Tyrosine hydroxylase and Parkinson's disease

@article{Haavik2007TyrosineHA,
  title={Tyrosine hydroxylase and Parkinson's disease},
  author={Jan Haavik and Karen Toska},
  journal={Molecular Neurobiology},
  year={2007},
  volume={16},
  pages={285-309}
}
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 ofl-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 hereditaryl-DOPA-responsive dystonia, a neurological disorder with clinical similarities to PD… 
A synopsis on the role of tyrosine hydroxylase in Parkinson's disease.
TLDR
A logical and efficient strategy for PD treatment is based on correcting or bypassing the enzyme deficiency by the treatment with L-DOPA, DA agonists, inhibitors of DA metabolism or brain grafts with cells expressing a high level of TH.
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TLDR
The molecular mechanism underlying the neurodegeneration process in dopamine-containing neurons is reviewed and the novel degradation pathway of TH through the ubiquitin-proteasome system is focused on to advance understanding of the etiology of Parkinson’s disease and dopa-responsive dystonia.
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TLDR
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TLDR
This mini review has tried to briefly outline the involvement of TH and α-synuclein in PD and the contributions of DJ-1 in TH regulation.
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TLDR
To determine if tyrosine hydroxylase (TH), the rate-limiting synthetic enzyme of dopamine, is implicated in the neuroprotective effect of CuSO4 pretreatment, and if this neuroProtective effect is able to prevent the hypokinetic state (measured as spontaneous locomotor activity, SLA) induced by the experimental model of PD.
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TLDR
Results suggest that preservation of THA participates in the neuroprotective effects derived from the copper supplementation, a phenomenon that avoid the hypokinetic state induced by the MPP+ experimental model of PD.
Intermittent Hypoxia and Experimental Parkinson’s Disease
TLDR
Inter intermittent hypoxia training increased dopamine synthesis in old and experimental PD animals, especially in the right striatum, restored partially the asymmetry of DA distribution between brain hemispheres, and decreased the intensity of lipid peroxidation.
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TLDR
The latest evidence on tyrosine hydroxylase genetic variants in PD is summarized, including the ongoing effort of using whole exome sequencing to search for rare variants inPD patients.
Neuroprotection of MAO-B inhibitor and dopamine agonist in Parkinson disease.
TLDR
Selegiline demonstrated stronger neuroprotective effect than Piribedil, and the two drugs have potential treatment effect in clinical for PD patients.
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References

SHOWING 1-10 OF 207 REFERENCES
Oxidative stress and antioxidant therapy in Parkinson's disease
Biochemistry of Parkinson's disease with special reference to the dopaminergic systems
TLDR
By contrast, the neurons that survive in Parkinson's disease are free of neuromelanin, calbindinD28-positive, contain low amounts of iron, and are better protected against oxidative stress.
Dopa‐responsive dystonia: Pathological and biochemical observations in a case
TLDR
It is concluded that disturbed dopamine synthetic capacity or a reduced arborization of striatal dopamine terminals may be the major disturbance in dopa‐responsive dystonia.
Does oxidative stress participate in nerve cell death in Parkinson's disease?
TLDR
It remains, however, to be determined whether oxidative stress participates to the cause of the disease or only represents a consequence of nerve cell death.
Oxidative stress as a cause of Parkinson's disease
TLDR
Present evidence points to oxidative stress as an important factor contributing to neuronal loss and future strategies for the treatment of Parkinson's disease should be aimed at preventing oxidative stress and stopping or slowing the progression of the underlying pathology.
The roles of neuromelanin, binding of metal ions, and oxidative cytotoxicity in the pathogenesis of Parkinson's disease: A hypothesis
TLDR
Parkinson's disease therefore may be a form of accelerated aging in the substantia nigra associated with environmental toxins in which neuromelanin has a central, active role.
Oxidative stress and the pathogenesis of Parkinson's disease
TLDR
Selegiline may act through a mechanism unrelated to MAO-B to increase neurotrophic factor activity and upregulate molecules such as glutathione, SOD, catalase, and BCL-2 protein, which protect against oxidant stress and apoptosis.
Specific A10 Dopaminergic Nuclei in the Midbrain Degenerate in Parkinson's Disease
TLDR
There was a reduction in tyrosine hydroxylase immunoreactivity but no overt neurodegeneration in other A10 regions, suggesting the disease may also influence the production of dopamine in some surviving neurons.
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