Abstract
AbstractBackgroundPositron emission tomography (PET) imaging is an increasingly widespread tool for the identification of Alzheimer’s disease (AD) pathophysiology. PET biomarkers of Aβ and tau pathology, together with fluid biomarkers and ex vivo pathology validation, have enabled detection of early regional changes and identification of individuals who are unimpaired but on the AD pathway. This presentation will address the changing and complementary role of PET biomarkers in relation to fluid biomarkers in AD clinical trials, research, and practice.MethodRecent PET imaging work from natural history studies targeting Aβ and tau pathology will be reviewed, with an emphasis on early detection of dynamic regional changes in unimpaired individuals in relation to fluid biomarkers and cognition. Relationships between Aβ and tau PET measurements to other biomarkers and pathology will be discussed, as well as the status of emerging PET markers of inflammation and synaptic integrity.ResultA key unique feature of PET imaging is that it offers a regionally‐specific view of fibrillar Aβ and paired helical filament (PHF) tau pathology in vivo. Initial Aβ and tau changes are detectable over a decade before the onset of clinically‐relevant cognitive symptoms. There is a predictable time course of Aβ and tau change over the course of disease, and regional tau accumulation predicts local neurodegenerative changes. In symptomatic individuals, inferolateral temporal tau accumulation is sensitive to AD and useful for differential diagnosis. However, tau accumulation is also highly variable even among symptomatic Aβ+ individuals, likely due to co‐pathology and the influence of poorly understood factors such as age, sex, genetics, and cardiovascular risk. There are a number of technical and cost considerations for successful implementation of PET relative to other biomarkers in research, trials, and clinical practice.ConclusionEarly, regionally‐specific Aβ and tau PET measurements predict downstream neurodegeneration and cognitive decline. Such early changes represent an opportunity for therapeutic intervention, but identification of individuals who are unimpaired but at risk remains challenging. Additional longitudinal research and development of PET biomarkers for other disease targets will address open questions about how AD develops.
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