{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,2]],"date-time":"2026-11-02T18:01:07Z","timestamp":1793642467226,"version":"4.5.1"},"reference-count":169,"publisher":"Wiley","issue":"S2","license":[{"start":{"date-parts":[[2016,6,3]],"date-time":"2016-06-03T00:00:00Z","timestamp":1464912000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100008897","name":"Janssen Pharmaceuticals","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100008897","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurochemistry"],"published-print":{"date-parts":[[2016,10]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:label\/>\n                    <jats:p>\n                      The first description of Alzheimer's disease (\n                      <jats:styled-content style=\"fixed-case\">AD<\/jats:styled-content>\n                      ) was made in 1907 by Alois Alzheimer (\n                      <jats:italic>Allgemeine Zeitschrift fur Psyciatrie und Psychisch\u2010Gerichtliche Medizin<\/jats:italic>\n                      <jats:bold>64,<\/jats:bold>\n                      3, 1907), although other contemporary physicians had made similar, and rather more complete, assessments of the neuropathological changes present in the\n                      <jats:styled-content style=\"fixed-case\">AD<\/jats:styled-content>\n                      brain (Fischer,\n                      <jats:italic>Monatsschr Psychiat Neurol<\/jats:italic>\n                      <jats:bold>22,<\/jats:bold>\n                      17, 1907). Our knowledge of\n                      <jats:styled-content style=\"fixed-case\">AD<\/jats:styled-content>\n                      has increased dramatically and continues to accelerate. This year is 25\u00a0years after the publication of a series of papers that, in various ways, articulated the amyloid cascade hypothesis (\n                      <jats:styled-content style=\"fixed-case\">ACH<\/jats:styled-content>\n                      ) for\n                      <jats:styled-content style=\"fixed-case\">AD<\/jats:styled-content>\n                      (Beyreuther and Masters,\n                      <jats:italic>Brain Pathol<\/jats:italic>\n                      <jats:bold>1,<\/jats:bold>\n                      241\u2013251, 1991; Hardy and Allsop,\n                      <jats:italic>Trends Pharmacol Sci<\/jats:italic>\n                      <jats:bold>12,<\/jats:bold>\n                      383\u2013388, 1991; Selkoe,\n                      <jats:italic>Neuron<\/jats:italic>\n                      <jats:bold>6,<\/jats:bold>\n                      487\u2013498, 1991; Hardy and Higgins,\n                      <jats:italic>Science<\/jats:italic>\n                      <jats:bold>256,<\/jats:bold>\n                      184\u2013185, 1992). This review will cover some familiar territory, but we shall also place the\n                      <jats:styled-content style=\"fixed-case\">ACH<\/jats:styled-content>\n                      into a wider context, compare it with other hypotheses for\n                      <jats:styled-content style=\"fixed-case\">AD<\/jats:styled-content>\n                      , explore the evolution of the hypothesis to encompass new findings, and determine, irrespective of the merits of the hypothesis itself, whether it has been useful for the research field, both in academia and in industry. Finally, we shall review how the\n                      <jats:styled-content style=\"fixed-case\">ACH<\/jats:styled-content>\n                      has led to a number of therapeutic approaches, all of which have, to date, failed to reach their primary efficacy end\u2010points in clinical trials and reflect upon what the future may hold.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:label\/>\n                    <jats:p>\n                      <jats:boxed-text content-type=\"graphic\" position=\"anchor\">\n                        <jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/jnc13632-fig-0003-m.png\">\n                          <jats:alt-text>image<\/jats:alt-text>\n                        <\/jats:graphic>\n                      <\/jats:boxed-text>\n                      We review the amyloid cascade hypothesis (ACH) and compare it with other hypotheses that have been posited to explain the initiation and progression Alzheimer's disease. We document the data that support the ACH, and also reflect upon its deficiencies. We list the recent clinical failures of amyloidocentric drugs and anticipate the results that new therapeutic approaches may deliver.\n                    <\/jats:p>\n                    <jats:p>\n                      <jats:bold>This article is part of the<\/jats:bold>\n                      \u00a0\n                      <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"http:\/\/onlinelibrary.wiley.com\/journal\/10.1111\/(ISSN)1471-4159\/homepage\/special_issues.htm\">60th Anniversary special issue<\/jats:ext-link>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/jnc.13632","type":"journal-article","created":{"date-parts":[[2016,6,3]],"date-time":"2016-06-03T03:43:07Z","timestamp":1464925387000},"page":"237-252","source":"Crossref","is-referenced-by-count":371,"title":["The amyloid cascade hypothesis: are we poised for success or 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