Abstract
Alzheimer's disease (AD) is a devastating and progressive neurodegenerative disease for which there is no cure. Mild cognitive impairment (MCI) is considered a prodromal stage of the disease. Molecular imaging with positron emission tomography (PET) allows for the in vivo visualisation and tracking of pathophysiological changes in AD and MCI. PET is a very promising methodology for differential diagnosis and novel targets of PET imaging might also serve as biomarkers for disease‐modifying therapeutic interventions. This review provides an overview of the current status and applications of in vivo molecular imaging of AD pathology, specifically amyloid, tau, and microglial activation. PET imaging studies were included and evaluated as potential biomarkers and for monitoring disease progression. Although the majority of radiotracers showed the ability to discriminate AD and MCI patients from healthy controls, they had various limitations that prevent the recommendation of a single technique or tracer as an optimal biomarker. Newer research examining amyloid, tau, and microglial PET imaging in combination suggest an alternative approach in studying the disease process.
Highlights
Alzheimer's disease (AD) is the most common cause of dementia worldwide
This review describes the recent developments and current applications of positron emission tomography (PET) imaging of amyloid, tau, and neuroinflammation in AD and mild cognitive impairment (MCI)
Both MCI and AD patients showed increased tau binding in inferior temporal, lateral temporal, lateral occipital, inferior parietal, anterior frontal, lateral occipital cortex, in addition to the precuneus compared to healthy controls
Summary
Alzheimer's disease (AD) is the most common cause of dementia worldwide. It is estimated that by 2050, 1 in 85 people worldwide will develop AD (Brookmeyer, Johnson, Ziegler-Graham, & Arrighi, 2007). Klunk et al discovered what would become the most heavily researched amyloid PET radiotracer, 11C-labelled Pittsburgh compound B ([11C]PiB; Table 1) (Klunk et al, 2004) In their seminal study, it was shown that this benzothiazole-based radioligand was capable of discriminating between patients with a diagnosis of extremely mild AD and healthy controls. It was shown that this benzothiazole-based radioligand was capable of discriminating between patients with a diagnosis of extremely mild AD and healthy controls Areas such as frontal and temporoparietal cortex, which are susceptible to Aβ pathology, demonstrated increased [11C]PiB retention in AD. MCI patients with elevated binding of [11C]PiB were more likely to
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