Abstract

Parkinson's disease, in most patients, is possibly caused by natural oxidative stress in dopaminergic neurons, insufficient exercise and galactose induced oxidative stress. Dopamine oxidizes to produce oxygen radicals that damage neurons. Exercise generates lactic acid and myokines that are essential for brain health. Galactose produces oxidative stress in the brain. These factors change with age and lifestyle. It is likely that lifestyle interventions, including daily exercise and much less alcohol and milk consumption, can delay or prevent Parkinson's disease.

Highlights

  • Alcohol Galactose Nicotine, high dose Nicotine, low dose Salbutamol Caffeine, theophylline, theobromine Lactic acid Cathepsin B Uric acid Vitamin E Ibuprofen

  • Heavy smoking and current smoking increase the onset of Parkinson’s disease with a hazard ratio of 3.2 [14, 15]. This may be because nicotine damages arteries including the blood brain barrier due to stimulation of non-neuronal nicotinic acetylcholine receptors (NAChR) which enhances oxygen radical formation [60]

  • It is possible that Parkinson’s disease is caused in most people by several factors that contribute to the damage of dopaminergic neurons in the substantia nigra

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Summary

Environmental causes

The discovery that manganese miners develop a parkinsonian syndrome led to the hypothesis that Parkinson’s disease is caused by an environmental factor [9]. This was backed up by the discovery that a contaminant of meperidine like drugs, MPTP causes a parkinsonian syndrome [10]. MPTP is metabolized by monoamine oxidase B to produce 1-methyl-4-phenylpyridine (MPP+) that induces oxidative stress by several mechanisms [11] including redox cycling in a two electron, hydride transfer, mechanism [12]. Exposure to pesticides is considered a risk factor for developing the disease [13]

Evidence from epidemiology
Alcohol
Dairy products
Smoking
10. Coffee
12. Physical activity
14. Vitamin E
15. Nonsteroidal anti-inflammatory drugs
17. Conclusions
Findings
23. References
Full Text
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