ReviewJournal of neural transmission (Vienna, Austria : 1996)2019
Human tyrosine hydroxylase in Parkinson's disease and in related disorders.
Review in Journal of neural transmission (Vienna, Austria : 1996), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
94 citing papers in PubMed, 173 citations in OpenAlex.
- Fungal-Derived Decahydrofluorene Alkaloids Promote Mitochondrial Resilience and Neuroprotection in Cellular and Animal Models of Parkinson's Disease.Antioxidants (Basel, Switzerland) · 2026Article
- NRF2 Deletion Results in Mobility Impairment in A53TSyn Model of Synucleinopathy.Antioxidants (Basel, Switzerland) · 2026Article
- Dopamine modulation of aggression.Psychopharmacology · 2026Review
- Tribolium castaneum with longer duration of tonic immobility have more variations corresponding to the human Parkinson's disease genomic region.Scientific reports · 2026Article
- Article
- Reducing Neuroinflammation via Inhibition of Fibrinogen Deposition and Microglial Activation as an Underlying Mechanism of Paning I Decoction in Ameliorating Parkinson's Disease Symptoms.Immunity, inflammation and disease · 2026Article
- Evaluation of a commercial AI-assisted cell counting software for dopaminergic neurons across species.PloS one · 2026Article
- Phenylalanine-tyrosine-catecholamine axis disorders: pathways, molecular diagnosis, therapeutics, and emerging translational monitoring technologies.Frontiers in molecular biosciences · 2026Review
- Stigmasterol exerts antioxidant effects through activation of the Keap1/Nrf2 signaling pathway in Parkinson's disease model.Journal of translational medicine · 2025Article
- Golexanolone Attenuates Neuroinflammation, Fatigue, and Cognitive and Motor Impairment in Diverse Neuroinflammatory Disorders.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Sympathetic Biomarker Dynamics Post-Myocardial Infarction: TH, PGP9.5, and SYN Expression Discordance in Murine Hearts.International journal of molecular sciences · 2025Article
- Sorghum bicolor supplement attenuates rotenone-induced behavioral derangements in rats through neuroprotective mechanisms and modulation of tyrosine hydroxylase and α-synuclein/NF-kB immunopositive cells expressions.Journal of molecular histology · 2025Article
- Quinoa extract restored behavioral damage and neurotoxicity induced by a Parkinson's disease-like model in Drosophila melanogaster.Metabolic brain disease · 2025Article
- Central biogenic amine deficiency with concomitant exploratory behavioral deficits in Dnajc12 knock-out mice.NPJ Parkinson's disease · 2025Article
- Article
- Computational Studies of Enzymes for C-F Bond Degradation and Functionalization.Chemphyschem : a European journal of chemical physics and physical chemistry · 2025Review
- Neuroprotective efficacy of berberine and caffeine against rotenone-induced neuroinflammatory and oxidative disturbances associated with Parkinson's disease via inhibiting α-synuclein aggregation and boosting dopamine release.Inflammopharmacology · 2025Article
- Phytochemicals Modulate Biosynthesis and Function of Serotonin, Dopamine, and Norepinephrine for Treatment of Monoamine Neurotransmission-Related Psychiatric Diseases.International journal of molecular sciences · 2025Review
- Metabolomics in Parkinson's Disease and Correlation with Disease State.Metabolites · 2025Review
- A comprehensive review of natural compounds and their structure-activity relationship in Parkinson's disease: exploring potential mechanisms.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
34 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD) is an aging-related movement disorder mainly caused by a deficiency of neurotransmitter dopamine (DA) in the striatum of the brain and is considered to be due to progressive degeneration of nigro-striatal DA neurons. Most PD is sporadic without family history (sPD), and there are only a few percent of cases of young-onset familial PD (fPD, PARKs) with the chromosomal locations and the genes identified. Tyrosine hydroxylase (TH), tetrahydrobiopterin (BH4)-dependent and iron-containing monooxygenase, catalyzes the conversion of L-tyrosine to L-3,4-dihydroxyphenylalanine (L-DOPA), which is the initial and rate-limiting step in the biosynthesis of catecholamines (DA, noradrenaline, and adrenaline). PD affects specifically TH-containing catecholamine neurons. The most marked neurodegeneration in patients with DA deficiency is observed in the nigro-striatal DA neurons, which contain abundant TH. Accordingly, TH has been speculated to play some important roles in the pathophysiology in PD. However, this decrease in TH is thought to be secondary due to neurodegeneration of DA neurons caused by some as yet unidentified genetic and environmental factors, and thus, TH deficiency may not play a direct role in PD. This manuscript provides an overview of the role of human TH in the pathophysiology of PD, covering the following aspects: (1) structures of the gene and protein of human TH in relation to PD; (2) similarity and dissimilarity between the phenotypes of aging-related sPD and those of young-onset fPD or DOPA-responsive dystonia due to DA deficiency in the striatum with decreased TH activity caused by mutations in either the TH gene or GTP cyclohydrolase I (GCH1) gene; and (3) genetic variants of the TH gene (polymorphisms, rare variants, and mutations) in PD, as discovered recently by advanced genome analysis.
Indexed as
Identifiers
What OpenQuestion holds
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.