Amyloid and Tau PET Imaging of Alzheimer Disease and Other Neurodegenerative Conditions

Abstract

Although diagnosing the syndrome of dementia is largely a clinical endeavor, neuroimaging plays an increasingly important role in accurately determining the underlying etiology, which extends beyond its traditional role in excluding other causes of altered cognition. New neuroimaging methods not only facilitate the diagnosis of the most common neurodegenerative conditions (particularly Alzheimer Disease [AD]) after symptom onset, but also show diagnostic promise even in the very early or presymptomatic phases of disease. Positron emission tomography (PET) is increasingly recognized as a key clinical tool for differentiating normal age-related changes in brain metabolism (using ¹⁸F-fluorodeoxyglucose [FDG]) from those seen in the earliest stages of specific forms of dementia. However, FDG PET only demonstrates nonspecific changes in altered parenchymal glucose uptake and not the specific etiologic proteinopathy causing the abnormal glucose uptake. A growing class of radiotracers targeting specific protein aggregates for amyloid-β (Aβ) and tau are changing the way AD is diagnosed, as these radiotracers directly label the underlying disease pathology. As these pathology-specific radiotracers are currently making their way to the clinic, it is important for the clinical neuroradiologist to understand the underlying patterns of Aβ and tau deposition in the context of AD (across its clinical continuum) and in other causes of dementia, as well as understand the implications of current research.