SynthesisInternational journal of molecular sciences2021
A Systematic Review of Parkinson's Disease Pharmacogenomics: Is There Time for Translation into the Clinics?
Synthesis in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Serum aromatic l-amino acid decarboxylase activity as a biomarker for prodromal and manifest Parkinson's disease.EBioMedicine · 2026Article
- Tailoring treatments: pharmacogenomics in the management of neurodegenerative diseases.Acta neurologica Belgica · 2026Review
- Long-term outcomes after caudal zona incerta-forel field ablation: three-year clinical follow-up in advanced Parkinson's disease.Frontiers in aging neuroscience · 2026Article
- Review
- Pharmacogenetics in advanced Parkinson's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2025Review
- Safety of COMT-inhibitors in parkinson's disease: a phase-IV comparative study on adverse events of Tolcapone, Entacapone and Opicapone.Journal of neural transmission (Vienna, Austria : 1996) · 2025Article
- MTHFR Gene Polymorphisms: A Single Gene with Wide-Ranging Clinical Implications-A Review.Genes · 2025Review
- Genetic risk variants in New Yorkers of Puerto Rican and Dominican Republic heritage with Parkinson's disease.NPJ Parkinson's disease · 2023Article
- Pharmacogenomics-a New Frontier for Individualized Treatment of Parkinson's Disease.Current neuropharmacology · 2023Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundParkinson's disease (PD) is the second most frequent neurodegenerative disease, which creates a significant public health burden. There is a challenge for the optimization of therapies since patients not only respond differently to current treatment options but also develop different side effects to the treatment. Genetic variability in the human genome can serve as a biomarker for the metabolism, availability of drugs and stratification of patients for suitable therapies. The goal of this systematic review is to assess the current evidence for the clinical translation of pharmacogenomics in the personalization of treatment for Parkinson's disease.
methodsWe performed a systematic search of Medline database for publications covering the topic of pharmacogenomics and genotype specific mutations in Parkinson's disease treatment, along with a manual search, and finally included a total of 116 publications in the review.
resultsWe analyzed 75 studies and 41 reviews published up to December of 2020. Most research is focused on levodopa pharmacogenomic properties and catechol-O-methyltransferase (COMT) enzymatic pathway polymorphisms, which have potential for clinical implementation due to changes in treatment response and side-effects. Likewise, there is some consistent evidence in the heritability of impulse control disorder via Opioid Receptor Kappa 1 (OPRK1), 5-Hydroxytryptamine Receptor 2A (HTR2a) and Dopa decarboxylase (DDC) genotypes, and hyperhomocysteinemia via the Methylenetetrahydrofolate reductase (MTHFR) gene. On the other hand, many available studies vary in design and methodology and lack in sample size, leading to inconsistent findings.
conclusionsThis systematic review demonstrated that the evidence for implementation of pharmacogenomics in clinical practice is still lacking and that further research needs to be done to enable a more personalized approach to therapy for each patient.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.