"high Doses Of Riboflavin And The Elimination Of Dietary Red Meat Promote The Recovery Of Some Motor Functions In Parkinson's Disease Patients. C.g. Coimbra And V.b.c. Junqueira. Brazilian Journal Of Medical And Biological Research, 36: 1409-1417, 2003"

[No abstract available]37912971299Coimbra, C.G., Junqueira, V.B.C., High doses of riboflavin and the elimination of dietary red meat promote the recovery of some motor functions in Parkinson's disease patients (2003) Brazilian Journal of Medical and Biological Research, 36, pp. 1409-1417Pare, S., Burr, S.I., Ross, S.E., Effect of day-time protein restriction on nutrient intakes of free-living Parkinson's disease patients (1992) American Journal of Clinical Nutrition, 55, pp. 701-707Simon, N., Gantcheva, R., Bruguerolle, B., Viallet, F., The effects of a normal protein diet on levodopa plasma kinetics in advanced Parkinson's disease (2004) Parkinsonism and Related Disorders, 10, pp. 137-142Fahn, S., Elton, R.L., Unified Parkinson's Disease Rating Scale (1987) Recent Developments in Parkinson's Disease, 2, pp. 153-164. , Members of the UPDRS Development Committee Fahn S, Marsden CD, Calne DB & Goldstein M (Editors), MacMillan Health Care Information, Florham Park, NJ, USABaldereschi, M., DiCarlo, A., Vanni, P., Ghetti, A., Carbonin, P., Amaducci, L., Inzitani, D., Italian longitudinal study on aging working group. Lifestyle related risk factors for Parkinson's disease: A populational study (2003) Acta Neurologica Scandinavica, 108, pp. 239-244Tsai, C.H., Lo, S.K., See, L.C., Chen, H.Z., Chen, R.S., Weng, Y.H., Chang, F.C., Lu, C.S., Environmental risk factors of young onset Parkinson's disease (2002) Clinical Neurology and Neurosurgery, 104, pp. 328-333Tanner, C.M., Epidemiological clues to the cause of Parkinson's disease (1994) Movement Disorders 3, pp. 124-146. , Marsden CD & Fahn S (Editors) Butterworth-Heinemann, Oxford, UKGolbe, L.I., Farrel, T.M., Davis, P.H., Case-control study of early life dietary factors in Parkinson's disease (1988) Archives of Neurology, 45, pp. 350-353Abbot, R.D., Ross, G.W., White, C.R., Sanderson, W.T., Burchfiel, C.M., Kashon, M., Sharp, D.S., Petrovitch, H., Environment, lifestyle, and physical precursors of clinical Parkinson's disease: Recent findings from the Honolulu-Asia aging study (2003) Journal of Neurology, 250 (SUPPL. 3), pp. III30-III3

DNAJC6 Mutations Associated with Early-Onset Parkinson's Disease

_Objective_ DNAJC6 mutations were recently described in two families with autosomal recessive juvenile parkinsonism (onset age < 11), prominent atypical signs, poor or absent response to levodopa, and rapid progression (wheelchair-bound within ∼10 years from onset). Here, for the first time, we report DNAJC6 mutations in early-onset Parkinson's disease (PD). _Methods_ The DNAJC6 open reading frame was analyzed in 274 patients with early-onset sporadic or familial PD. Selected variants were followed up by cosegregation, homozygosity mapping, linkage analysis, whole-exome sequencing, and protein studies. _Results_ We identified two families with different novel homozygous DNAJC6 mutations segregating with PD. In each family, the DNAJC6 mutation was flanked by long runs of homozygosity within highest linkage peaks. Exome sequencing did not detect additional pathogenic variants within the linkage regions. In both families, patients showed severely decreased steady-state levels of the auxilin protein in fibroblasts. We also identified a sporadic patient carrying two rare noncoding DNAJC6 variants possibly effecting RNA splicing. All these cases fulfilled the criteria for a clinical diagnosis of early-onset PD, had symptoms onset in the third-to-fifth decade, and slow disease progression. Response to dopaminergic therapies was prominent, but, in some patients, limited by psychiatric side effects. The phenotype overlaps that of other monogenic forms of early-onset PD. _Interpretation_ Our findings delineate a novel form of hereditary early-onset PD. Screening of DNAJC6 is warranted in all patients with early-onset PD compatible with autosomal recessive inheritance. Our data provide further evidence for the involvement of synaptic vesicles endocytosis and trafficking in PD pathogenesis

Selegiline increases heme oxygenase-1 expression and the cytotoxicity produced by dopamine treatment of neuroblastoma SK-N-SH cells

Increased dopamine catabolism may be associated with oxidative stress and neuronal cell death in Parkinson's disease. The present study was carried out to examine the effect of dopamine on the expression of heme oxygenase-1 and -2 (HO-1 and HO-2) in human neuroblastomas (SK-N-SH cell line) and the effects of selegiline and antioxidants on this expression. Cells were kept with close control of pH and were incubated with varying concentrations of dopamine (0.1-100 µM) for 24 h. HO-1 and HO-2 cDNA probes were prepared by reverse transcription-polymerase chain reaction amplification. The mRNA expression of HO-1 and HO-2 was measured by Northern blot analysis. The levels of HO-1 mRNA increased after dopamine treatment, in a dose-dependent manner, in all cell lines studied, whereas levels of the two HO-2 transcripts did not. The HO-1 and HO-2 protein expression was analyzed by Western blotting. HO-1 protein was undetectable in untreated SK-N-SH cells and increased after treatment with dopamine. In contrast, the HO-2 protein (36 kDa) was detected in untreated cells and the levels did not change as a result of treatment. alpha-Tocopherol (10-100 µM) and ascorbic acid (100 µM) did not attenuate the effects of dopamine. Selegiline (10 µM) produced significant increase (P < 0.01) in the induction of HO-1 by dopamine (more than six times the control values). The increased expression of HO-1 following dopamine treatment indicates that dopamine produces oxidative stress in this cell line