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Neurosci Biobehav Rev. 2016 May;64:148-66. doi: 10.1016/j.neubiorev.2016.02.017. Epub 2016 Feb 23.

Mapping inflammation onto mood: Inflammatory mediators of anhedonia.

Author information

1
University of Toronto, Department of Pharmacology & Toxicology, Canada; Sunnybrook Research Institute, Hurvitz Brain Sciences Program, Canada; University Health Network Toronto Rehabilitation Institute, Canada. Electronic address: w.swardfager@utoronto.ca.
2
University Health Network Toronto Western Research Institute, Mood Disorders Psychopharmacology Unit, Canada; University of Toronto, Department of Psychiatry, Canada.
3
University of Toronto Mississauga, Institute of Medical Sciences, Canada.
4
University of Toronto, Department of Pharmacology & Toxicology, Canada; University Health Network Toronto Western Research Institute, Mood Disorders Psychopharmacology Unit, Canada; University of Toronto, Department of Psychiatry, Canada.

Abstract

Evidence supports inflammatory involvement in mood and cognitive symptoms across psychiatric, neurological and medical disorders; however, inflammation is not a sensitive or specific characteristic of these diagnoses. The National Institute of Mental Health Research Domain Criteria (RDoC) ask for a shift away from symptom-based diagnoses toward a transdiagnostic neurobiological focus in the study of brain illnesses. The RDoC matrix may provide a useful framework for integrating the effects of inflammation on brain function. Based on preclinical and clinical findings, relevant relationships span negative and positive valence systems, cognitive systems, systems for social processes and arousal/regulatory systems. As an exemplar, we consider the psychopathological domain of anhedonia, conceptualizing the relevance of inflammation (e.g., cellular immunity) and downstream processes (e.g., indoleamine 2,3-dioxygenase activation and oxidative inactivation of tetrahydrobiopterin) across RDoC units of analysis (e.g., catecholamine neurotransmitter molecules, nucleus accumbens medium spiny neuronal cells, dopaminergic mesolimbic and mesocortical reward circuits, animal paradigms, etc.). We discuss implications across illnesses affecting the brain, including infection, major depressive disorder, stroke, Alzheimer's disease and type 2 diabetes.

KEYWORDS:

Anhedonia; Cytokine; Depression; Dopamine; Inflammation; Research Domain Criteria; Reward

PMID:
26915929
DOI:
10.1016/j.neubiorev.2016.02.017
[Indexed for MEDLINE]

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