Current understanding of Alzheimer's disease (AD) pathogenesis relies on the observed accumulations of amyloid β and phosphorylated tau aggregates that are thought to play key roles in initiating or propagating disease. However, other processes including changes in synaptic proteins and neurotransmitter loss have been suggested as important etiologies or contributors. Positron emission tomography (PET) imaging allows in vivo investigations of molecular changes associated with AD. PET imaging with multiple radiotracers can be used in combination with other modalities such as magnetic resonance imaging (MRI), and with assessments of cognition and neuropsychiatric symptoms to investigate the molecular underpinnings of AD. Studies of synaptic protein changes may improve the understanding of disease mechanisms and provide valuable markers of disease progression and therapeutic efficacy. This chapter will illustrate the importance of in vivo molecular imaging in the study of AD with a specific emphasis on PET and radioligands for several non-amyloid targets.
Keywords: Alzheimer's disease; PET; Positron emission tomography; SV2A; Serotonin; [(11)C]UCB-J; [(18)F]FPEB; mGluR5.
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