Semin Neurol 2017; 37(05): 546-557
DOI: 10.1055/s-0037-1608715
Review Article
Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

TSPO-PET Imaging to Assess Cerebral Microglial Activation in Multiple Sclerosis

Tarun Singhal
1   Partners Multiple Sclerosis Center, Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts
,
Howard L. Weiner
1   Partners Multiple Sclerosis Center, Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts
,
Rohit Bakshi
1   Partners Multiple Sclerosis Center, Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts
2   Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts
› Author Affiliations
Further Information

Publication History

Publication Date:
05 December 2017 (online)

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Abstract

The adaptive immune system, particularly T cells and more recently B cells, is considered to play a major role in the pathogenesis of multiple sclerosis (MS). In addition to adaptive immune mechanisms, innate central nervous system (CNS) immunity, particularly mediated by microglia, may play a key role in MS pathogenesis. Microglial activation has been demonstrated throughout the MS disease course and at various locations in the CNS, including white and gray matter lesions as well as normal appearing white and gray matter. Activated microglia overexpress an 18 kilodalton mitochondrial translocator protein (TSPO), which is otherwise expressed at low levels during the resting state. Several positron emission tomography (PET) ligands targeting TSPO have been developed to enable the assessment of microglial activation. In this article, we review the biological basis, methodological aspects, and current status of TSPO-PET imaging in MS and discuss future research directions.

Funding

This work was supported by research grants from the Race to Erase MS foundation and the Harvard NeuroDiscovery Center.