Blood serotonin and tryptophan in Tourette syndrome

Comings, David E.

doi:10.1002/ajmg.1320360410

Cited by 79 publications

(29 citation statements)

References 85 publications

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“…Also, significantly decreased serum tryptophan levels of TS patients have been reported in two large-scale studies, 50,51 which would be compatible with increased turnover of tryptophan along the kynurenine pathway. However, cerebrospinal fluid tryptophan levels were found to be normal in a different study.…”

Section: Altered Tryptophan Metabolism and Data On Cytokinesmentioning

confidence: 78%

Is Tourette's syndrome an autoimmune disease?

Hoekstra¹,

Kallenberg²,

Korf

et al. 2002

Mol Psychiatry

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We provide a review of recent research findings which support the involvement of autoimmunity in childhood-onset tic disorders, in particular the presence of antineuronal autoantibodies, D8/17 B lymphocyte overexpression, a marker of chorea associated with streptococcal infection, and possible beneficial effects of immunomodulatory intervention. One of the most controversial areas in this field is the validity of the proposed PANDAS concept. Some researchers have delineated a putatively unique subgroup of patients, from the spectrum of illness encompassing Tourette's syndrome and obsessive-compulsive disorder (OCD), whose tics and obsessive-compulsive symptoms are shown to arise in response to beta-hemolytic streptococcal infections. They designated it by the term pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS). Herein we additionally present pros and cons concerning the concept of PANDAS. Finally, recommendations for future research directions are given.

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Section: Altered Tryptophan Metabolism and Data On Cytokinesmentioning

confidence: 78%

Is Tourette's syndrome an autoimmune disease?

Hoekstra¹,

Kallenberg²,

Korf

et al. 2002

Mol Psychiatry

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“…However, our study also includes the concomitant 5-HT 2A R measure, indicative of a trend for elevations in 5-HT 2A BP. 5-HT abnormalities have been hypothesized in TS, although there are conflicting reports regarding 5-HT metabolism (Comings, 1990;Leckman et al, 1984). Some abnormalities that have been hypothesized to be related to co-morbidity with OCD include decreased SERT in platelets (Weizman et al, 1992).…”

Section: -Ht and Da Relationshipsmentioning

confidence: 99%

Mechanisms of Dopaminergic and Serotonergic Neurotransmission in Tourette Syndrome: Clues from an In Vivo Neurochemistry Study with PET

Wong

Brašić

Singer

et al. 2007

Neuropsychopharmacol

233

172

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Tourette syndrome (TS) is a neuropsychiatric disorder with childhood onset characterized by motor and phonic tics. Obsessivecompulsive disorder (OCD) is often concomitant with TS. Dysfunctional tonic and phasic dopamine (DA) and serotonin (5-HT) metabolism may play a role in the pathophysiology of TS. We simultaneously measured the density, affinity, and brain distribution of dopamine D 2 receptors (D 2 -R's), dopamine transporter binding potential (BP), and amphetamine-induced dopamine release (DA rel ) in 14 adults with TS and 10 normal adult controls. We also measured the brain distribution and BP of serotonin 5-HT 2A receptors (5-HT 2A R), and serotonin transporter (SERT) BP, in 11 subjects with TS and 10 normal control subjects. As compared with controls, DA rel was significantly increased in the ventral striatum among subjects with TS. Adults with TS + OCD exhibited a significant D 2 -R increase in left ventral striatum. SERT BP in midbrain and caudate/putamen was significantly increased in adults with TS (TS + OCD and TS-OCD). In three subjects with TS + OCD, in whom D 2 -R, 5-HT 2A R, and SERT were measured within a 12-month period, there was a weakly significant elevation of DA rel and 5-HT 2A BP, when compared with TS-OCD subjects and normal controls. The current study confirms, with a larger sample size and higher resolution PET scanning, our earlier report that elevated DA rel is a primary defect in TS. The finding of decreased SERT BP, and the possible elevation in 5-HT 2A R in individuals with TS who had increased DA rel , suggest a condition of increased phasic DA rel modulated by low 5-HT in concomitant OCD.

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“…A role for serotonin is suggested by a reduction in cerebrospinal fluid of 5-hydroxyindoleacetic acid (Leckman et al, 1995), the principal metabolite of serotonin and by a reduction of plasma tryptophan, whole blood serotonin, and the 24-h urine secretion of serotonin in some patients with TS (Comings, 1990). Moreover, a PET study suggested decreased serotonin transporter (SERT) binding potential (Wong et al, 2008).…”

Section: Neurotransmitter Abnormalities Associated With Tsmentioning

confidence: 99%

Genetic Susceptibility and Neurotransmitters in Tourette Syndrome

Paschou

Fernandez

Sharp

et al. 2013

International Review of Neurobiology

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Family studies have consistently shown that Tourette syndrome (TS) is a familial disorder and twin studies have clearly indicated a genetic contribution in the etiology of TS. Whereas early segregation studies of TS suggested a single-gene autosomal dominant disorder, later studies have pointed to more complex models including additive and multifactorial inheritance and likely interaction with genetic factors. While the exact cellular and molecular base of TS is as yet elusive, neuroanatomical and neurophysiological studies have pointed to the involvement of cortico-striato-thalamocortical circuits and abnormalities in dopamine, glutamate, gamma-aminobutyric acid, and serotonin neurotransmitter systems, with the most consistent evidence being available for involvement of dopamine-related abnormalities, that is, a reduction in tonic extracellular dopamine levels along with hyperresponsive spike-dependent dopamine release, following stimulation. Genetic and gene expression findings are very much supportive of involvement of these neurotransmitter systems. Moreover, intriguingly, genetic work on a two-generation pedigree has opened new research pointing to a role for histamine, a so far rather neglected neurotransmitter, with the potential of the development of new treatment options. Future studies should be aimed at directly linking neurotransmitter-related genetic and gene expression findings to imaging studies (imaging genetics), which enables a better understanding of the pathways and mechanisms through which the dynamic interplay of genes, brain, and environment shapes the TS phenotype.

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Blood serotonin and tryptophan in Tourette syndrome

Cited by 79 publications

References 85 publications

Is Tourette's syndrome an autoimmune disease?

Is Tourette's syndrome an autoimmune disease?

Mechanisms of Dopaminergic and Serotonergic Neurotransmission in Tourette Syndrome: Clues from an In Vivo Neurochemistry Study with PET

Genetic Susceptibility and Neurotransmitters in Tourette Syndrome

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