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We present a case of a 66-year-old man, where 18F-FDG PET/CT revealed intense FDG uptake in the tongue, lips, cheeks, and chewing musculature and distinct activation of the somatosensory and motor cortex corresponding to the mouth and tongue. The patient suffered from buccolingual masticatory syndrome, characterized by tardive dyskinesia, meaning uncontrollable, repetitive movements of the tongue, lips, cheeks, and masticatory musculature. In this case, the buccolingual masticatory syndrome was caused by metoclopramide antiemetic treatment.

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We present a case of a 66-year-old man, where 18F-FDG PET/CT revealed intense FDG uptake in the tongue, lips, cheeks, and chewing musculature and distinct activation of the somatosensory and motor cortex corresponding to the mouth and tongue. The patient suffered from buccolingual masticatory syndrome, characterized by tardive dyskinesia, meaning uncontrollable, repetitive movements of the tongue, lips, cheeks, and masticatory musculature. In this case, the buccolingual masticatory syndrome was caused by metoclopramide antiemetic treatment.

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Background: Deutetrabenazine is a widely used drug for the treatment of tardive dyskinesia (TD), and post-marketing testing is important. There is a lack of real-world, large-sample safety studies of deutetrabenazine. In this study, a pharmacovigilance analysis of deutetrabenazine was performed based on the FDA Adverse Event Reporting System (FAERS) database to evaluate its relevant safety signals for clinical reference.

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Positron emission tomography (PET) is frequently used to obtain target occupancy (%TO) of central nervous system (CNS) drug candidates during clinical development. Obtaining %TO with PET can be particularly powerful when the %TO associated with efficacy is known for a protein target. Using the radiotracer [F]AV-133, the relationship between plasma concentration (PK) and %TO of NBI-750142, an experimental inhibitor of the vesicular monoamine transporter type 2 (VMAT2) was obtained in both nonhuman primate (NHP) and human.

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Drug inhibition and substrate transport mechanisms of human VMAT2.

Nat Commun

January 2025

Shanghai Fifth People's Hospital, Fudan University, and Shanghai Key Laboratory of Medical Epigenetics, International Co-laboratory of Medical Epigenetics and Metabolism (Ministry of Science and Technology), Institutes of Biomedical Sciences, Fudan University, Shanghai, China.

Vesicular monoamine transporter 2 (VMAT2) is crucial for packaging monoamine neurotransmitters into synaptic vesicles, with their dysregulation linked to schizophrenia, mood disorders, and Parkinson's disease. Tetrabenazine (TBZ) and valbenazine (VBZ), both FDA-approved VMAT2 inhibitors, are employed to treat chorea and tardive dyskinesia (TD). Our study presents the structures of VMAT2 bound to substrates serotonin (5-HT) and dopamine (DA), as well as the inhibitors TBZ and VBZ.

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