Recreational physical activity and risk of Parkinson's disease

Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts, USA. <>
Movement Disorders (Impact Factor: 5.68). 01/2008; 23(1):69-74. DOI: 10.1002/mds.21772
Source: PubMed


The purpose of this study was to investigate associations between recreational physical activity and Parkinson's disease (PD) risk. We prospectively followed 143,325 participants in the Cancer Prevention Study II Nutrition Cohort from 1992 to 2001 (mean age at baseline = 63). Recreational physical activity was estimated at baseline from the reported number of hours per week on average spent performing light intensity activities (walking, dancing) and moderate to vigorous intensity activities (jogging/running, lap swimming, tennis/racquetball, bicycling/stationary bike, aerobics/calisthenics). Incident cases of PD (n = 413) were confirmed by treating physicians and medical record review. Relative risks (RR) were estimated using proportional hazards models, adjusting for age, gender, smoking, and other risk factors. Risk of PD declined in the highest categories of baseline recreational activity. The RR comparing the highest category of total recreational activity (men > or = 23 metabolic equivalent task-hours/week [MET-h/wk], women > or = 18.5 MET-h/wk) to no activity was 0.8 (95% CI: 0.6, 1.2; P trend = 0.07). When light activity and moderate to vigorous activity were examined separately, only the latter was found to be associated with PD risk. The RR comparing the highest category of moderate to vigorous activity (men > or = 16 MET-h/wk, women > or = 11.5 MET-h/wk) to the lowest (0 MET-h/wk) was 0.6 (95% CI: 0.4, 1.0; P trend = 0.02). These results did not differ significantly by gender. The results were similar when we excluded cases with symptom onset in the first 4 years of follow-up. Our results may be explained either by a reduction in PD risk through moderate to vigorous activity, or by decreased baseline recreational activity due to preclinical PD.

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    • "Taken together, these studies suggest that physical activity prior to neurotoxic 6-OHDA insult may provide neuroprotective benefit in terms of behavioral performance. This mirrors the results seen in human epidemiological studies, which have shown that increased physical activity decreases the risk for PD (Chen et al., 2005; Sasco et al., 1992; Thacker et al., 2008). Forced exercise has also been shown to decrease the behavioral and neurochemical deficits when implemented after a 6-OHDA lesion. "
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    ABSTRACT: Studies on exercise before and after toxin-induced hemiparkinsonism have reported promising findings in terms of amelioration of motor asymmetry in adult, 6-hydroxydopamine (6-OHDA) rats. However, recent studies have had more mixed results. Therefore, the purpose of this study was to further explore the notion of exercise, in particular forced exercise, as a potential neuroprotective therapy when implemented before and after 6-OHDA hemiparkinsonism. To explore this, two experiments were conducted: Experiment 1 - exercise before a 6-OHDA lesion; and, Experiment 2 - exercise after a 6-OHDA lesion. In Experiment 1, rats were randomly assigned into one of two 4-week experimental conditions, a forced exercise condition and a non-exercise control condition. Then, after the experimental conditions rats were injected with 6-OHDA into the right medial forebrain bundle. In Experiment 2, rats were first injected with 6-OHDA and were then randomly assigned into one of two 4-week experimental groups, a forced exercise group and a non-exercise control group. Outcomes in both experiments did not show any differences in terms of motor behavioral tests (i.e., apomorphine rotations, forelimb placement asymmetry, exploratory rearing) between the forced exercise and sedentary control groups. Based on our results and in light of the body of literature, it is possible that the stress of shock-motivated forced running utilized in this study may have cancelled beneficial behavioral effects. Additionally, it is possible that the one-week delay in the forced exercise protocol implementation in Experiment 2 may have prevented behavioral rescue.
    Brain research 11/2013; 1543. DOI:10.1016/j.brainres.2013.10.054 · 2.84 Impact Factor
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    • "In comparison to the number of studies of cognitive function in AD, there have been much fewer examinations of the potential disease modifying effects of physical activity on the development of cognitive impairment in Parkinson's disease (PD). The clinical evidence supporting a benefit of engaging physical activity associated with reduced risk of developing PD remains inconclusive (Thacker et al., 2008; Sasco, 1992) although a community-based randomised study examining Tango dancing reported improvements of Unified Parkinson's disease Rating scores of offmedication patients (Duncan and Earhart, 2012). By comparison, the findings of a randomised controlled trial of training on a rotating treadmill based on the hypothesis that this would limit turning movement-related falls revealed limited short-term benefits (McNeely and Earhart, 2012) which was largely consistent with the findings of a meta-analysis that reported no significant effect of motor training on the risk ratio of falling incidence (Allen et al., 2011). "
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    ABSTRACT: This review will provide an overview of the non-drug based approaches that have been demonstrated to enhance cognitive function of the compromised brain, primarily focussed on the two most widely adopted paradigms of environmental enrichment and enhanced physical exercise. Environmental enrichment involves the generation of novelty and complexity in animal housing conditions which facilitates enhanced sensory and cognitive stimulation as well as physical activity. In a wide variety of animal models of brain disorders, environmental enrichment and exercise have been found to have beneficial effects, including cognitive enhancement, delayed disease onset, enhanced cellular plasticity and associated molecular processes. Potential cellular and molecular mechanisms will also be discussed, which have relevance for the future development of 'enviromimetics', drugs which could mimic or enhance the beneficial effects of environmental stimulation. This article is part of a Special Issue entitled 'Cognitive Enhancers'.
    Neuropharmacology 07/2012; 64(1):515-28. DOI:10.1016/j.neuropharm.2012.06.029 · 5.11 Impact Factor
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    • "In fact, studies have shown that although persons with PD reduce their level of physical activity, only 12–15 percent of diagnosed individuals are referred to physical therapy for an exercise intervention (Goodwin, Richards, Taylor, Taylor, & Campbell, 2008; Thacker et al., 2008). However, optimal levels, quality, and timing of PD-specific therapies remain unclear. "
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    ABSTRACT: Parkinson's disease (PD) is a neurodegenerative disorder primarily characterized by sensorimotor dysfunction. The neuropathology of PD includes a loss of dopamine (DA) neurons of the nigrostriatal pathway. Classic signs of the disease include rigidity, bradykinesia, and postural instability. However, as many as 90% of patients also experience significant deficits in speech, swallowing (including mastication), and respiratory control. Oromotor deficits such as these are underappreciated, frequently emerging during the early, often hemi-Parkinson, stage of the disease. In this paper, we review tests commonly used in our labs to model early and hemi-Parkinson deficits in rodents. We have recently expanded our tests to include sensitive models of oromotor deficits. This paper discusses the most commonly used tests in our lab to model both limb and oromotor deficits, including tests of forelimb-use asymmetry, postural instability, vibrissae-evoked forelimb placing, single limb akinesia, dry pasta handling, sunflower seed shelling, and acoustic analyses of ultrasonic vocalizations and pasta biting strength. In particular, we lay new groundwork for developing methods for measuring abnormalities in the acoustic patterns during eating that indicate decreased biting strength and irregular intervals between bites in the hemi-Parkinson rat. Similar to limb motor deficits, oromotor deficits, at least to some degree, appear to be modulated by nigrostriatal DA. Finally, we briefly review the literature on targeted motor rehabilitation effects in PD models. LEARNING OUTCOMES: Readers will: (a) understand how a unilateral lesion to the nigrostriatal pathway affects limb use, (b) understand how a unilateral lesion to the nigrostriatal pathway affects oromotor function, and (c) gain an understanding of how limb motor deficits and oromotor deficits appear to involve dopamine and are modulated by training.
    Journal of Communication Disorders 09/2011; 44(5):529-37. DOI:10.1016/j.jcomdis.2011.04.005 · 1.45 Impact Factor
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