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Histidine Decarboxylase Deficiency Causes Tourette Syndrome: Parallel Findings in Humans and Mice
12017-11-19T13:07:10-08:00Dylan Rasmussend0b1b774d22a2c8ccf09bff36e3254513a79fb2e253262study exploring the link between deficiency in histidine decarboxylase enzyme and tics and tic-like symptoms by Lissandra Castellan Baldan et al.plain2017-11-19T13:09:33-08:00Dylan Rasmussend0b1b774d22a2c8ccf09bff36e3254513a79fb2e
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12017-11-13T09:15:03-08:00Causes of Tourette's11Explores a study linking deficient histidine decarboxylase enzyme to tics and tic-like symptomsplain2017-11-19T23:20:36-08:00
by Dylan Rasmussen
Despite the prevalence and increasing awareness of the disorder, the exact causes of Tourette syndrome are unknown. According to the study “Histidine Decarboxylase Deficiency Causes Tourette Syndrome: Parallel Findings in Humans and Mice,” as well as several other promising studies, a mutation in histidine decarboxylase (Hdc)—a key enzyme responsible for the biosynthesis of histamine—is seen as a probable cause of the disorder in a family with a high incidence of Tourette syndrome. A solid understanding of the enzymatic activity of Hdc, as well as the “hypothesized ability of [histamine] to modulate [dopamine] levels in the [central nervous system],” lends itself to optimal testing in animal models (Baldan et al. 77-78). By observing patterns which appeared in both the animal model and human cases, we may begin to understand the underlying causes of Tourette syndrome.
Baldan et al. introduced two categories of mice: Hdc+/- mice (KO mice), with inhibited enzymatic activity and subsequently reduced levels of histamine, and Hdc-/- mice, which possessed normal behavior of Hdc. D-amphetamine, a psychostimulant which can induce ticcing behavior in specific animals, was administered to individuals of both categories. Physical responses of the animals were quantified before and after the introduction of D-amphetamine (Baldan et al. 78). Baseline tests revealed similar tendencies in both groups, with animals exhibiting “exploratory rearing and center occupancy in an open field.” Baldan et al. continue, describing behaviors after D-amphetamine was introduced. “The majority consisted of repetitive focused sniffing and orofacial movements. KO mice showed markedly increased motor stereotypies.” This trend was exhibited quite clearly through extended trials. Baldan et al. were able to identify that “Hdc deficiency potentiates tic-like stereotypes” (78).
Although this study represents a great leap in our understanding of Tourette syndrome, we are far from describing its exact causes. It is likely that a combination of genetic variables, environmental factors, and individual lifestyle all play a role in the manifestation of Tourette’s. Yet no matter the cause, individuals with the disorder continue to encounter the social and professional barriers created by those who are unfamiliar with Tourette’s. To further break down these barriers, we will now address the societal attitudes and stigma surrounding the disorder through a variety of perspectives.