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In addition to criticisms, however, we believe that the field would benefit from having alternative narratives and disease models that can either replace or function alongside of an amyloid\u2010centric view of Alzheimer's. This review is an attempt to meet that need. We offer three experimentally verified amyloid\u2010independent mechanisms, each of which plausibly contributes substantially to the aetiology of Alzheimer's disease: loss of <jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content> integrity, faulty cell cycle regulation, regression of myelination. We outline the ways in which the failure of each can contribute to <jats:styled-content style=\"fixed-case\">AD<\/jats:styled-content> initiation and progression, and review how, acting alone or in combination with each other, they are sufficient for explaining the full range of <jats:styled-content style=\"fixed-case\">AD<\/jats:styled-content> pathologies. Yet, these three alternatives represent only a few of the many non\u2010amyloid mechanisms that can explain <jats:styled-content style=\"fixed-case\">AD<\/jats:styled-content> pathogenesis. Therefore instead of proposing a single \u2018alternative hypothesis\u2019 to the amyloid cascade theory, sporadic <jats:styled-content style=\"fixed-case\">AD<\/jats:styled-content> is pictured as the result of independent yet intersecting age\u2010related pathologies that afflict the ageing human brain.<\/jats:p><jats:p><jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"http:\/\/onlinelibrary.wiley.com\/journal\/10.1111\/(ISSN)1471-4159\/homepage\/virtual_issues.htm#Amyloid\">This article is part of the series \u201cBeyond Amyloid\u201d<\/jats:ext-link>.<\/jats:p><jats:p><jats:bold>Cover Image<\/jats:bold> for this issue: doi. <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"doi\" xlink:href=\"10.1111\/jnc.13823\">10.1111\/jnc.13823<\/jats:ext-link>.<\/jats:p><\/jats:sec><jats:sec><jats:label\/><jats:p>\n<jats:boxed-text content-type=\"graphic\" position=\"anchor\"><jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/jnc14079-fig-0003-m.png\"><jats:alt-text>image<\/jats:alt-text><\/jats:graphic><\/jats:boxed-text>\n<\/jats:p><\/jats:sec>","DOI":"10.1111\/jnc.14079","type":"journal-article","created":{"date-parts":[[2017,5,26]],"date-time":"2017-05-26T07:52:43Z","timestamp":1495785163000},"page":"432-444","source":"Crossref","is-referenced-by-count":100,"title":["Re\u2010imagining Alzheimer's disease \u2013 the diminishing importance of amyloid and a glimpse of what lies ahead"],"prefix":"10.1111","volume":"143","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7287-3984","authenticated-orcid":false,"given":"Kai\u2010Hei","family":"Tse","sequence":"first","affiliation":[{"name":"Division of Life Science and the State Key Laboratory of Molecular Neuroscience The Hong Kong University of Science and Technology Clear Water Bay Kowloon Hong Kong"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7786-5844","authenticated-orcid":false,"given":"Karl","family":"Herrup","sequence":"additional","affiliation":[{"name":"Division of Life Science and the State Key Laboratory of Molecular Neuroscience The Hong Kong University of Science and Technology Clear Water Bay Kowloon Hong Kong"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2017,6,21]]},"reference":[{"key":"e_1_2_10_2_1","doi-asserted-by":"publisher","DOI":"10.1038\/nature.2016.21045"},{"key":"e_1_2_10_3_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.neurobiolaging.2008.11.012"},{"key":"e_1_2_10_4_1","doi-asserted-by":"publisher","DOI":"10.1111\/bpa.12216"},{"key":"e_1_2_10_5_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.1912-12.2012"},{"key":"e_1_2_10_6_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.18-16-06241.1998"},{"key":"e_1_2_10_7_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.22-02-00455.2002"},{"key":"e_1_2_10_8_1","doi-asserted-by":"publisher","DOI":"10.1093\/jnen\/61.2.197"},{"key":"e_1_2_10_9_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0908867107"},{"key":"e_1_2_10_10_1","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000199348.10580.1d"},{"key":"e_1_2_10_11_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.neurobiolaging.2003.03.001"},{"key":"e_1_2_10_12_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.neurobiolaging.2009.08.007"},{"key":"e_1_2_10_13_1","doi-asserted-by":"publisher","DOI":"10.1001\/archpsyc.58.5.461"},{"key":"e_1_2_10_14_1","doi-asserted-by":"publisher","DOI":"10.1001\/archneur.60.3.393"},{"key":"e_1_2_10_15_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.biopsych.2007.03.024"},{"key":"e_1_2_10_16_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuroimage.2015.10.030"},{"key":"e_1_2_10_17_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.nbd.2013.10.007"},{"key":"e_1_2_10_18_1","doi-asserted-by":"publisher","DOI":"10.1161\/STROKEAHA.108.537704"},{"key":"e_1_2_10_19_1","doi-asserted-by":"publisher","DOI":"10.1038\/nrn3887"},{"key":"e_1_2_10_20_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jalz.2014.07.155"},{"key":"e_1_2_10_21_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.18-08-02801.1998"},{"key":"e_1_2_10_22_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.freeradbiomed.2007.05.037"},{"key":"e_1_2_10_23_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbadis.2014.06.010"},{"key":"e_1_2_10_24_1","doi-asserted-by":"publisher","DOI":"10.1001\/archneurol.2009.174"},{"key":"e_1_2_10_25_1","doi-asserted-by":"publisher","DOI":"10.1038\/nrn3900"},{"key":"e_1_2_10_26_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.ajpath.2011.03.036"},{"key":"e_1_2_10_27_1","first-page":"4223","article-title":"Induction of cell cycle entry and cell death in postmitotic lens fiber cells by overexpression of E2F1 or E2F2","volume":"41","author":"Chen Q.","year":"2000","journal-title":"Invest. 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