Altered immunoglobulin profiles in children with Tourette syndrome

Bos-Veneman, Netty G. P.; Olieman, Renske; Tobiásová, Zuzana; Hoekstra, Pieter J.; Katsovich, Lily; Bothwell, Alfred L.M.; Leckman, James F.; Kawikova, Ivana

doi:10.1016/j.bbi.2010.12.003

Cited by 47 publications

(30 citation statements)

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“…In keeping with Landau et al (2012), this study found elevated levels of IgG4, bolstering evidence for a drive toward autoimmune disturbance. A trend toward an increase in IgG1 during tic exacerbations was found in a prospective analysis in the same study (Bos-Veneman et al, 2011). IgA dysgammaglobulinemia has been reported in another study of children with TS.…”

Section: Introductionsupporting

confidence: 58%

“…Another study reporting elevated IgE levels in subjects with TS additionally noted elevated levels of IgG4 (Landau et al, 2012), consistent with a possible vulnerability to the development of autoimmune disease (Takahashi et al, 2010). In contrast, one report based on two independent cross-sectional study samples noted that IgE serum levels tended to be decreased in one of the two samples, and also reported decreased levels of IgG3 and a trend toward a decrease in IgM levels (Bos-Veneman et al, 2011). In keeping with Landau et al (2012), this study found elevated levels of IgG4, bolstering evidence for a drive toward autoimmune disturbance.…”

Section: Introductionmentioning

confidence: 92%

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Immune-mediated animal models of Tourette syndrome

Hornig

Lipkin

2013

Neuroscience & Biobehavioral Reviews

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An autoimmune diathesis has been proposed in Tourette syndrome (TS) and related neuropsychiatric disorders such as obsessive-compulsive disorder, attention-deficit/hyperactivity disorder, autism and anorexia nervosa. Environmental triggers including infection and xenobiotics are hypothesized to lead to the production of brain-directed autoantibodies in a subset of genetically susceptible individuals. Although much work has focused on Group A Streptococcus (GAS), the role of this common childhood infection remains controversial. Animal model studies based on immune and autoantibody findings in TS have demonstrated immunoglobulin (Ig) deposits and stereotypic movements and related behavioral disturbances reminiscent of TS following exposure to GAS and other activators of host anti-microbial responses, soluble immune mediators and anti-GAS or anti-neuronal antibodies. Demonstration of the ability to recreate these abnormalities through passive transfer of serum IgG from GAS-immunized mice into naïve mice and abrogation of this activity through depletion of IgG has provided compelling evidence in support of the autoimmune hypothesis. Immunologically-based animal models of TS are a potent tool for dissecting the pathogenesis of this serious neuropsychiatric syndrome.

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Section: Introductionsupporting

confidence: 58%

Section: Introductionmentioning

confidence: 92%

Immune-mediated animal models of Tourette syndrome

Hornig

Lipkin

2013

Neuroscience & Biobehavioral Reviews

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“…In particular, the risk for TS has been shown to be significantly enhanced in patients with a history of adverse events and/or stress in the prenatal and perinatal period (Leckman et al, 1990; Motlagh et al, 2010; Bos-Veneman et al, 2011), as well as maternal smoking (Mathews et al, 2006). Given that obstetric complications and maternal smoke have been linked to multiple mental disorders, several animal models have been developed in the attempt of reproducing the pathophysiological sequence leading to their sequelae (Boksa, 2004; Yochum et al, 2014).…”

Section: Animal Models Based On Environmental Etiologymentioning

confidence: 99%

Animal models of tic disorders: A translational perspective

Godar

Mosher

Giovanni

et al. 2014

Journal of Neuroscience Methods

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Tics are repetitive, sudden movements and/or vocalizations, typically enacted as maladaptive responses to intrusive premonitory urges. The most severe tic disorder, Tourette syndrome (TS), is a childhood-onset condition featuring multiple motor and at least one phonic tic for a duration longer than 1 year. The pharmacological treatment of TS is mainly based on antipsychotic agents; while these drugs are often effective in reducing tic severity and frequency, their therapeutic compliance is limited by serious motor and cognitive side effects. The identification of novel therapeutic targets and development of better treatments for tic disorders is conditional on the development of animal models with high translational validity. In addition, these experimental tools can prove extremely useful to test hypotheses on the etiology and neurobiological bases of TS and related conditions. In recent years, the translational value of these animal models has been enhanced, thanks to a significant re-organization of our conceptual framework of neuropsychiatric disorders, with a greater focus on endophenotypes and quantitative indices, rather than qualitative descriptors. Given the complex and multifactorial nature of TS and other tic disorders, the selection of animal models that can appropriately capture specific symptomatic aspects of these conditions can pose significant theoretical and methodological challenges. In this article, we will review the state of the art on the available animal models of tic disorders, based on genetic mutations, environmental interventions as well as pharmacological manipulations. Furthermore, we will outline emerging lines of translational research showing how some of these experimental preparations have led to significant progress in the identification of novel therapeutic targets for tic disorders.

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“…A subsequent study suggesting that GTS individuals have immune deficiency was that of an immunoglobulin: Bos-Veneman et al 71 demonstrated that at least some GTS patients have decreased IgG3 and possibly also low IgM levels, although only a few subjects had Ig immunodeficiency 71. Another study showed that patients with GTS when compared with controls had higher rates of IgA/IgG antibody titres to Chlamydia trachomatis and a trend with Toxoplasma gondi 72 and Mycoplasma pneumoniae 73 with the authors suggesting that infections contribute to GTS by triggering an immune response.…”

Section: Aetiological Theoriesmentioning

confidence: 99%

The Gilles De La Tourette syndrome: the current status

Robertson

2012

Arch Dis Child Educ Pract Ed

162

115

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Gilles de la Tourette syndrome (GTS) is characterised by multiple motor and one or more vocal/phonic tics. GTS was once thought to be rare, but many relatively recent studies suggest that the prevalence is about 1% of the worldwide community, apart from in Sub-Saharan Black Africa. Comorbidity and coexistent psychopathology are common, occurring in about 90% of clinical cohorts and individuals in the community. The most common comorbidities are attention deficit hyperactivity disorder, obsessive-compulsive behaviours, and disorder, and autistic spectrum disorders, while the most common coexisting psychopathologies are depression, anxiety and behavioural disorders such as oppositional defiant and conduct disorder. There has been an increasing amount of evidence to show that the quality of life in young people is reduced when compared with normative data or healthy control populations. It is widely accepted that most cases of GTS are inherited, but the genetic mechanisms appear much more complex than previously understood, as evidenced by many recent studies; indeed, there have been suggestions of 'general neurodevelopmental genes' which affect the brain development after which the 'specific GTS gene(s)' may further affect the phenotype. Other aetiopathogenetic suggestions have included environmental factors such as neuro-immunological factors, infections, prenatal and peri-natal difficulties and androgen influences. Few studies have addressed aetiology and phenotype, but initial results are exciting. The search for endophenotypes has followed subsequently. Intriguing neuroanatomical and brain circuitry abnormalities have now been suggested in GTS; the most evidence is for cortical thinning and a reduction in the size of the caudate nucleus. Thorough assessment is imperative and multidisciplinary management is the ideal. Treatment should be 'symptom targeted', and in mild cases, psycho-education and reassurance for the patient and the family may be sufficient. Behavioural treatments such as Comprehensive Behavioural Intervention for Tics including Habit Reversal Training have been shown to be significantly better than other behavioural/psychological treatments and 'placebo'. Medication is often necessary for moderately affected individuals. In more severe cases, medical treatment is not simple and referral to an expert may be advisable. In general, neuroleptics and clonidine or guanfacine are the medications of choice for the tics. Other treatments which may be needed for loud and severe phonic tics include botulinum toxin. In severe adult GTS patients who are refractory to medication and other therapies, deep brain stimulation looks promising.

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Altered immunoglobulin profiles in children with Tourette syndrome

Abstract: BACKGROUND-Post-infectious autoimmunity and immune deficiency have been implicated in the pathogenesis of Tourette syndrome (TS). We asked here whether B cell immunity of patients with TS differs from healthy subjects.

Cited by 47 publications

References 48 publications

Immune-mediated animal models of Tourette syndrome

Immune-mediated animal models of Tourette syndrome

Animal models of tic disorders: A translational perspective

The Gilles De La Tourette syndrome: the current status

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