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This article is part of the Research Topic Innate immunity and neurodegenerative disorders


Front. Pharmacol., 29 May 2012 | http://dx.doi.org/10.3389/fphar.2012.00096

Imaging of microglia in patients with neurodegenerative disorders

Marios Politis*, Paul Su and Paola Piccini
  • Division of Experimental Medicine, Faculty of Medicine, Centre for Neuroscience, Hammersmith Hospital, Imperial College London, London, UK

Microglia constitute the main immune defense in the central nervous system. In response to neuronal injury, microglia become activated, acquire phagocytic properties, and release a wide range of pro-inflammatory mediators that are essential for the annihilation of the neuronal insult. Although the role of microglial activation in acute neuronal damage is well defined, the pathophysiological processes underlying destructive or protective role to neurons following chronic exposure to microglial activation is still a subject of debate. It is likely that chronic exposure induces detrimental effects by promoting neuronal death through the release of neurotoxic factors. Positron emission tomography (PET) imaging with the use of translocator protein (TSPO) radioligands provides an in vivo tool for tracking the progression and severity of neuroinflammation in neurodegenerative disease. TSPO expression is correlated to the extent of microglial activation and the measurement of TSPO uptake in vivo with PET is a useful indicator of active disease. Although understanding of the interaction between radioligands and TSPO is not completely clear, there is a wide interest in application of TSPO imaging in neurodegenerative disease. In this article, we aim to review the applications of in vivo microglia imaging in neurodegenerative disorders such as Parkinson’s disease, Huntington’s disease, Dementias, and Multiple Sclerosis.

Keywords: dementia, Huntington, microglia, multiple sclerosis, Parkinson, PET, PK11195

Citation: Politis M, Su P and Piccini P (2012) Imaging of microglia in patients with neurodegenerative disorders. Front. Pharmacol. 3:96. doi: 10.3389/fphar.2012.00096

Received: 27 January 2012; Accepted: 01 May 2012;
Published online: 29 May 2012.

Edited by:

Roger A. Barker, University of Cambridge and Addenbrooke’ Hospital, UK

Reviewed by:

Jason B. Wu, Cedars-Sinai Medical Center, USA
Roger A. Barker, University of Cambridge and Addenbrooke’ Hospital, UK

Copyright: © 2012 Politis, Su and Piccini. This is an openaccess article distributed under the terms of the Creative Commons Attribution Non Commercial License, which permits non-commercial use, distribution, and reproduction in other forums, provided the original authors and source are credited.

*Correspondence: Marios Politis, Hammersmith Hospital, Imperial College London, Cyclotron Building, London W12 0NN, UK. e-mail: marios.politis@imperial.ac.uk