Physical activity and the risk of Parkinson disease

Department of Nutrition, Harvard School of Public Health, 665 Huntington Ave., Boston, MA 02115, USA.
Neurology (Impact Factor: 8.29). 03/2005; 64(4):664-9. DOI: 10.1212/01.WNL.0000151960.28687.93
Source: PubMed


To investigate whether greater physical activity is associated with a lower risk of Parkinson disease (PD).
The authors prospectively followed 48,574 men and 77,254 women who provided information on physical activity in 1986 or in early adulthood. During the follow-up, a total of 252 (male) and 135 (female) incident PD cases were identified.
In men, greater baseline physical activity was associated with a lower PD risk; compared with the lowest quintile, the multivariate relative risk (RR) of PD for the highest quintile was 0.7 (95% CI 0.5 to 1.1; p value, test for trend = 0.007), and the inverse association was still present after excluding the first 10 years of follow-up (RR = 0.5; p value, test for trend = 0.02). Further, strenuous exercise in early adult life was also inversely related to PD risk in men: compared with men who regularly exercised < or =2 months/year, those with > or =10 months of strenuous exercise had a 60% lower PD risk (RR = 0.4; p value, test for trend = 0.005). In women, physical activity assessed at baseline was not related to PD risk, whereas strenuous exercise in early adulthood tended to be inversely related to PD risk later in life (highest vs lowest categories, RR = 0.5, 95% CI 0.2 to 1.4; p value, test for trend = 0.06).
This study suggests either that higher levels of physical activity may lower the risk of Parkinson disease (PD) in men or that men predisposed to PD tend to avoid strenuous physical activity in their early adult years.

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    • "In 1999, van Praag et al. showed the increase of neurogenesis following exercise in the adult brain rats [5]. Since then, other scientists have replicated this finding and clinicians have tried to assess and quantify the effect of exercise on a variety of neurological disorders [6] [7]. Multiple clinical studies demonstrated the benefit of exercise on motor symptoms of PD by applying different exercise models such as treadmill training [8] [9] [10], resistance training [11] [12] [13], biking [14], Tai Chi [15] [16], tango [17] [18], and boxing [19]. "
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    ABSTRACT: Background. Novel rehabilitation strategies have demonstrated potential benefits for motor and non-motor symptoms of Parkinson’s disease (PD). Objective. To compare the effects of Lee Silverman Voice Therapy BIG (LSVT BIG therapy) versus a general exercise program (combined treadmill plus seated trunk and limb exercises) on motor and non-motor symptoms of PD. Methods. Eleven patients with early-mid stage PD participated in the prospective, double-blinded, randomized clinical trial. Both groups received 16 one-hour supervised training sessions over 4 weeks. Outcome measures included the Unified Parkinson’s Disease Rating Scale (UPDRS), Beck Depression Inventory (BDI), Beck Anxiety Inventory (BAI) and Modified Fatigue Impact Scale (MFIS). Five patients performed general exercise and six patients performed LSVT BIG therapy. Post-intervention evaluations were conducted at weeks 4, 12 and 24. Results. The combined cohort made improvements at all follow-up evaluations with statistical significance for UPDRS total and motor, BDI, and MFIS (p<0.05). Conclusion. This study demonstrated positive effects of general exercise and LSVT BIG therapy on motor and non-motor symptoms of patients with PD. Our results suggest that general exercise may be as effective as LSVT BIG therapy on symptoms of PD for patients not able to readily access outpatient LSVT BIG therapy.
    Parkinson's Disease 02/2015; 2015. DOI:10.1155/2015/586378 · 2.01 Impact Factor
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    • "Exercise is known to raise free radical content and can precondition against ischemia (Frasier et al. 2011; Powers et al. 2011; Zhang et al. 2011). Many studies have supported the long-term benefits of exercise in humans, even in Alzheimer's and Parkinson's patients (Chen et al. 2005; Xu et al. 2010; Erickson et al. 2012; Mayeux and Stern 2012; Fisher et al. 2013; Intlekofer and Cotman 2013; Winchester et al. 2013). Animal studies have also shown convincingly that exercise is protective in experimental models of neurodegeneration (for some examples, see Adlard et al. 2005; Nichol et al. 2009; Pothakos et al. 2009; Zigmond et al. 2009; Gerecke et al. 2010; Vuckovic et al. 2010; Intlekofer and Cotman 2013; Souza et al. 2013). "
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    ABSTRACT: Although severe stress can elicit toxicity, mild stress often elicits adaptations. Here we review the literature on stress-induced adaptations versus stress sensitization in models of neurodegenerative diseases. We also describe our recent findings that chronic proteotoxic stress can elicit adaptations if the dose is low but that high-dose proteotoxic stress sensitizes cells to subsequent challenges. In these experiments, long-term, low-dose proteasome inhibition elicited protection in a superoxide dismutase-dependent manner. In contrast, acute, high-dose proteotoxic stress sensitized cells to subsequent proteotoxic challenges by eliciting catastrophic loss of glutathione. However, even in the latter model of synergistic toxicity, several defensive proteins were upregulated by severe proteotoxicity. This led us to wonder whether high-dose proteotoxic stress can elicit protection against subsequent challenges in astrocytes, a cell type well known for their resilience. In support of this new hypothesis, we found that the astrocytes that survived severe proteotoxicity became harder to kill. The adaptive mechanism was glutathione dependent. If these findings can be generalized to the human brain, similar endogenous adaptations may help explain why neurodegenerative diseases are so delayed in appearance and so slow to progress. In contrast, sensitization to severe stress may explain why defenses eventually collapse in vulnerable neurons.
    Dose-Response 03/2014; 12(1):24-56. DOI:10.2203/dose-response.13-016.Leak · 1.22 Impact Factor
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    • "Individuals who are suffering from obesity have lower dopamine D2 receptor availability in the striatum [13]. Obese people are also usually less active than normal weight people [14, 15], and lower levels of physical activity may increase the risk of developing PD [16]. Although recent epidemiological studies have shown a potential association between obesity/overweight and the risk of PD [17, 18], some studies have not provided evidence in support of this viewpoint [19, 20]. "
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    ABSTRACT: Objective. Parkinson's disease (PD) is a severe neurological disease and its risk factors remain largely unknown. A meta-analysis was carried out to investigate the relationship of overweight and obesity with PD. Methods. We used PubMed, EMBASE, and the Chinese National Knowledge Infrastructure (CNKI) databases to identify studies of associations between overweight/obesity and PD. Overweight, obesity, and PD were used as keywords, and published works were retrieved until September 30, 2013. The extracted data were classified (BMI ≥ 30, 25 ≤ BMI < 30, and BMI < 25) according to BMI values and analyzed using RevMan5.2 and Stata11.0. Results. Four cohort studies and three case-control studies were used to evaluate the association between overweight/obesity and PD, including 2857 PD patients and 5, 683, 939 cases of non-PD controls. There was a statistically significant difference between 25 ≤ BMI < 30 and BMI < 25 in the cohort study (RR = 1.17, 95% CI, 1.03-1.32, P = 0.03), but there was no difference between BMI ≥ 30 and BMI < 25 or BMI ≥ 30 and 25 ≤ BMI < 30, where the respective RR was 1.16 and 0.84; the respective 95% CI was 0.67-2.01 and 0.61-1.15, respectively, and the P values were 0.60 and 0.28, respectively. Case-control studies showed that there was no statistical difference between any two groups. Conclusion. Meta-analysis showed that overweight might be a potential risk factor of PD. Demonstration of a causal role of overweight/obesity in PD development could have important therapeutic implications.
    International Journal of Endocrinology 02/2014; 2014(1):203930. DOI:10.1155/2014/203930 · 1.95 Impact Factor
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