Development of Alzheimer’s disease (AD) has been attributed to neurodegeneration as a result of the neuronal overexpression, secretion, and deposition of the neurotoxic amyloid β (Aβ) fragment of the Aβ protein precursor in the brain (1). No specific treatment for AD is currently available, and clinicians are increasingly focused on developing ways to either prevent or delay the formation of Aβ plaques in the brain of AD patients (2). In addition, several hundred clinical trials approved by the United States Food and Drug Administration have been completed or are in progress to develop drugs for the prevention, onset delay, or treatment of AD. Early detection of Aβ plaques by non-invasive techniques such as positron emission tomography (PET) is often used to identify individuals who are prone to get the disease and also to monitor the efficacy of drugs used to treat or delay onset of the disease (3).
The 11C-labeled Pittsburgh compound B ([11C]PIB) is the most commonly used PET tracer for detection of Aβ plaques, but due to the short half-life (20.4 min) of 11C the use of this label is restricted to clinical facilities that have the capability to generate the agent on-site (3). Some 18F-labeled compounds have also been generated for the visualization of Aβ plaques, but these labeled compounds have low specificity (3), and the PIB analogs [18F]BAY94-9172 (4) and [18F]GE067 (5) or its derivative, [18F]flutemetamol (6), are currently under clinical evaluation. In an ongoing effort to develop 18F-labeled compounds for the detection of Aβ plaques and to monitor the efficacy of drugs used to treat AD, Serdons et al. (3) synthesized three new 18F-labeled derivatives of 2-phenylbenzothiazoles (designated [18F]2, [18F]3, and [18F]6, respectively), determined the in vitro affinity of these tracers for Aβ fibrils, and investigated their biodistribution in mice, pharmacokinetics in rats, and pharmacokinetics and uptake in monkeys.