Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Selegiline (Deprenyl, Jumex, Movergan etc.) is primarily used in the therapy of Parkinson's disease due to its neuroprotective, antidepressive and oxidative stress-preventing activities. Its prime effect is based upon the inhibition of the monoamine oxidase enzyme (MAO-B). The cofactor of this flavoenzyme is riboflavin (vitamin B2). Riboflavin, on the other hand, is an effective photosensitizer, with the capacity to promote the photodegradation of molecules (drugs, biological systems) which are otherwise stable against daylight. It has been studied whether this property of riboflavin is expressed against selegiline as well. This experiments proved that in the presence of riboflavin, both daylight and the light of daylight-lamps are sufficient to significantly decompose selegiline. The major decomposition product is methamphetamine.
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PMID:[In vitro interaction of selegiline, riboflavin and light. Sensitized photodegradation of drugs. I]. 1040 Nov 52

Abnormal riboflavin status in the absence of a dietary deficiency was detected in 31 consecutive outpatients with Parkinson's disease (PD), while the classical determinants of homocysteine levels (B6, folic acid, and B12) were usually within normal limits. In contrast, only 3 of 10 consecutive outpatients with dementia without previous stroke had abnormal riboflavin status. The data for 12 patients who did not complete 6 months of therapy or did not comply with the proposed treatment paradigm were excluded from analysis. Nineteen PD patients (8 males and 11 females, mean age +/- SD = 66.2+/-8.6 years; 3, 3, 2, 5, and 6 patients in Hoehn and Yahr stages I to V) received riboflavin orally (30 mg every 8 h) plus their usual symptomatic medications and all red meat was eliminated from their diet. After 1 month the riboflavin status of the patients was normalized from 106.4+/-34.9 to 179.2+/-23 ng/ml (N = 9). Motor capacity was measured by a modification of the scoring system of Hoehn and Yahr, which reports motor capacity as percent. All 19 patients who completed 6 months of treatment showed improved motor capacity during the first three months and most reached a plateau while 5/19 continued to improve in the 3- to 6-month interval. Their average motor capacity increased from 44 to 71% after 6 months, increasing significantly every month compared with their own pretreatment status (P < 0.001, Wilcoxon signed rank test). Discontinuation of riboflavin for several days did not impair motor capacity and yellowish urine was the only side effect observed. The data show that the proposed treatment improves the clinical condition of PD patients. Riboflavin-sensitive mechanisms involved in PD may include glutathione depletion, cumulative mitochondrial DNA mutations, disturbed mitochondrial protein complexes, and abnormal iron metabolism. More studies are required to identify the mechanisms involved.
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PMID:High doses of riboflavin and the elimination of dietary red meat promote the recovery of some motor functions in Parkinson's disease patients. 1533 94

The kynurenine pathway (KP) of L-tryptophan metabolism produces several neuroactive metabolites with an amino acid structure. These metabolites may play an important role in the pathophysiology of irritable bowel syndrome, Alzheimer's disease, Parkinson's disease, Huntington's disease, schizophrenia, AIDS-dementia complex, depression, epilepsy and the aging process. Modulation of the KP through inhibition or stimulation of enzyme synthesis and activity can be an alternative approach to traditional therapy. Furthermore, it may be responsible for the altered functioning of the enteric nervous system and the central nervous system. There is evidence that the KP is sensitive to changes in the concentration of many vitamins and minerals that play a crucial role as coenzymes and cofactors in the de novo synthesis of nicotinamide adenine dinucleotide coenzyme. A reduction in the availability of the active form of vitamin B6 (pyridoxal 5'-phosphate, PLP) is known to affect tryptophan hydroxylase, kynurenine aminotransferase and kynureninase (KYNU). Vitamin B2 deficiencies result in a reduction in the activity of the flavin adenine dinucleotide dependent enzyme, kynurenine 3-monooxygenase. Minerals are also responsible for the proper functioning of enzymes engaged in L-tryptophan metabolism. Mn(2+), Zn(2+), Co(2+) and Cu(2+) influence KYNU activity, and Mg(2+) regulates quinolinate phosphoribosyl transferase. Fe(2+) is responsible for the proper functioning of both indoleamine 2,3-dioxygenase and 3-hydroxy-anthranilic acid dioxygenase. Changes in the concentration of KP metabolites and in enzymatic activity have been found in many pathological states. Therefore, it is justifiable to regulate the concentration of certain kynurenines or enzymes in the KP which may provide a potential therapeutic target for the treatment of various health impairments. This review demonstrates the role of vitamin and mineral activity on the KP, which may have an effect on the proper functioning of the human organism. Surplus administration of vitamins did not elicit any beneficial effects on L-tryptophan metabolism. Whether a mineral surplus influences L-tryptophan metabolism is still not established. It seems that cofactor deficiencies influence the KP far more than surpluses.
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PMID:Overview of the role of vitamins and minerals on the kynurenine pathway in health and disease. 2701 Aug 91

Riboflavin is a water-soluble vitamin, which was initially isolated from milk. There are two coenzyme forms of riboflavin, flavin mononucleotide and flavin adenine dinucleotide, in which riboflavin plays important roles in the enzymatic reactions. Riboflavin is found in a wide variety of animal and plant foods. Meat and dairy products are the major contributors of riboflavin dietary intake. In this chapter, the latest evidence on the relationship between riboflavin status and specific health risks will be reviewed. Also, some of the mechanisms by which riboflavin exerts its roles will be discussed. The evidence accrued suggests that riboflavin is an antioxidant nutrient which may prevent lipid peroxidation and reperfusion oxidative injury. Moreover, riboflavin deficiency may increase the risk of some cancers. Riboflavin may also exert a neuroprotective effects in some neurological disorders (e.g., Parkinson disease, migraine, and multiple sclerosis) through its role in some pathways that are hypothesized to be impaired in neurological disorders such as antioxidation, myelin formation, mitochondrial function, and iron metabolism.
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PMID:Riboflavin in Human Health: A Review of Current Evidences. 2947 26