Nutritional or pharmacological activation of HCA(2) ameliorates neuroinflammation.

Stefan Offermanns, Markus Schwaninger

Trends in molecular medicine 2015 Apr

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Neuroinflammation is a pathology common to many neurological diseases, including multiple sclerosis (MS) and stroke. However, therapeutic attempts to modulate neuroinflammation have proved difficult. Neuroinflammatory cells express HCA2, a receptor for the endogenous neuroprotective ketone body β-hydroxybutyrate (BHB) as well as for the drugs dimethyl fumarate (DMF) and nicotinic acid, which have established efficacy in the treatment of MS and experimental stroke, respectively. This review summarizes the evidence that HCA2 is involved in the therapeutic effects of DMF, nicotinic acid, and ketone bodies in reducing neuroinflammation. Furthermore, we discuss the mechanisms underlying the beneficial effects of HCA2 activation in neuroinflammatory diseases and the therapeutic potential of recently developed synthetic ligands of HCA2. Copyright © 2015 Elsevier Ltd. All rights reserved.

Citation

Stefan Offermanns, Markus Schwaninger. Nutritional or pharmacological activation of HCA(2) ameliorates neuroinflammation. Trends in molecular medicine. 2015 Apr;21(4):245-55