Abstract
Gilles de la Tourette syndrome (GTS) is a childhood-onset neurodevelopmental and -psychiatric tic-disorder of complex etiology which is often comorbid with obsessive-compulsive disorder (OCD) and/or attention deficit hyperactivity disorder (ADHD). Twin and family studies of GTS individuals have shown a high level of heritability suggesting, that genetic risk factors play an important role in disease etiology. However, the identification of major GTS susceptibility genes has been challenging, presumably due to the complex interplay between several genetic factors and environmental influences, low penetrance of each individual factor, genetic diversity in populations, and the presence of comorbid disorders. To understand the genetic components of GTS etiopathology, we conducted an extensive review of the literature, compiling the candidate susceptibility genes identified through various genetic approaches. Even though several strong candidate genes have hitherto been identified, none of these have turned out to be major susceptibility genes yet.
Highlights
Gilles de la Tourette syndrome (GTS) is a complex early-onset neurodevelopmental/-psychiatric disorder with a prevalence between 0.52% and 0.77% in children [1,2]
The first association and linkage studies reported in GTS individuals [22], and dopamine receptor blockers have successfully been were conducted at the end of the previous century, where Comings et al showed assoused for the treatment of tics in GTS [21]
Suggest that the altered epigenetic regulation of dopamine-related genes may play a role in GTS etiology, but this finding should be replicated in larger cohorts
Summary
Gilles de la Tourette syndrome (GTS) is a complex early-onset neurodevelopmental/. -psychiatric disorder with a prevalence between 0.52% and 0.77% in children [1,2]. Provisional tic disorder meets all of the criteria for GTS except for the fact that tics do not last longer than 12 months. It is categorized as other specified and unspecified tic disorder when none of the above criteria are met [3]. The identification of susceptibility genes has been challenging, which is likely due to the complex and heterogeneous genetic architecture of GTS, wherein common and rare variants in several different genes and biological pathways are involved. We will highlight some of the most recent and notable studies in tic genetics, genes of historical significance in tic research, and studies focusing on candidate biological systems, such as the dopaminergic and serotonergic neurotransmission pathways
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