β-Amyloid Imaging In Vivo and Its Possible Implications for Alzheimer’s Disease
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A central and initiating biochemical feature of most forms of Alzheimer’s disease (AD) is mis-processing of the neurotoxic amyloid β-peptide (Aβ). Promising therapeutic strategies are being developed directed at various steps in the Aβ biochemical cascade, resulting in reduction of accumulated Aβ. Promising radiotracers such as [18F]FDDNP, [11C]PIB and [11C]SB-13 have been developed for PET imaging of cerebral Aβ accumulation in vivo. The combination of these promising therapeutic strategies and radiotracers will hopefully allow for early detection and preventative treatment of AD. This will need to be studied prospectively in subjects at risk for AD, such as amnestic mild cognitive impairment (MCI), with adequate follow-up. Longitudinal Aβ PET studies may also help us resolve the question whether aging subjects without detectable cognitive impairment but with Aβ accumulation are at increased risk for developing AD. Repeated Aβ PET could be used to study the efficacy of β-amyloid-reducing medications.
KeywordsPositron Emission Tomography Single Photon Emission Compute Tomography Mild Cognitive Impairment Amnestic Mild Cognitive Impairment Amyloid Image
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