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This review concerns how the primary inflammation preceding the generation of certain key damage‐associated molecular patterns ( DAMPs ) arises in  A lzheimer's disease ( AD ). In doing so, it places soluble amyloid β (Aβ), a protein hitherto considered as a primary initiator of AD, in a novel perspective. We note here that increased soluble Aβ is one of the proinflammatory cytokine‐induced  DAMPs  recognized by at least one of the toll‐like receptors on and in various cell types. Moreover, Aβ is best regarded as belonging to a class of  DAMPs , as do the S100 proteins and  HMBG 1, that further exacerbate production of these same proinflammatory cytokines, which are already enhanced, and induces them further. Moreover, variation in levels of other  DAMPs  of this same class in  AD  may explain why normal elderly patients can exhibit high Aβ plaque levels, and why removing Aβ or its plaque does not retard disease progression. It may also explain why mouse transgenic models, having been designed to generate high Aβ, can be treated successfully by this approach.

Amyloid β: one of three danger‐associated molecules that are secondary inducers of the proinflammatory cytokines that mediate A lzheimer's disease