New insights into the various molecular imaging techniques for assessment of the Alzheimer’s disease.

Learning Objectives 1-To review the role of different PET radiotracers in mechanism and diagnosis of AD 2-To discuss the future trend in utilizing various molecular imaging techniques and modalities in AD

Alzheimer’s disease (AD) is the most common neurodegenerative disorder. Despite the great advances in our understanding of the mechanisms of AD a significant gap in pathophysiology of this disorder remains to be addressed. PET has a potential to increase our knowledge about the mechanisms of AD. 18F-FDG PET as an indicator of cellular metabolism, has shown reliable alterations in AD including characteristic hypometabolism in hippocampus, posterior cingulate, lateral temporopairetal and precuneous cortices of which the most reliable early alterations are seen in the posterior cingulate cortex. Moreover, similar but less severe changes are seen in mild cognitive impairment which has been shown to predict progression to AD. Besides FDG there are new emerging radio-tracers that target the accumulated proteins in brain. 11C-Pittsburgh compound B (PiB) was the first tracer used to detect Amyloid plaques (Aβ). Tau protein which can be detected in neurofibrillary tangles (NFT) is another target and recently the 18F- and 11C- labeled tau agents have been introduced. These agents enable assessing the temporal separation between Aβ and NFT development in brain. PET radiotracers provide an opportunity to study the formation of these agents in normal and AD population. The current and future trend in AD imaging is to utilize the tau and Aβ radio-tracers in AD patients and compare those results with in vitro and animal studies. In this review we discuss these topics: 1- Description of the PET radiotracers in understanding the mechanism if AD and its diagnosis a- Radiotracers targeting cellular metabolism i- 18F-FDG b-Radiotracers targeting tau c- Beta-amyloid tracers 2- Current and future trends in diagnostic techniques for AD pathophysiology