The influence of dopamine β-hydroxylase gene polymorphism rs1611115 on levodopa/carbidopa treatment for cocaine dependence: a preliminary study
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Updated: Apr 30, 2026

Induction and Assessment of Levodopa-induced Dyskinesias in a Rat Model of Parkinson's Disease
Published on: October 14, 2021
Shijing Liu1, Charles E Green, Scott D Lane
1aDepartment of Psychiatry and Behavioral Sciences, University of Texas Health Science Center at Houston bDepartment of Psychiatry and Behavioral Sciences, Baylor College of Medicine and Michael E. DeBakey V.A. Medical Center, MEDVAMC, Houston, Texas cDepartment of Psychiatry and Pharmacology and Toxicology, Virginia Commonwealth University Medical School, Richmond, Virginia, USA.
Abstract:
Recent studies have suggested that heterogeneity in the level of dopamine activity and function might be useful for identifying a subgroup of cocaine-dependent patients responding better to dopamine-enhancement pharmacotherapy. Here we hypothesized that response to levodopa/carbidopa treatment would be greater in patients with genetically determined low levels of the dopamine metabolizing enzyme dopamine β-hydroxylase (DβH). Seventy-one cocaine-dependent patients who participated in a 12-week randomized double-blind placebo-controlled trial of levodopa/carbidopa were genotyped for the DβH gene (DBH) polymorphism rs1611115. Our results showed that for patients with the low DβH activity genotypes (CT/TT) who received levodopa, the odds of having cocaine-positive urine decreased significantly over treatment compared with placebo-treated patients with the CT/TT genotypes (P=0.004). Individuals with the normal DβH activity genotype (CC) showed no differential response to levodopa. These preliminary results need to be confirmed in a larger sample focusing on the DBH polymorphism.
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