ArticleParkinsonism & related disorders2016
The V81M variant of tyrosine hydroxylase is associated with more severe freezing of gait in Parkinson's disease.
Article in Parkinsonism & related disorders, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 4 citations in OpenAlex.
- Contribution of dopaminergic polymorphisms to levodopa treatment response and drug concentration in Chinese patients with Parkinson's disease.Clinical parkinsonism & related disorders · 2025Article
- Freezing of gait: overview on etiology, treatment, and future directions.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022Review
- Freezing of gait: understanding the complexity of an enigmatic phenomenon.Brain : a journal of neurology · 2020Review
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Authors and funding
6 authors at 2 institutions in 1 country.
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Abstract
introductionMany of the symptoms and signs of Parkinson's disease (PD) arise from the death of midbrain dopamine neurons that utilize tyrosine hydroxylase (TH) as the rate-limiting enzyme in catecholamine biosynthesis.
methodsWe investigated whether the presence of a common TH polymorphism affects the clinical outcomes in 101 PD subjects. We further examined the effect of this polymorphism on the purified recombinant enzyme.
resultsPD subjects homozygous for the common V81M polymorphism, have higher overall freezing of gait scores after controlling for disease duration, although this polymorphism does not associate with the occurrence of PD or FOG. In vitro functional assays on pure recombinant wild type TH and V81M TH revealed that the Km of the mutant enzyme for tyrosine was twice that of the wild-type. This polymorphism, however, did not change the stability of the enzyme, nor did it affect the Vmax or Km for the co-substrate BH4.
conclusionThe data suggest that presence of a homozygous V81M polymorphism is associated with more severe FOG, possibly due to lower catecholamine synthetic capacity. Further studies are warranted to investigate the role of subtle changes in catecholamine availability in the development of FOG.
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