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Moreover, variation in levels of other <jats:styled-content style=\"fixed-case\">DAMPs<\/jats:styled-content> of this same class in <jats:styled-content style=\"fixed-case\">AD<\/jats:styled-content> may explain why normal elderly patients can exhibit high A\u03b2 plaque levels, and why removing A\u03b2 or its plaque does not retard disease progression. It may also explain why mouse transgenic models, having been designed to generate high A\u03b2, can be treated successfully by this approach.<\/jats:p>","DOI":"10.1111\/bph.13181","type":"journal-article","created":{"date-parts":[[2015,5,4]],"date-time":"2015-05-04T07:31:10Z","timestamp":1430724670000},"page":"3714-3727","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":83,"title":["Amyloid \u03b2: one of three danger\u2010associated molecules that are secondary inducers of the proinflammatory cytokines that mediate <scp>A<\/scp>lzheimer's disease"],"prefix":"10.1111","volume":"172","author":[{"given":"I A","family":"Clark","sequence":"first","affiliation":[{"name":"Biomedical Sciences and Biochemistry Research School of Biology Australian National University  Canberra ACT 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