Beschreibung:
<jats:title>Abstract</jats:title><jats:sec><jats:title>Background</jats:title><jats:p>With the introduction of the NINCDS‐ADRDA criteria in 1984, Alzheimer’s disease (AD) could for the first time be diagnosed with high probability during life. The pathological characteristics of AD were not mentioned at all however, since they could not yet be measured in living individuals.</jats:p></jats:sec><jats:sec><jats:title>Method</jats:title><jats:p>In the following decades, advances in MRI measures, markers in Cerebrospinal Fluid (CSF), and amyloid‐imaging using PET can be counted among the largest successes of AD research. As a result, the AD disease process can now be demonstrated during life. In addition, these novel diagnostic tests allow the measurement of Alzheimer’s pathology before the stage of dementia. Nonetheless, until well into the 21<jats:sup>st</jats:sup> century, the 1984 criteria remained common standard.</jats:p></jats:sec><jats:sec><jats:title>Result</jats:title><jats:p>The publication of the IWG‐criteria in 2007 was a first attempt to integrate biomarker knowledge into diagnostic criteria. These criteria allowed a diagnosis of AD before dementia. In 2011 a roundtable under auspices of NIA‐AA published separate sets of criteria for dementia and MCI due to AD, and even for preclinical AD –the latter reading more like a research agenda than a set of criteria. The 2018 NIA‐AA research framework defines AD as a biological construct, independently of clinical staging. A diagnosis of AD can hence entirely be based on biomarkers. The most recent publication of the IWG in 2021 however proposes that a diagnosis of AD should be reserved to those with symptoms only, otherwise individuals should be considered ‘at risk’ of progression to AD.</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p>Questions remain with respect to operationalization, e.g. choices and cut‐offs, for the biomarkers of use. Among the most fundamental questions is the question whether you can have disease but no symptoms, and <jats:italic>when</jats:italic> disease is symptomatic. Ultimately, truly longitudinal studies are needed to answer the question whether everybody with abnormal amyloid and tau will develop dementia, given enough time of life. This is particularly important now disease modifying treatment are at the horizon. In this presentation, I provide an overview of the different sets of criteria, outlining a number of open questions to be addressed before these criteria can be fully used in clinical practice.</jats:p></jats:sec>