This case report details the clinical presentation, diagnosis, management and prognosis of paroxysmal dyskinesia (PD) in four small-breed dogs, each weighing under 6 kg: A 7-year-old spayed female Pomeranian, an 8-year-old female mixed breed, a 1-year-old female Pomeranian and a 9-year-old castrated male Poodle. These dogs were referred to our hospital due to movement disorders. Diagnosis was facilitated by video recordings of the episodes, assessing motor activity, consciousness, episode duration, any pre- or post-episodic behaviour as well as the presence of autonomic signs. Magnetic resonance imaging conducted on two of the dogs returned unremarkable results. Treatment trials included a gluten-free diet for all four dogs, with two also receiving acetazolamide. This intervention led to a decrease in the frequency of abnormal movement in all patients. Our findings suggest that PD in dogs can be effectively diagnosed through detailed symptom description using videos and questionnaires. Furthermore, once diagnosed, a combination of nutritional and medical management can be beneficial.
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http://dx.doi.org/10.1002/vms3.70015 | DOI Listing |
Neuropsychopharmacology
January 2025
Neurocrine Biosciences, Inc., San Diego, CA, USA.
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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Movement Disorders Unit, Department of Neurology, University Hospital Josep Trueta, Girona - Hospital Santa Caterina, Salt, Spain.
Neurochem Res
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Diagnostic Radiology Department, National Cancer Institute, Misrata, Libya.
Huntington's disease (HD) is a progressive neurodegenerative disease resulting from a mutation in the huntingtin (HTT) gene and characterized by progressive motor dysfunction, cognitive decline, and psychiatric disturbances. Currently, no disease-modifying treatments are available. Recent research has developed therapeutic agents that may have the potential to directly target the disease pathology, such as gene silencing or clearing the mutant protein.
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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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January 2025
The First Hospital of Peking University, Beijing, China.
Background: Glucose transporter 1 deficiency syndrome (Glut1DS) was initially reported by De Vivo and colleagues in 1991. This disease arises from mutations in the SLC2A1 and presents with a broad clinical spectrum. It is a treatable neuro-metabolic condition, where prompt diagnosis and initiation of ketogenic dietary therapy can markedly enhance the prognosis.
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