In the CNS tryptophan degradation takes place especially in microglia (also partly in astrocytes and neurons)

In the CNS tryptophan degradation takes place especially in microglia (also partly in astrocytes and neurons). and are therefore involved in the pathology. In tic disorders, infections with group A streptococci, infectious agents and pro-inflammatory cytokines. Tryptophan breakdown leads to neuroactive metabolites that can influence the neurotransmitter balance [9]. Especially in microglia, which are the resident innate immune cells of the brain, tryptophan gets degraded to serotonin and to other products of this metabolism [10], which function either as a NMDA-receptor agonist or antagonist and control the neurotransmitter availability [11]. So far, an imaging study of Behen Protopanaxatriol might be associated with tic symptoms [19, 20]. This assumption was strengthened by a study that compared 29 Tourette patients to healthy controls regarding the Mycoplasma infection rates. The study found significantly more elevated antibody titers against in TS patients as compared to controls [21]. Furthermore, an association between herpes simplex virus 1 and the exacerbation of tics was stated [22]. Also an acute infection with as compared to controls and trend towards a higher prevalence in the Tourettes group was shown for [24]. Unitl now, none of these infectious agents has been linked consistently with TS. Thus a hypothesis is that infections do not directly cause symptoms of the disease, instead they could contribute to TS by triggering an immune response. Therefore the observations of a dysbalanced immune system will be discussed for TS. IMMUNE PARAMETERS IN TOURETTES SYNDROME AND POSSIBLE UNDERLYING MECHANISMS OF THE ASSOCIATION OF TS AND INFECTIOUS AGENTS In TS patients nonspecific markers of immune activation have been found to be elevated: The parameter neopterin serves as a biomarker of cell-mediated immunity. It is produced by human monocytes/macrophages during Th1-type immune responses, after stimulation with interferon-. Increased levels of neopterin have been observed in association with several autoimmune diseases [25, 26]. Also in TS, neopterin levels at baseline were elevated in patients compared to healthy controls [13]. Another marker is c-reactive protein (CRP), which is an acute-phase protein. It gets secreted mainly in the liver and is modulating inflammatory responses, although the exact mechanism remains controversial. Luo infectious providers and elevated proinflammatory cytokines [9]. In the CNS tryptophan degradation takes place especially in microglia (also partly in astrocytes and neurons). The essential amino acid tryptophan gets degraded either to serotonin or over the kynurenine pathway (KP) to additional products [10], which function either like a NMDA- receptor agonist or antagonist and control the neurotransmitter availability [11]. The activation of this KP has been shown to play an important part in the pathophysiology of neuropsychiatric disorders (e.g. schizophrenia) [38]. Also for TS, Behen Protopanaxatriol the tryptophan catabolism. The association of infections and the kynurenic pathway could EPAS1 have restorative implications, Protopanaxatriol as at present inhibitors of particular metabolites of this pathway are available [9]. ACKNOWLEDGEMENTS None declared. CONFLICT OF INTEREST The authors confirm that this article content has no conflicts of interest. Referrals 1. Jankovic J. Tourette’s syndrome. N Engl J Med. 2001;18(345(16)):1184C92. [PubMed] [Google Scholar] 2. Tanner CM, Goldman SM, Lyons KE, et al. Essential tremor in twins an assessment of genetic vs environmental determinants of etiology. Neurology. 2001;23(57(8) ):1389C91. [PubMed] [Google Scholar] 3. Mell LK, Davis RL, Owens D. Association between streptococcal illness and obsessive-compulsive disorder Tourette’s syndrome and tic disorder. Pediatrics. 2005;116(1 ):56C60. [PubMed] [Google Scholar] 4. Leckman JF, Katsovich L, Kawikova I, et al. Improved serum levels of interleukin-12 and tumor necrosis factor-alpha in Tourette’s syndrome. Biol Psychiatry. 2005;15(57(6) ):667C73. [PubMed] [Google Scholar] 5. Morris CM, Pardo-Villamizar C, Gause CD, Singer HS. Serum autoantibodies measured by immunofluorescence confirm a failure to differentiate PANDAS and Tourette syndrome from settings. J Neurol Sci. 2009;15 (276(1-2) ):45C8. [PubMed] [Google Scholar] 6. Snider LA, Swedo SE. PANDAS: current status and directions for study. Mol Psychiatry. 2004;9(10 ):900C7. [PubMed] [Google Scholar] 7. Krause KH, Dresel S, Krause J, Kung HF,.