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Tourette Syndrome (TS)

The main therapeutic difficulty in Tourette syndrome (TS) is alleviating tics without overly sedating or dulling the patient's cognitive functioning. In relation to this condition, Protheragen is allocating resources to advanced technologies and specialists dedicated to the development of therapeutic solutions to manage TS. With our full-service support, you will benefit from our extensive expertise in the areas of preclinical drug development to bring your drug candidate to market.

Overview of Tourette Syndrome (TS)

Tourette syndrome, or TS, is a form of a neurodevelopmental disorder marked by the presence of numerous motor tics and at least one vocal tic for over a year. Hallmark features of TS include fluctuating tic severity, the presence of premonitory sensory urges before the tic, and high rates of comorbid conditions like attention-deficit hyperactivity disorder (ADHD) and obsessive-compulsive disorder (OCD). TS affects about 0.3-1% of children globally, with males outnumbering females, and the onset of TS symptoms is usually before the age of 18.

Fig.1 Graphical representation of the cortical-striatal-thalamus-cortical (CSTC) circuit and its changes in patients with Tourette syndrome (TS). (Lamanna J, et al., 2023)

Pathogenesis of Tourette Syndrome (TS)

Genetic factors are the primary focus in the pathogenesis of Tourette syndrome (TS), which includes the development and function of cortico-striato-thalamo (CSTC) circuits and their neurotransmission flow, particularly overactive dopamine signaling in the striatum. Other factors like neurotransmitter systems involved in the lack of control like SLITRK1 and HDC are also involved, as well as polygenic risk variants affecting histamine signaling. Furthermore, immune and prenatal factors like PANS/PANDAS are capable of modifying gene expression which in turn, can increase symptom severity.

Fig.2 Summary of the possible underlying mechanism leading to immune dysfunction in Tourette syndrome (TS). (Hsu C J, et al., 2021)

Therapeutic Development for Tourette Syndrome (TS)

Drug Name	Mechanism of Action	Targets	NCT Number	Research Phase
Deutetrabenazine	Selective vesicular monoamine transporter 2 (VMAT2) inhibitor. Reduces synaptic dopamine availability by inhibiting its packaging into synaptic vesicles.	VMAT2	NCT02674321	Approved
Pimavanserin	Selective inverse agonist and antagonist of serotonin 5-HT₂A receptors with minimal dopamine receptor binding. Modulates serotonin-glutamate-dopamine interactions in CSTC circuits.	5-HT₂A receptor	NCT04794413	Phase II
Dronabinol + Palmitoylethanolamide	Combined cannabinoid receptor modulation: Dronabinol acts as a partial CB1 agonist, while PEA enhances endocannabinoid tone through PPAR-α activation and allosteric modulation. Proposed synergistic effect on tic suppression and neuroinflammation reduction.	Cannabinoid receptor type 1 (CB1), PPAR-α	NCT03066193	Phase I

Disclaimer: Protheragen focuses on providing preclinical research services. This table is for information exchange purposes only. This table is not a treatment plan recommendation. For guidance on treatment options, please visit a regular hospital.

Our Services

Protheragen provides a full diagnostic and therapeutic development services to manage Tourette syndrome( TS) more effectively. We are focused on fulfilling the unmet medical needs with the innovative therapies aimed at TS's diverse molecular mechanisms. Our team specializes in the development of precise disease models which allows thorough testing of the safety, efficacy, and mechanism of action of TS therapies.

Therapeutic Development Services

By Molecule Types

By Mechanism of Action

Disease Model Development Services

Model Types	Model Names
In Vitro Models	Patient-Derived Cell Model Neuronal Cell Model Glial Cell Model	Co-Culture Model Brain Organoid Spinal Cord Organoid
Microfluidic Models	Neurovascular Unit Model Axon Degeneration Model Neuroinflammation Model	Neuromuscular Junction Model Synaptic Plasticity Model Organoid-on-a-Chip Model
Animal Models	Tonic Activation of Striatal Neurons (TANs) Model: This model uses optogenetic or chemogenetic techniques to induce sustained, abnormal firing in striatal projection neurons, disrupting corticostriatal circuitry to recapitulate tic-like repetitive movements and behavioral disinhibition. Fast-Spiking Interneurons (FSIs) Dysfunction Model: This approach involves selectively impairing the function of striatal fast-spiking interneurons, leading to disrupted GABAergic inhibition and resulting in spontaneous, repetitive hyperkinetic behaviors resembling tics. Histidine Decarboxylase (HDC) Knockout Model: This genetic model deletes the HDC gene, eliminating brain histamine synthesis and producing a robust phenotype of motor tics, vocalizations, and sensorimotor gating deficits that are responsive to dopamine antagonists.

At Protheragen, we are committed to supporting the development of innovative therapeutics through comprehensive preclinical research services, including pharmacodynamics (PD), pharmacokinetic (PK) and toxicology studies. Our customized approach addresses the unique challenges of your studies and helps you optimize your drug candidates for commercial success. If you are interested in our services, please feel free to contact us for more details and quotation information of related services.

References

Lamanna J, Ferro M, Spadini S, et al. The dysfunctional mechanisms throwing tics: structural and functional changes in Tourette syndrome[J]. Behavioral Sciences, 2023, 13(8): 668.
Hsu C J, Wong L C, Lee W T. Immunological dysfunction in Tourette syndrome and related disorders[J]. International journal of molecular sciences, 2021, 22(2): 853.

For research use only. Not intended for any clinical use.