Dietary Antioxidants and Parkinson Disease

Rijk, Maarten C. de

doi:10.1001/archneur.1997.00550180070015

Cited by 212 publications

(138 citation statements)

References 36 publications

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“…There was no significant association between PD and flavonoid intake reported by one cross-sectional study (de Rijk et al 1997a).…”

Section: Fruits Vegetables and Antioxidantsmentioning

confidence: 74%

“…One cross-sectional study is included because the methods were similar to the CC studies, and because it was included in one of the published meta-analyses (de Rijk et al 1997a). The quality of evidence is not as strong, but results are presented as supporting evidence.…”

Section: Literature Searchmentioning

confidence: 99%

“…Intake was classified by quartiles (Hellenbrand et al 1996a;Anderson et al 1999;Johnson et al 1999;Powers et al 2003), quintiles , median intake (Scheider et al 1997), or specified amounts of intake (de Rijk et al 1997a).…”

Section: Fruits Vegetables and Antioxidantsmentioning

confidence: 99%

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A systematic review of nutritional risk factors of Parkinson's disease

Ishihara

Brayne

2005

Nutr. Res. Rev.

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A wide variety of nutritional exposures have been proposed as possible risk factors for Parkinson's disease (PD) with plausible biological hypotheses. Many studies have explored these hypotheses, but as yet no comprehensive systematic review of the literature has been available. MEDLINE, EMBASE, and WEB OF SCIENCE databases were searched for existing systematic reviews or meta-analyses of nutrition and PD, and one meta-analysis of coffee drinking and one meta-analysis of antioxidants were identified. The databases were searched for primary research articles, and articles without robust methodology were excluded by specified criteria. Seven cohort studies and thirty-three case -control (CC) studies are included in the present systematic review. The majority of studies did not find significant associations between nutritional factors and PD. Coffee drinking and alcohol intake were the only exposures with a relatively large number of studies, and meta-analyses of each supported inverse associations with PD. Factors that were reported by at least one CC study to have significantly increased consumption among cases compared with controls were: vegetables, lutein, xanthophylls, xanthins, carbohydrates, monosaccharides, junk food, refined sugar, lactose, animal fat, total fat, nuts and seeds, tea, Fe, and total energy. Factors consumed significantly less often among cases were: fish, egg, potatoes, bread, alcohol, coffee, tea, niacin, pantothenic acid, folate and pyridoxine. In three cohort studies, two reported borderline decreased relative risks and one a significant increased risk with vitamin C intake. One cohort reported an inverse association between caffeine intake and PD. Three cohorts reported significant positive association in men between dairy products and PD.

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“…There was no significant association between PD and flavonoid intake reported by one cross-sectional study (de Rijk et al 1997a).…”

Section: Fruits Vegetables and Antioxidantsmentioning

confidence: 74%

Section: Literature Searchmentioning

confidence: 99%

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A systematic review of nutritional risk factors of Parkinson's disease

Ishihara

Brayne

2005

Nutr. Res. Rev.

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“…In three US case-control studies [487,489,501], no associations of PD with vitamin C, E, A (or carotenoid) intake were reported. Similarly, retrospective data from the Rotterdam study showed no associations of PD with vitamin C or beta-carotene intake, although an inverse association with vitamin E intake was reported (OR 0.3, 95% CI 0.1-0.9 for the highest versus the lowest tertile, p for trend 0.03) [502]. A population-based case-control study conducted in Washington found no associations for vitamin C, E, A, or beta-carotene intake in the initial study [488] nor in an extended dataset [492].…”

Section: Antioxidantsmentioning

confidence: 94%

Epidemiology and etiology of Parkinson’s disease: a review of the evidence

et al. 2011

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“…Watanabe et al [211] reported that G. biloba supplementation in mice had neuromodulatory effects as indicated by a more than three-fold increase of mRNA expression for neuronal tyrosine/threonine phosphatases-1, microtubule-associated tau, prolactin, different calcium, and chloride channels as well as transthyretin. Flavonoidassociated antioxidant interventions have also been proposed to be beneficial in hypoxia/ischemia, seizures, Parkinson's disease, increased survival in brain cancers, and general age-related neurodegeneration [50,73,89,125]. However, since the flavonoids used in these studies were given as food extracts or preparations containing other potential bioactive or antioxidant components rather than as a pure flavonoid fraction, the results may not reflect solely the effects of flavonoids.…”

Section: Flavonoids: Neuroprotective Agents In Vivo and In Vitro?mentioning

confidence: 99%

MAPK signaling in neurodegeneration: influences of flavonoids and of nitric oxide

Schroeter

Boyd

Spencer

et al. 2002

Neurobiology of Aging

308

178

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Oxidative and nitrosative stress is increasingly associated with the pathology of neurodegeneration and aging. The molecular mechanisms underlying oxidative/nitrosative stress-induced neuronal damage are emerging and appear to involve a mode of death in which mitogen-activated protein kinase (MAPK) signaling pathways are strongly implicated. Thus, attention is turning towards the modulation of intracellular signaling as a therapeutic approach against neurodegeneration. Both endogenous and dietary agents have been suggested as potent modulators of intracellular signal transduction, e.g. nitric oxide and flavonoids, respectively. This review addresses recent findings on the biological effects of flavonoids and nitric oxide in neurodegeneration and aims to elucidate the rationale for their prospective use as modulators of cellular signal transduction. © 2002 Elsevier Science Inc. All rights reserved.Keywords: Apoptosis; Oxidative stress; Neuron; Flavonoids; MAP kinase; JNK; ERK; Epicatechin; Nitric oxide; Mitochondria; Redox status; Polyphenols Abbreviations: AKT, serine/threonine kinase (also known as protein kinase B); AP-1, activator protein-1; Apaf-1, apoptosis protease activating factor-1; ASK1, apoptosis signal-regulating kinase-1; Bad, Bcl-2/BclX Lassociated death promoting protein; Bax, pro-apoptotic protein of the Bcl-2 family; Bcl-2, B-cell lymphoma 2: protein with anti-apoptotic properties; BclX L , long form of Bclx: anti-apoptotic protein of the Bcl-2 family; Caspase, cysteinyl aspartic acid-protease; c-Jun, mammalian equivalent of Jun: part of the AP-1 transcription complex; CREB, cAMP response element binding protein; DIABLO/smac, mitochondria-related pro-apoptotic protein: inhibits XIAP; ERK1/2, extracellular signal-related kinase; Fas, CD95: member of the TNF receptor family; GSHST, glutathione Stransferase; JNK, c-Jun amino-terminal kinase; MAPK, mitogen-activated protein kinase; MAPKK, MAPK kinase; MAPKKK, MAPKK kinase; MEK1/2, ERK1/2-specific MAPKK; MKK4/7, JNK-specific MAPKK; MSK1, mitogen-and stress-activated kinase-1; NF-B, nuclear factor of immunoglobulin k locus in B-cells; ONOO − , peroxynitrite anion; p53, pro-apoptotic tumor suppressor gene product; PI3-kinase, phosphoinositol 3-kinase; Ras, small G-protein; RNS, reactive nitrogen species; ROS, reactive oxygen species; RSK, pp90 ribosomal S6 kinase; SAPK, stressactivated protein kinase; XIAP, X-linked inhibitor of apoptosis: inhibits the activation of caspase-9

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Dietary Antioxidants and Parkinson Disease

Abstract: Our data suggest that a high intake of dietary vitamin E may protect against the occurrence of PD.

Cited by 212 publications

References 36 publications

A systematic review of nutritional risk factors of Parkinson's disease

A systematic review of nutritional risk factors of Parkinson's disease

Epidemiology and etiology of Parkinson’s disease: a review of the evidence

MAPK signaling in neurodegeneration: influences of flavonoids and of nitric oxide

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