vitamin-k-semiquinone-radical and Parkinson-Disease

This umbrella review aimed to systematically review the available literature and assess the association of dietary intake or serum levels of different vitamins and the risk of PD, to help find out more efficient treatments for PD patients by replenishing the deficiency of vitamins.. Pubmed/Medline, Scopus, Google Scholar and hand searching bibliographies of retrieved articles in duplicate, were used to detect all relevant meta-analyses investigating the relationship between vitamins and PD. After study selection, data were extracted from previously published meta-analyses and pooled by Review Manager version 5.4 and CMA software version 2.2.064 to achieve effect sizes. Level of statistical significance was set at P ≤ 0.05.. 14 meta-analyses were included in the meta-review. Serum vitamin D and B12 levels were significantly lower in PD (SMD = -0.67 and SMD = -0.40 respectively). Homocysteine (Hcy) levels were significantly higher in PD patients (SMD = 1.26). Also the odds ratio for highest vs. lowest vitamin E intake was 0.73 which was significant. However, there was no significant difference between vitamin A, C and B6 intake or serum levels in PD vs. control groups.. Serum vitamin D and B12 levels were significantly lower in PD in comparison to healthy individuals, while Hcy level was significantly higher in PD patients. Also higher vitamin E intake was associated with significantly lower risk of development of PD in comparison to lower vitamin E intake. However, there was no significant difference between risk of PD and higher vitamin A, C and B6 intake or serum levels of folate.

Topics: Humans; Parkinson Disease; Systematic Reviews as Topic; Vitamin A; Vitamin B 12; Vitamin D; Vitamin E; Vitamin K; Vitamins

Neurodegenerative disease refers to a group of disorders that predominantly damage the neurons in the brain. Despite significant progress in the knowledge of neurodegenerative diseases, there is currently no disease-modifying drug available. Vitamin K was first established for its involvement in blood clotting, but there is now compelling evidence indicating its role in the neurological system. In particular, the results of recent studies on the effects of vitamin K2 on preventing apoptosis, oxidative stress, and microglial activation in neuron cells through its role in electron transport are very promising against Alzheimer's disease. In addition to its protective effect on cognitive functions, its inhibitory effects on inflammation and α-synuclein fibrillization in Parkinson's disease, which has been revealed in recent years, are remarkable. Although there are many studies on the mechanism and possible treatment methods of neurodegenerative diseases, especially Parkinson's and Alzheimer's disease, studies on the relationship between vitamin K and neurodegenerative diseases are very limited, yet have promising findings. Vitamin K has also been proposed for therapeutic use in multiple sclerosis patients to lower the intensity or to slow down the progression of the disease. Accordingly, the aim of this study is to review the current evidence for the use of vitamin K supplementation in neurodegenerative diseases, in particular Alzheimer's disease, Parkinson's disease, and multiple sclerosis.

Topics: Alzheimer Disease; Humans; Multiple Sclerosis; Neurodegenerative Diseases; Parkinson Disease; Vitamin K

Parkinson's disease (PD) is designated as a convoluted nerve cell devastating disorder that encompasses the profound declination of dopaminergic (DArgic) nerve cells of the mesencephalon region. The condition is sketched by four eminent motor manifestations, namely, slow movement, muscle tension, shaking, and disrupted balance, but the pathology behind these manifestations is still vague. Modern-day medicinal treatment emphasizes curbing the manifestations via introducing a gold standard (levodopa) instead of forestalling the DArgic nerve cell destruction. Therefore, the invention and utilization of novel neuroprotective candidates are of paramount importance in overcoming PD. Vitamins are organic molecules engaged in the modulation of evolution, procreation, biotransformation, and other operations of the body. Numerous studies employing varying experimental models have promulgated a prominent linkage between vitamins and PD. Vitamins, owing to their antioxidant and gene expression modulation abilities, might be efficacious in PD therapy. Recent corroborations depict that adequate augmentation of vitamins might de-escalate the manifestations and emergence of PD; however, the safety of daily vitamin intake must be considered. By assembling the comprehensive information obtained from existing publications via searching various renowned medical portals, the investigators render in-depth insights into the physiological association amongst vitamins (D, E, B3, and C) and PD and concerned pathological processes and their safeguarding actions in varied PD models. Furthermore, the manuscript delineates the remedial aptitude of vitamins in PD therapy. Conclusively, augmentation of vitamins (owing to their antioxidant and gene expression regulation capabilities) might appear as a novel and terribly efficacious ancillary therapeutic approach for PD.

Topics: Antioxidants; Humans; Levodopa; Parkinson Disease; Vitamin A; Vitamin K; Vitamins

Topics: Antiparkinson Agents; Female; Humans; Indoles; Intracranial Hemorrhages; Middle Aged; Parkinson Disease; Vitamin K

To assess the influence of vitamin K on bone mineral density (BMD) in vitamin-D-deficient women with Parkinson's disease (PD).. Cross-sectional study.. Neurology department at a university medical center in Japan.. Sixty-two women with PD (mean age, 70.7yr) and 62 age-matched controls. Patients were divided into 2 groups according to their functional capabilities: group A (independent: stages I-II of Hoehn and Yahr stages of Parkinson's disease, n = 26); and group B (dependent: Hoehn and Yahr stages 3-5; n = 36).. Not applicable.. Sera were analyzed to relate vitamin K concentrations to bone-related biochemical indices. BMD was measured by computed radiograph densitometry.. Group B had significantly lower metacarpal BMD (P <.0001) lower serum concentrations of vitamin K1 (P <.01) and 25-hydroxyvitamin D (25-OHD; P <.0001) than group A. Serum undercarboxylated osteocalcin levels were higher in group B than in group A (P <.0001). The serum concentration of vitamin K1 correlated positively with that of 25-OHD (r =.735, P <.0001), and negatively with undercarboxylated osteocalcin (r = -.751, P <.0001) and Hoehn and Yahr stages (r =.787, P <.0001). Multiple regression analysis identified Hoehn and Yahr stages, vitamin K1, 25-OHD, and undercarboxylated osteocalcin as independent determinants of BMD (P <.0364.0003).. In functionally dependent women with PD, nutritional vitamin K1 deficiency is believed to reduce production of fully carboxylated osteocalcin, causing reduced BMD.

Topics: Aged; Aged, 80 and over; Analysis of Variance; Bone Density; Bone Diseases, Metabolic; Chi-Square Distribution; Cross-Sectional Studies; Female; Humans; Linear Models; Middle Aged; Osteocalcin; Parkinson Disease; Vitamin D Deficiency; Vitamin K; Vitamin K Deficiency

Linkage of alpha-synuclein (alpha-SN) mutations to familial Parkinson's disease (PD) and presence of alpha-SN as a major constituent of Lewy body in both sporadic and familial PD implicate alpha-SN abnormality in PD pathogenesis. Here we demonstrate that overexpression of wild-type or mutant alpha-SN does not cause any deleterious effect on the growth or continued propagation of transfected human cells, but overproduction of mutant alpha-SN heightens their sensitivity to menadione-induced oxidative injury. Such enhanced vulnerability is more pronounced in neuronal transfectants than in their nonneuronal counterparts and is associated with increased production of reactive oxygen species. The data suggest that mutated alpha-SN, especially with an alanine-to-proline substitution at residue 30, sensitizes neuronal cells to oxidative damage.

Topics: alpha-Synuclein; Cell Line; Cell Survival; Dose-Response Relationship, Drug; Humans; Immunoblotting; Kidney; Mutation; Nerve Tissue Proteins; Neurons; Oxidative Stress; Parkinson Disease; Reactive Oxygen Species; RNA, Messenger; Sulfhydryl Compounds; Synucleins; Tetrazolium Salts; Thiazoles; Transfection; Vitamin K