Table of Contents Author Guidelines Submit a Manuscript
Journal of Immunology Research
Volume 2016, Article ID 8606057, 8 pages
http://dx.doi.org/10.1155/2016/8606057
Review Article

Microglial Dysregulation in OCD, Tourette Syndrome, and PANDAS

1Department of Psychiatry, Yale University, New Haven, CT, USA
234 Park Street, 3rd floor, W306, New Haven, CT 06519, USA
3Department of Psychology, Yale University, New Haven, CT, USA
4Department of Interdepartmental Neuroscience Program, Yale University, New Haven, CT, USA
5Department of Child Study Center, Yale University, New Haven, CT, USA

Received 23 September 2016; Accepted 15 November 2016

Academic Editor: Fabiano Carvalho

Copyright © 2016 Luciana Frick and Christopher Pittenger. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

There is accumulating evidence that immune dysregulation contributes to the pathophysiology of obsessive-compulsive disorder (OCD), Tourette syndrome, and Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections (PANDAS). The mechanistic details of this pathophysiology, however, remain unclear. Here we focus on one particular component of the immune system: microglia, the brain’s resident immune cells. The role of microglia in neurodegenerative diseases has been understood in terms of classic, inflammatory activation, which may be both a consequence and a cause of neuronal damage. In OCD and Tourette syndrome, which are not characterized by frank neural degeneration, the potential role of microglial dysregulation is much less clear. Here we review the evidence for a neuroinflammatory etiology and microglial dysregulation in OCD, Tourette syndrome, and PANDAS. We also explore new hypotheses as to the potential contributions of microglial abnormalities to pathophysiology, beyond neuroinflammation, including failures in neuroprotection, lack of support for neuronal survival, and abnormalities in synaptic pruning. Recent advances in neuroimaging and animal model work are creating new opportunities to elucidate these issues.