In The Lancet Neurology, Frisoni and colleagues1 present a thought ful and topical Insight, but I dis agree with their recommendations. They point out that, although the National Institute on Aging–Alzheimer’s Association (NIA-AA) research framework2 recommends defining the dis ease bio logically (by abnormal biomark ers denoting both amyloid and tau deposits) indepen dent from symp to matic presentation, most in the lay community under stand the term Alzheimer’s disease to mean a progress ive cognitive impair ment that leads to dementia. This disparity creates a conceptual dis connect between the lay and scien tific communities. The solution recommended by Frisoni and col leagues1 is that the term Alzheimer’s disease be reserved for symptomatic individuals.

Although Frisoni and colleagues1 accurately recount many aspects of the NIA-AA research framework, 2 their Insight includes one common but important misinterpretation, which is:“to refrain from using the Alzheimer’s disease label for cognitively intact people showing abnormal amyloid markers (CSF or PET) but normal or unknown tau markers”. Implying that the framework defines Alzheimer’s disease as isolated amyloidosis without evidence of tauopathy is an error. The fact is that the NIA-AA research framework did not apply the label Alzheimer’s disease to such individuals. The label Alzheimer’s disease is reserved exclusively for individuals with abnormal biomarkers of both amyloid and tau. This label aligns the in-vivo, biomarker-based definition of Alzheimer’s disease with the neuropathological definition. 3 Frisoni and colleagues1 also propose that abnormal biomarkers in asymptomatic people should be labelled as risk factors for disease, rather than evidence of disease itself. It is well established that biomarkers of