The Pathogenesis of Tourette's Syndrome

Kurlan, Roger

doi:10.1001/archneur.1992.00530320106020

Cited by 63 publications

(3 citation statements)

References 19 publications

(2 reference statements)

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“…There is a sharp rise in the incidence of Alzhiemer's disease after menopause [15]. Some diseases that involve DA neurotransmission are less prevalent or different in premenopausal females vs. postmenopausal females and males (Parkinson's, Tourette's, ADHD [16-20]), also suggesting an influence of estrogens on disease status. Other studies suggest an involvement of estrogens in cognitive function [21] and attention [22-24].…”

Section: Introductionmentioning

confidence: 99%

Estradiol effects on the dopamine transporter – protein levels, subcellular location, and function

Watson

Alyea

Hawkins

et al. 2006

JMS

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BackgroundThe effects of estrogens on dopamine (DA) transport may have important implications for the increased incidence of neurological disorders in women during life stages when hormonal fluctuations are prevalent, e.g. during menarche, reproductive cycling, pregnancy, and peri-menopause.ResultsThe activity of the DA transporter (DAT) was measured by the specific uptake of 3H-DA. We found that low concentrations (10-14 to 10-8 M) of 17β-estradiol (E2) inhibit uptake via the DAT in PC12 cells over 30 minutes, with significant inhibition taking place due to E2 exposure during only the last five minutes of the uptake period. Such rapid action suggests a non-genomic, membrane-initiated estrogenic response mechanism. DAT and estrogen receptor-α (ERα) were elevated in cell extracts by a 20 ng/ml 2 day NGFβ treatment, while ERβ was not. DAT, ERα and ERβ were also detectable on the plasma membrane of unpermeabilized cells by immunocytochemical staining and by a fixed cell, quantitative antibody (Ab)-based plate assay. In addition, PC12 cells contained RNA coding for the alternative membrane ER GPR30; therefore, all 3 ER subtypes are candidates for mediating the rapid nongenomic actions of E2. At cell densities above 15,000 cells per well, the E2-induced inhibition of transport was reversed. Uptake activity oscillated with time after a 10 nM E2 treatment; in a slower room temperature assay, inhibition peaked at 9 min, while uptake activity increased at 3 and 20–30 min. Using an Ab recognizing the second extracellular loop of DAT (accessible only on the outside of unpermeabilized cells), our immunoassay measured membrane vs. intracellular/nonvesicular DAT; both were found to decline over a 5–60 min E2 treatment, though immunoblot analyses demonstrated no total cellular loss of protein.ConclusionOur results suggest that physiological levels of E2 may act to sequester DAT in intracellular compartments where the transporter's second extramembrane loop is inaccessible (inside vesicles) and that rapid estrogenic actions on this differentiated neuronal cell type may be regulated via membrane ERs of several types.

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Section: Introductionmentioning

confidence: 99%

Estradiol effects on the dopamine transporter – protein levels, subcellular location, and function

Watson

Alyea

Hawkins

et al. 2006

JMS

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“…It was proved that basal ganglia, particularly the caudatus nucleus and ventral striatolimbic complex played a significant role in the pathogenesis of OCD and primitive reproductive behavior ( 11 ). The influence of sex hormones on the development of these structures can explain the difference in TS among sexes, the exacerbation of puberty and estrogenic stages of the menstrual cycle, and the characteristic occurrence of complex motor and sound tics, as well as behavioral manifestations with sexual content ( 12 ).…”

Section: Etiology and Pathophysiologymentioning

confidence: 99%

Tourette Syndrome: A Mini-Review

2018

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The purpose of this mini-review is to provide the latest information on epidemiology, pathophysiology, diagnosis, and treatment of Tourette syndrome (TS). The authors conducted a literature search of available sources describing the issue of tic disorders with special focus on TS and made a comparison and evaluation of relevant findings. The results of this mini-review indicate that TS is a complex disorder, which has a significant impact on the quality of life of both the patients and his/her family. Therefore, early and proper diagnosis and treatment are necessary in order to reduce or even eliminate both symptoms and social burden of the patient. This requires a multidisciplinary management approach in order to meet the patients’ special needs. Future research should focus on neuroimaging, new neurotransmitter targets, in functional neurosurgery, as well as the effect of non-pharmacological psychotherapies for these people.

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“…A provocative hypothesis for the pathogenesis of Tourette's syndrome proposes that the brain regions involved in Tourette's, specifically the basal ganglia and limbic system, are the phylogenetic counterparts in humans of the regions that functioned in primitive reproductive behavior (Kurlan, 1992a). From an evolutionary standpoint, these areas would have been responsible for vestigial reproductive motor programs such as mating dances and sexual foreplay, as well as vestigial vocal programs such as mating songs and noises.…”

Section: Gilles De La Tourette's Syndromementioning

confidence: 99%

Defining features, clinical conditions, and theoretical constructs of stereotyped movements.

Shulman¹,

Sanchez‐Ramos²,

Weiner³

Stereotyped Movements: Brain and Behavior Relationships.

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tereotyped behavior is a difficult concept to define. This difficulty is S not dissimilar to that faced in the accurate diagnosis of other movement disorders. Identification and classification can be hindered by a number of obstacles. In contrast to a paralysis of motor function or an incoordination of movement, the "material evidence" of a movement disorder is ephemeral and fleeting, occurring with variable frequency and characterized by morphologic variability. Some movement disorders are stimulus sensitive, activated by vocalization or motor activity. Most are exacerbated by emotional stress. In addition, the presence of movement disorders in the setting of psychiatric disease (e.g., schizophrenia, autism) combined with the existence of psychogenic movement disorders adds to the complexity of accurate diagnosis.The characteristics of a given movement disorder may not be unique to a specific disease process. For example, the chorea of Huntington's disease may not appear strikingly different from the chorea that occurs as a drug-induced side effect. Therefore, a given movement disorder may cross

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The Pathogenesis of Tourette's Syndrome

Cited by 63 publications

References 19 publications

Estradiol effects on the dopamine transporter – protein levels, subcellular location, and function

Estradiol effects on the dopamine transporter – protein levels, subcellular location, and function

Tourette Syndrome: A Mini-Review

Defining features, clinical conditions, and theoretical constructs of stereotyped movements.

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