Increased serum levels of interleukin-12 and tumor necrosis factor-alpha in Tourette’s syndrome

Leckman, James F.; Katsovich, Liliya; Kawikova, Ivana; Lin, Haiqun; Zhang, Heping; Krönig, Holger; Morshed, Syed A.; Parveen, Salina; Grantz, Heidi; Lombroso, Paul J.; King, Robert A.

doi:10.1016/j.biopsych.2004.12.004

Cited by 143 publications

(132 citation statements)

References 45 publications

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“…IRF5 is involved in delayed induction of TNF-α in response to a viral or bacterial TLR response (Takaoka et al, 2005). This is consistent with the previously reported increased TNF-α in TS (Leckman et al, 2005). Moreover, IRF5 specifically induces IFNα subtype 8 (IFNA8) (Barnes et al, 2001).…”

Section: Hypothesis Generation For Further Studysupporting

confidence: 90%

“…Moreover, IRF5 specifically induces IFNα subtype 8 (IFNA8) (Barnes et al, 2001). Thus while total IFNα levels might not show significant differences within TS in this study or previous reports (Leckman et al, 2005), it is possible that the IFNα protein produced in TS might be a different subtype than that in NC (Kumaran et al, 2007). This might account for increased TNF-α in TS, as well as suggest a mechanism for differential viral responses in younger children with TS compared to controls.…”

Section: Hypothesis Generation For Further Studycontrasting

confidence: 52%

“…Blood markers have been used to differentiate TS subjects on various medications from controls (Kawikova et al, 2007;Leckman et al, 2005). Changes of gene expression in peripheral blood have been demonstrated in subjects with stroke, which only affects brain, and in genetic neurological diseases where there are brain and peripheral manifestations of the diseases (Tang et al, 2001;Tang et al, 2003).…”

Section: Limitationsmentioning

confidence: 99%

“…These include autoimmune responses, altered cytokine profiles [see reviews (Dale, 2003;Hoekstra et al, 2004;Martino & Giovannoni, 2005)] and correlations of inflammatory mediators with symptom exacerbation (Leckman et al, 2005). Age-related changes in tic severity (Leckman et al, 1998) suggest immune-associated gene expression in TS might vary with age if the immune system is involved in the disease process.…”

Section: Introductionmentioning

confidence: 99%

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Age-related gene expression in Tourette syndrome

Lit

Enstrom

Sharp

et al. 2009

Journal of Psychiatric Research

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Because infection and immune responses have been implicated in the pathogenesis of Tourette Syndrome (TS), we hypothesized that children with TS would have altered gene expression in blood compared to controls. In addition, because TS symptoms in childhood vary with age, we tested whether gene expression changes that occur with age in TS differ from normal control children. Whole blood was obtained from 30 children and adolescents with TS and 28 healthy children and adolescents matched for age, race and gender. Gene expression (RNA) was assessed using whole genome Affymetrix microarrays. Age was analyzed as a continuous covariate and also stratified into three groups: 5-9 (common age for tic onset), 10-12 (when tics often peak), and 13-16 (tics may begin to wane). No global differences were found between TS and controls. However, expression of many genes and multiple pathways differed between TS and controls within each age group (5-9, 10-12, and 13-16), including genes involved in the immune-synapse, and proteasome-and ubiquitinmediated proteolysis pathways. Notably, across age strata, expression of interferon response, viral processing, Natural Killer and cytotoxic T-lymphocyte cell genes differed. Our findings suggest agerelated interferon, immune and protein degradation gene expression differences between TS and controls.

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Section: Hypothesis Generation For Further Studysupporting

confidence: 90%

Section: Hypothesis Generation For Further Studycontrasting

confidence: 52%

Section: Limitationsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Age-related gene expression in Tourette syndrome

Lit

Enstrom

Sharp

et al. 2009

Journal of Psychiatric Research

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“…A number of laboratories have examined serum from affected individuals and found evidence for autoantibodies [22][23][24][25]. Recent studies have also found evidence for the involvement of cytokines and regulatory T cells [26] [27].…”

Section: Pediatric Autoimmune Neuropsychiatric Disorder Associated Wimentioning

confidence: 99%

Tourette syndrome and obsessive–compulsive disorder

Lombroso

Scahill

2008

Brain and Development

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Tourette syndrome and obsessive-compulsive disorder are neuropsychiatric disorders that have sparked considerable interest over the decades. They are the focus of research for a remarkable diversity of disciplines, ranging from neuroimagers and prenatal epidemiologists to experts in the neural circuits that connect the cortex with the basal ganglia, as well as neuroimmunologists focusing on brain-based autoimmune phenomena. Several hypotheses have been put forward to explain the onset and exacerbation of these illnesses. Here we discuss the clinical phenomenology and treatment options that are currently available. New psychopharmacological agents are being used that are based on a greater understanding of the neurobiology and are being used in combination with behavioral interventions. Longitudinal clinical investigations into clinical symptoms and the natural course are providing additional clues on the underlying pathophysiology. Recent advances in research models are also reviewed in an attempt to clarify some of the molecular etiologies that lead to these disorders. KeywordsTorrette syndrome; obsessive-compulsive disorder; basal ganglia; autoimmune disorders; streptococcal infections; neuroleptic treatment Tourette syndrome (TS) and obsessive-compulsive disorder (OCD) are model neuropsychiatric disorders that have been the subject of medical interest for centuries [1]. Many explanations have been suggested for the etiology of tics and OCD symptoms and have included genetic factors, the influence of toxins, psychological, and infectious processes. There have been significant advances of our understanding of the neurobiological mechanisms at work in these disorders, as well as improvements in the treatments available. Several reviews on more specialized aspect of TS, OCD and related disorders have appeared over the last several years [2][3][4]. Here we concentrate on the clinical features of tic disorders and OCD and discuss evidence-based interventions for these disorders. Tourette syndromeTourette syndrome is one of several tic disorders that are classified either by their type (motor or phonic tic) or their duration (transient or chronic). The diagnosis of a transient tic is made if the tics are present for less than 12 months. If the tics persist for more than 12 months, they

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Molecular Genetics of Tourette Syndrome

Valenti

Grados

2012

Encyclopedia of Life Sciences

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Tourette Syndrome (TS) is a neurodevelopmental disorder characterised by chronic motor and vocal tics, which fluctuate over time. The molecular genetics of TS is supported by genetic epidemiology studies, which strongly suggest the presence of susceptibility genes for TS. Epidemiologic family, segregation and linkage studies, as well as candidate gene studies, have yielded limited specific results to date, however, pathophysiology models that support a molecular genetics approach in TS are emerging. Whole‐genome approaches, including genome‐wide association studies (GWAS) and whole‐genome sequencing, may yield more definitive genomic findings. Uncovering the biological substrate of TS will spur the development of novel, more precisely targeted, treatments for this disabling disorder.

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Increased serum levels of interleukin-12 and tumor necrosis factor-alpha in Tourette’s syndrome

Cited by 143 publications

References 45 publications

Age-related gene expression in Tourette syndrome

Age-related gene expression in Tourette syndrome

Tourette syndrome and obsessive–compulsive disorder

Molecular Genetics of Tourette Syndrome

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