The neuroimmune basis of fatigue.
Trends in Neurosciences. 2014-01-01; 37(1): 39-46
DOI: 10.1016/j.tins.2013.10.003
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Dantzer R(1), Heijnen CJ(2), Kavelaars A(3), Laye S(4), Capuron L(4).
Author information:
(1)The University of Texas MD Anderson Cancer Center, Division of Internal
Medicine, Department of Symptom Research, Houston, TX 77030, USA. Electronic
address: .
(2)The University of Texas MD Anderson Cancer Center, Division of Internal
Medicine, Department of Symptom Research, Houston, TX 77030, USA; University
Medical Center, Laboratory of Neuroimmunology of Developmental Origin of Disease,
Utrecht, The Netherlands.
(3)The University of Texas MD Anderson Cancer Center, Division of Internal
Medicine, Department of Symptom Research, Houston, TX 77030, USA.
(4)NutriNeuro, INRA, UMR 1286, University of Bordeaux 2, Bordeaux, France.
The exact nature and pathophysiology of fatigue remain largely elusive despite
its high prevalence in physically ill patients. Studies on the relationship
between the immune system and the central nervous system provide a new
perspective on the mechanisms of fatigue. Inflammatory mediators that are
released by activated innate immune cells at the periphery and in the central
nervous system alter the metabolism and activity of neurotransmitters, generate
neurotoxic compounds, decrease neurotrophic factors, and profoundly disturb the
neuronal environment. The resulting alterations in fronto-striatal networks
together with the activation of insula by inflammatory interoceptive stimuli
underlie the many dimensions of fatigue including reduced incentive motivation,
decreased behavioral flexibility, uncertainty about usefulness of actions, and
awareness of fatigue.
Published by Elsevier Ltd.