Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P02794 (ferritin)
17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Parkinson's disease, known also as striatal dopamine deficiency syndrome, is a degenerative disorder of the central nervous system characterized by akinesia, muscular rigidity, tremor at rest, and postural abnormalities. In early stages of parkinsonism, there appears to be a compensatory increase in the number of dopamine receptors to accommodate the initial loss of dopamine neurons. As the disease progresses, the number of dopamine receptors decreases, apparently due to the concomitant degeneration of dopamine target sites on striatal neurons. The loss of dopaminergic neurons in Parkinson's disease results in enhanced metabolism of dopamine, augmenting the formation of H2O2, thus leading to generation of highly neurotoxic hydroxyl radicals (OH.). The generation of free radicals can also be produced by 6-hydroxydopamine or MPTP which destroys striatal dopaminergic neurons causing parkinsonism in experimental animals as well as human beings. Studies of the substantia nigra after death in Parkinson's disease have suggested the presence of oxidative stress and depletion of reduced glutathione; a high level of total iron with reduced level of ferritin; and deficiency of mitochondrial complex I. New approaches designed to attenuate the effects of oxidative stress and to provide neuroprotection of striatal dopaminergic neurons in Parkinson's disease include blocking dopamine transporter by mazindol, blocking NMDA receptors by dizocilpine maleate, enhancing the survival of neurons by giving brain-derived neurotrophic factors, providing antioxidants such as vitamin E, or inhibiting monoamine oxidase B (MAO-B) by selegiline. Among all of these experimental therapeutic refinements, the use of selegiline has been most successful in that it has been shown that selegiline may have a neurotrophic factor-like action rescuing striatal neurons and prolonging the survival of patients with Parkinson's disease.
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PMID:Oxidative stress and antioxidant therapy in Parkinson's disease. 883 Mar 46

This study investigated the effect of acupuncture on iron-related oxidative damage in a mouse model designed as a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced parkinsonism model. To generate the chronic parkinsonism model, mice were intraperitoneally injected with MPTP (20mg/kg, one daily injection) for 30 days and acupuncture was performed at acupoints LR3 (Taichong) and GB34 (Yanglingquan) at 48h intervals. Acupuncture inhibited decreases in the immunoreactivities of tyrosine hydroxylase (TH) and dopamine transporter (DAT) that occurred as a result of MPTP neurotoxicity. The presence of ferric iron (Fe(3+)), but not ferrous iron (Fe(2+)), was strongly increased in the substantia nigra (SN) as a result of chronic loading of MPTP, whereas the ferritin-heavy chain (F-H) was significantly decreased. However, acupuncture treatment inhibited the increase in ferric iron and the decrease in the F-H that was induced by MPTP. Additionally, treatment with MPTP and acupuncture caused no changes in the presence of ferrous iron and ferritin-light chain (F-L) as a result of the treatments. The mRNA of F-H was also not affected. These results suggest that acupuncture may inhibit iron-related oxidative damage and may prevent the deleterious alteration of iron metabolism in the MPTP model.
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PMID:Acupuncture inhibits ferric iron deposition and ferritin-heavy chain reduction in an MPTP-induced parkinsonism model. 1905 64

A 57-year-old woman had been suffered from insomnia due to restlessness and abnormal sensation of the left side of the body for 33 years. Since the preceding year of the first visit frequency of the symptoms increased, and the abnormal sensation was spread to the right leg. Her daughter had restless legs syndrome (RLS) since age 20. Neurological examination showed no abnormality. Laboratory test results showed normal ferritin levels. There was no renal dysfunction or anemia. A diagnosis of RLS was made, and her symptoms responded well to pramipexole treatment. However, the patient developed right shoulder pain and right-hand tremor one year and one and a half year after the first visit, respectively. Based on clinical findings and the findings of dopamine transporter scan and cardiac 123I-MIBG scintigraphy, the patient was diagnosed with Parkinson's disease (PD). Careful observation of changes in RLS symptoms is required as an increased frequency and spread of symptoms of RLS could be the early manifestation of PD.
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PMID:[Increased frequency and spread of restlessness as the early manifestation of Parkinson's disease in a woman with restless legs syndrome]. 3027 Mar 36