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Mediators of Inflammation
Volume 2016, Article ID 1924603, 10 pages
http://dx.doi.org/10.1155/2016/1924603
Review Article

Histamine and Immune Biomarkers in CNS Disorders

1Chair of Genomic Medicine, Camilo José Cela University, C/Castillo de Alarcón 49, Villanueva de la Cañada, 28692 Madrid, Spain
2EuroEspes Biomedical Research Center, Institute for CNS Disorders and Genomic Medicine, Santa Marta de Babio, Bergondo, 15165 Corunna, Spain
3Neuropsychopharmacology Unit, Hospital 12 de Octubre Research Institute (i+12), Avenida de Córdoba, s/n, 28041 Madrid, Spain

Received 19 November 2015; Revised 14 March 2016; Accepted 20 March 2016

Academic Editor: Vinod K. Mishra

Copyright © 2016 Ramón Cacabelos et al. 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

Neuroimmune dysregulation is a common phenomenon in different forms of central nervous system (CNS) disorders. Cross-links between central and peripheral immune mechanisms appear to be disrupted as reflected by a series of immune markers (CD3, CD4, CD7, HLA-DR, CD25, CD28, and CD56) which show variability in brain disorders such as anxiety, depression, psychosis, stroke, Alzheimer’s disease, Parkinson’s disease, attention-deficit hyperactivity disorder, migraine, epilepsy, vascular dementia, mental retardation, cerebrovascular encephalopathy, multiple sclerosis, brain tumors, cranial nerve neuropathies, mental retardation, and posttraumatic brain injury. Histamine (HA) is a pleiotropic monoamine involved in several neurophysiological functions, neuroimmune regulation, and CNS pathogenesis. Changes in brain HA show an age- and sex-related pattern, and alterations in brain HA levels are present in different CNS regions of patients with Alzheimer’s disease (AD). Brain HA in neuronal and nonneuronal compartments plays a dual role (neurotrophic versus neurotoxic) in a tissue-specific manner. Pathogenic mechanisms associated with neuroimmune dysregulation in AD involve HA, interleukin-1β, and TNF-α, whose aberrant expression contributes to neuroinflammation as an aggravating factor for neurodegeneration and premature neuronal death.