{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,4]],"date-time":"2026-11-04T02:17:08Z","timestamp":1793758628501,"version":"4.6.1"},"reference-count":44,"publisher":"American Medical Association (AMA)","issue":"12","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JAMA Neurol"],"published-print":{"date-parts":[[2024,12,1]]},"abstract":"<jats:sec id=\"ab-nsc240001-1\">\n                    <jats:title>Importance<\/jats:title>\n                    <jats:p>Since 2018, a movement has emerged to define Alzheimer disease (AD) as a purely biological entity based on biomarker findings. The recent revision of the Alzheimer\u2019s Association (AA) criteria for AD furthers this direction. However, concerns about a purely biological definition of AD being applied clinically, the understanding of AD by society at large, and the translation of blood-based biomarkers into clinical practice prompt these International Working Group (IWG) updated recommendations.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"ab-nsc240001-2\">\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>To consider the revised AA criteria and to offer an alternative definitional view of AD as a clinical-biological construct for clinical use. The recommendations of the 2021 IWG diagnostic criteria are updated for further elaborating at-risk and presymptomatic states.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"ab-nsc240001-3\">\n                    <jats:title>Evidence Review<\/jats:title>\n                    <jats:p>PubMed was searched for articles published between July 1, 2020, and March 1, 2024, using the terms \u201cbiomarker\u201d OR \u201camyloid\u201d OR \u201ctau\u201d OR \u201cneurodegeneration\u201d OR \u201cpreclinical\u201d OR \u201cCSF\u201d OR \u201cPET\u201d OR \u201cplasma\u201d AND \u201cAlzheimer\u2019s disease.\u201d The references of relevant articles were also searched.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"ab-nsc240001-4\">\n                    <jats:title>Findings<\/jats:title>\n                    <jats:p>In the new AA diagnostic criteria, AD can be defined clinically as encompassing cognitively normal people having a core 1 AD biomarker. However, recent literature shows that the majority of biomarker-positive cognitively normal individuals will not become symptomatic along a proximate timeline. In the clinical setting, disclosing a diagnosis of AD to cognitively normal people with only core 1 AD biomarkers represents the most problematic implication of a purely biological definition of the disease.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"ab-nsc240001-5\">\n                    <jats:title>Conclusions and Relevance<\/jats:title>\n                    <jats:p>The ultimate aim of the field was to foster effective AD treatments, including preventing symptoms and dementia. The approach of diagnosing AD without a clinical and biological construct would be unwarranted and potentially concerning without a clear knowledge of when or whether symptoms will ever develop. It is recommended that those who are amyloid-positive only and, more generally, most biomarker-positive cognitively normal individuals, should not be labeled as having AD. Rather, they should be considered as being at risk for AD. The expansion of presymptomatic AD is viewed as a better diagnostic construct for those with a specific pattern of biomarkers, indicating that they are proximate to the expression of symptoms in the near future.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1001\/jamaneurol.2024.3770","type":"journal-article","created":{"date-parts":[[2024,11,1]],"date-time":"2024-11-01T04:30:31Z","timestamp":1730435431000},"page":"1304","source":"Crossref","is-referenced-by-count":449,"title":["Alzheimer Disease as a Clinical-Biological Construct\u2014An International Working Group Recommendation"],"prefix":"10.1001","volume":"81","author":[{"given":"Bruno","family":"Dubois","sequence":"first","affiliation":[{"name":"D\u00e9partement de Neurologie, Groupe Hospitalier Piti\u00e9-Salp\u00eatri\u00e8re, AP-HP Sorbonne Universit\u00e9, Institute of Memory and Alzheimer\u2019s Disease, Paris, France"},{"name":"Sorbonne Universit\u00e9, INSERM U1127, CNRS 7225, Institut du Cerveau - ICM, FrontLab, Paris, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicolas","family":"Villain","sequence":"additional","affiliation":[{"name":"D\u00e9partement de Neurologie, Groupe Hospitalier Piti\u00e9-Salp\u00eatri\u00e8re, AP-HP Sorbonne Universit\u00e9, Institute of Memory and Alzheimer\u2019s Disease, Paris, France"},{"name":"Sorbonne Universit\u00e9, INSERM U1127, CNRS 7225, Institut du Cerveau - 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