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dc.rights.licenseopenen_US
hal.structure.identifierBordeaux population health [BPH]
dc.contributor.authorDALY, Timothy
dc.contributor.authorOLLURI, Andi
dc.contributor.authorKURKINEN, Markku
dc.date.accessioned2025-01-08T10:14:08Z
dc.date.available2025-01-08T10:14:08Z
dc.date.issued2024-12-19
dc.identifier.issn1899-5276en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/204191
dc.description.abstractEnThe so-called "amyloid cascade hypothesis" provides an elegant explanation of Alzheimer's disease (AD), has motivated the amyloid-lowering therapeutic strategy, and led to the elaboration of a rich experimental and conceptual toolkit for the field to progress. But it might be incorrect. The scientific evidence base supporting the efficacy and safety of current anti-amyloid antibody treatments in AD is weak. Nevertheless, we argue that there is a bias towards the amyloid-lowering therapeutic strategy amongst key opinion leaders in the research and advocacy communities. To demonstrate this, we first focus on the AD lexicon: while any accrual of amyloid on a brain PET scan can now permit diagnosis/definition of AD, lowering positron emission tomography (PET) amyloid is considered disease modification, and treatment-induced side-effects are hidden behind neutral-sounding acronyms: ARIA (amyloid-β (Aβ)-related imaging abnormalities: brain bleeding and swelling) and ARPA (amyloid-β (Aβ) removal-related pseudo-atrophy: brain shrinkage). Second, we underline that drugmakers did not test anti-amyloid antibodies against the best proven interventions and did not adequately inform trial participants of risks, thus violating research ethics of the Declaration of Helsinki on 2 counts. In conclusion, we are critical of over-reliance on the idea that PET amyloid-lowering treatments for AD are a therapeutic revolution as claimed, and consider that optimism does not excuse a lack of scientific, regulatory, and ethical integrity. We argue for rigorous, properly controlled (e.g. donepezil) anti-amyloid trials demonstrating cognitive and functional benefit before accepting amyloid-lowering drugs as the new standard of care for AD patients.
dc.language.isoENen_US
dc.rightsAttribution 3.0 United States*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/us/*
dc.subject.enAlzheimer’s Disease
dc.subject.enAmyloid Hypothesis
dc.subject.enBias
dc.subject.enClinical Trials
dc.subject.enEthics
dc.titleAnti-amyloid treatments in Alzheimer’s disease: elegance, evidence and ethics
dc.title.alternativeAdv Clin Exp Meden_US
dc.typeArticle de revueen_US
dc.identifier.doi10.17219/acem/198674en_US
dc.subject.halSciences du Vivant [q-bio]/Santé publique et épidémiologieen_US
dc.identifier.pubmed39698778en_US
bordeaux.journalAdvances in Clinical and Experimental Medicineen_US
bordeaux.page1303-1309en_US
bordeaux.volume33en_US
bordeaux.hal.laboratoriesBordeaux Population Health Research Center (BPH) - UMR 1219en_US
bordeaux.issue12en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionINSERMen_US
bordeaux.teamACTIVE_BPHen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
bordeaux.import.sourcecrossref
hal.identifierhal-04873123
hal.version1
hal.date.transferred2025-01-08T10:14:11Z
hal.popularnonen_US
hal.audienceInternationaleen_US
hal.exporttrue
workflow.import.sourcecrossref
dc.rights.ccPas de Licence CCen_US
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