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Huntingtin (Htt) is the protein coded for in humans by the HTT gene, also known as the IT15 ("interesting transcript 15") gene. [5] Mutated HTT is the cause of Huntington's disease (HD), and has been investigated for this role and also for its involvement in long-term memory storage. [6]
Tetrabenazine is a drug for the symptomatic treatment of hyperkinetic movement disorders.It is sold under the brand names Nitoman and Xenazine among others. On August 15, 2008, the U.S. Food and Drug Administration approved the use of tetrabenazine to treat chorea associated with Huntington's disease.
Huntington's disease has autosomal dominant inheritance, meaning that an affected individual typically inherits one copy of the gene with an expanded trinucleotide repeat (the mutant allele) from an affected parent. [26] Since the penetrance of the mutation is very high, those who have a mutated copy of the gene will have the disease.
Branaplam (development codes LMI070 and NVS-SM1) is a pyridazine derivative that is being studied as an experimental drug.It was originally developed by Novartis to treat spinal muscular atrophy (SMA); since 2020 it was being developed to treat Huntington's disease but the trial ended in 2023 due to toxicity concerns.
Treatment; Huntington's-related: A common treatment is dopaminergic antagonists, although treatment is largely supportive. Tetrabenazine, deutetrabenazine and valbenazine are FDA-approved drugs for the treatment of Huntington's disease-related chorea. Sydenham's chorea: Haloperidol, carbamazepine and valproic acid.
Huntington's disease stems from a defect that consists of an expanded CAG repeat in the huntingtin gene (HTT) located on the short arm p of chromosome 4. [7] Evidence shows that the basal ganglia in patients with Huntington's disease show a decrease in activity of the mitochondrial pathway , complex II-III.
These agents are associated with fewer neuromotor side effects and a lower risk of developing tardive dyskinesia. [ 37 ] Studies have tested the use of melatonin , high dosage vitamins , and different antioxidants in concurrence with antipsychotic drugs (often used to treat schizophrenia ) as a way of preventing and treating tardive dyskinesia.
These often are translated into polyglutamine-containing proteins that form inclusions and are toxic to neuronal cells. Examples of the disorders caused by this mechanism include Huntington's disease and Huntington disease-like 2, spinal-bulbar muscular atrophy, dentatorubral-pallidoluysian atrophy, and spinocerebellar ataxia 1–3, 6–8, and 17.
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