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The application of biomarkers to clinical Alzheimer disease (AD) research has transformed the way we think about the disorder. Probable AD was defined as a clinical syndrome, generally amnestic, that progressed to global dementia. Poor prediction of the underlying pathology has made it clear that this approach is inadequate, particularly for patients with atypical or mild symptoms. The recent proposal of a biomarker-based framework for diagnosis has moved our thinking about AD from the syndromic to the biological.1 In this framework, evidence of β-amyloid and tau deposition in the brain constitutes AD, regardless of clinical presentation. Using this biomarker approach with PET imaging, Therriault et al.2 report in this issue of Neurology® the patterns of β-amyloid (denoted A) and tau (denoted T) PET abnormalities in a group of persons with cognitive impairment recruited from a dementia-specialty clinic population. Their observations allow us to judge the added value of the PET biomarkers and to compare clinical and biomarker diagnoses.
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