Imaging Brain Metabolism and Pathology in AlzheimerÃ¢ÂÂs Disease with Positron Emission Tomography
- Corresponding Author:
- Sepideh Shokouhi
Department of Radiology & Radiological Sciences
Vanderbilt University Institute of Imaging Science
1161 21st Avenue South, AA 1105 MCN
Nashville, TN 37232-2310, USA
Fax: (615) 322-0734
E-mail: [email protected]
Received date: January 21, 2014; Accepted date: February 27, 2014; Published date: March 15, 2014
Citation: Shokouhi S, Claassen D, Riddle WR (2014) Imaging Brain Metabolism and Pathology in Alzheimer’s Disease with Positron Emission Tomography. J Alzheimers Dis Parkinsonism 4:143. doi:10.4172/2161-0460.1000143
Copyright: © 2014 Shokouhi S, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Current Positron Emission Tomography (PET) biomarkers for Alzheimer’s disease (AD) assess either neuronal function, or associated pathological features of this common neurodegenerative disease. The most widely accepted clinical PET tool for AD is 18-fluorodeoxyglucose PET (FDG-PET), which measures cerebral metabolic glucose utilization rate (CMRglc). FDG-PET is a marker of synaptic activity, neuronal function, and neuronal metabolic activity. AD is characterized by a distinct pattern of hypometabolism, as seen with the FDG images. This pattern can show variability across different subjects and is present before a patient is demented, specifically in amnestic mild cognitive impairment a clinical diagnosis defined as an intermediate state from normal aging to dementia. In addition to FDG PET, novel PET approaches assess known pathological hallmarks of AD including extracellular amyloid-beta plaques (Aβ) and intracellular neurofibrillary tangles composed of tau fibrils. Already, amyloid PET imaging is a tool that allows in vivo imaging of extracellular beta-amyloid levels. Efforts to bring tau imaging into clinical use continue, but this approach is hampered by the intracellular nature of tau protein deposition, subsequent weak radiotracer binding, and low image contrast. Several new candidate probes for tau-specific PET imaging are currently available but have not found their way into broad clinical applications. This study gives an overview of the most recent PET-based neuroimaging techniques for AD. We place special emphasis on PET data analysis and interpretation techniques, as well as radiochemistry for imaging metabolism and assessing Aβ and tau pathology.