around plaques. This reactive and resorptive response has been discussed in our field for years, though in different terms. The comparison of transcriptomics datasets we now have available further clarifies this point of view, as articulated in Lemke’s perspective.
In my opinion, perhaps the term granuloma is not fully accurate from a pathologist’s point of view, but the underlying message is correct and well argued: In amyloid plaques, a non-physiological protein aggregate becomes attacked and resorbed by the responsible cells, just like foreign material in a foreign body type granuloma or the pathogenic agents/necrotic tissue in a TBC granuloma.
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Salk Institute
This perspective by Youtong Huang and I argues that the dense-core plaques of Alzheimer's disease are in fact granulomas constructed by microglia. We highlight structural, functional, and transcriptomic correspondences between dense-core plaques and the granulomas constructed by macrophages in other settings, including tuberculosis.
Katholieke Universiteit Leuven, Department of Imaging and Pathology, Laboratory of Neuropathology
In this interesting paper, Greg Lemke uses the somewhat provocative term granuloma to highlight the reactive/resorptive nature of the glial cell response around plaques. This reactive and resorptive response has been discussed in our field for years, though in different terms. The comparison of transcriptomics datasets we now have available further clarifies this point of view, as articulated in Lemke’s perspective.
In my opinion, perhaps the term granuloma is not fully accurate from a pathologist’s point of view, but the underlying message is correct and well argued: In amyloid plaques, a non-physiological protein aggregate becomes attacked and resorbed by the responsible cells, just like foreign material in a foreign body type granuloma or the pathogenic agents/necrotic tissue in a TBC granuloma.
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