{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,5]],"date-time":"2026-09-05T06:06:38Z","timestamp":1788588398386,"version":"build-2803163510"},"reference-count":128,"publisher":"eLife Sciences Publications, Ltd","license":[{"start":{"date-parts":[[2025,2,17]],"date-time":"2025-02-17T00:00:00Z","timestamp":1739750400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2025,2,17]],"date-time":"2025-02-17T00:00:00Z","timestamp":1739750400000},"content-version":"am","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2025,2,17]],"date-time":"2025-02-17T00:00:00Z","timestamp":1739750400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100010269","name":"Wellcome Trust","doi-asserted-by":"publisher","award":["10.35802\/217150"],"award-info":[{"award-number":["10.35802\/217150"],"id":[{"id":"10.35802\/217150","id-type":"DOI","asserted-by":"publisher"}]}],"id":[{"id":"10.13039\/100010269","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Leonard Wolfson PhD Programme in Neurodegeneration"}],"content-domain":{"domain":["elifesciences.org"],"crossmark-restriction":false},"short-container-title":[],"abstract":"<jats:p>\n                    By exposing genes associated with disease, genomic studies provide hundreds of starting points that should lead to druggable processes. However, our ability to systematically translate these genomic findings into biological pathways remains limited. Here, we combine rapid loss-of-function mutagenesis of Alzheimer\u2019s risk genes and behavioural pharmacology in zebrafish to predict disrupted processes and candidate therapeutics.\n                    <jats:ext-link ext-link-type=\"uri\" xlink:href=\"https:\/\/github.com\/francoiskroll\/FramebyFrame\">FramebyFrame<\/jats:ext-link>\n                    , our expanded package for the analysis of larval behaviours, revealed that decreased night-time sleep was common to F0 knockouts of all four late-onset Alzheimer\u2019s risk genes tested. We developed an online tool,\n                    <jats:ext-link ext-link-type=\"uri\" xlink:href=\"https:\/\/francoiskroll.shinyapps.io\/zoltar\/\">ZOLTAR<\/jats:ext-link>\n                    , which compares any behavioural fingerprint to a library of fingerprints from larvae treated with 3677 compounds. ZOLTAR successfully predicted that\n                    <jats:italic>sorl1<\/jats:italic>\n                    mutants have disrupted serotonin signalling and identified betamethasone as a drug which normalises the excessive day-time sleep of\n                    <jats:italic>presenilin-2<\/jats:italic>\n                    knockout larvae with minimal side effects. Predictive behavioural pharmacology offers a general framework to rapidly link disease-associated genes to druggable pathways.\n                  <\/jats:p>","DOI":"10.7554\/elife.96839","type":"journal-article","created":{"date-parts":[[2024,5,29]],"date-time":"2024-05-29T12:26:01Z","timestamp":1716985561000},"update-policy":"https:\/\/doi.org\/10.7554\/elife.96839","source":"Crossref","is-referenced-by-count":10,"title":["Behavioural pharmacology predicts disrupted signalling pathways and candidate therapeutics from zebrafish mutants of Alzheimer\u2019s disease risk genes"],"prefix":"10.7554","volume":"13","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9908-2648","authenticated-orcid":true,"given":"Fran\u00e7ois","family":"Kroll","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/02jx3x895","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Cell and Developmental Biology, University College London","place":["London, United 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