ReviewMolecular neurobiology1998
Tyrosine hydroxylase and Parkinson's disease.
Review in Molecular neurobiology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers.
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Who cites it
114 citing papers in PubMed, 259 citations in OpenAlex.
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- Tribolium castaneum with longer duration of tonic immobility have more variations corresponding to the human Parkinson's disease genomic region.Scientific reports · 2026Article
- Integrative Transcriptomic Analysis Identifies Novel Mitochondrial Gene Targets in Parkinson's Disease.Molecular neurobiology · 2026Article
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- Bacopaside-I ameliorates motor dysfunction and neurodegeneration in rat model of Parkinson's disease.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
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- Bifenthrin Caused Parkinson's-Like Symptoms Via Mitochondrial Autophagy and Ferroptosis Pathway Stereoselectively in ParkinMolecular neurobiology · 2024Article
- Repetitive transcranial magnetic stimulation alleviates motor impairment in Parkinson's disease: association with peripheral inflammatory regulatory T-cells and SYT6.Molecular neurodegeneration · 2024Article
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- Social defeat stress impairs systemic iron metabolism by activating the hepcidin-ferroportin axis.FASEB bioAdvances · 2024Article
- New Step in Understanding the Pathogenetic Mechanism of Sudden Infant Death Syndrome: Involvement of the Pontine Reticular Gigantocellular Nucleus.International journal of molecular sciences · 2024Article
- Persistent Neurological Deficits in Mouse PASC Reveal Antiviral Drug Limitations.bioRxiv : the preprint server for biology · 2024Article
- Optimization of the Preparation Process of Glucuronomannan Oligosaccharides and Their Effects on the Gut Microbiota in MPTP-Induced PD Model Mice.Marine drugs · 2024Article
- Neuronal-type-specific epigenome editing to decreaseMolecular therapy. Nucleic acids · 2024Article
- Serping1 associated with α-synuclein increase in colonic smooth muscles of MPTP-induced Parkinson's disease mice.Scientific reports · 2024Article
54 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
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A consistent neurochemical abnormality in Parkinson's disease (PD) is degeneration of dopaminergic neurons in substantia nigra, leading to a reduction of striatal dopamine (DA) levels. As tyrosine hydroxylase (TH) catalyses the formation of L-DOPA, the rate-limiting step in the biosynthesis of DA, the disease can be considered as a TH-deficiency syndrome of the striatum. Similarly, some patients with hereditary L-DOPA-responsive dystonia, a neurological disorder with clinical similarities to PD, have mutations in the TH gene and decreased TH activity and/or stability. Thus, a logical and efficient treatment strategy for PD is based on correcting or bypassing the enzyme deficiency by treatment with L-DOPA, DA agonists, inhibitors of DA metabolism, or brain grafts with cells expressing TH. A direct pathogenetic role of TH has also been suggested, as the enzyme is a source of reactive oxygen species (ROS) in vitro and a target for radical-mediated oxidative injury. Recently, it has been demonstrated that L-DOPA is effectively oxidized by mammalian TH in vitro, possibly contributing to the cytotoxic effects of DOPA. This enzyme may therefore be involved in the pathogenesis of PD at several different levels, in addition to being a promising candidate for developing new treatments of this disease.
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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.