Surprisingly, factors that are being associated to other serious and fatal diseases have been shown to reduce the risk of Parkinson’s disease. Louis Tan et al. explained that the nicotine acquired from cigarette smoking and the caffeine in coffee are active components that protect against the disease. This is because nicotine can stimulate dopamine release and alter the activity of monoamine oxidase B while caffeine may improve motor deficits by building a blockade against adenosine A2 receptors.
Monoamine oxidase B is an inhibitor drug that can boost the level of dopamine and reduce the risk of complications of Parkinson’s disease but can also cause the patient receiving it to experience nausea, insomnia, occasional confusion and hallucination while adenosine A2 receptors, on the other hand, play a role in regulating myocardial oxygen consumption and coronary blood flow but are said to have increased amounts along with alteration in its mRNA expression in patients with Parkinson’s disease.
Research revealed that there is a high risk of acquiring the disease for those who never smoked while current smokers have low risk. The risk of former smokers stands between never smokers and current smokers. Furthermore, it is found that, among current smokers, lower risk is associated to those who began smoking at an earlier age and those who smoked a higher number of cigarettes per day. Recent Research Concerning the Disease There are numerous researches being conducted to help prevent, minimize the effect, or cure Parkinson’s disease.
Primary of these researches is the identification of genes that are responsible for the hereditary factor of the disease. There are currently over 100 identified genes associated with Parkinson’s disease. Some of these genes are identified to have been mutated which cause sporadic Parkinson’s disease—that is a person acquiring the disease instead of the disease being inherited. Scientists are also working to learn how these genes function and how the mutations cause the disease. Studies about environmental toxins are continuously performed such that precautions could be made to help reduce the risk of acquiring the disease.
Other research focus on the protein disposal system of cells which are necessary for the prevention of toxins to build up to harmful levels while some research focus on excitotoxicity, particularly of the overactivity of neurons in the subthalmic nucleus due to dopamine deficiency. Inflammation in the brain is another focus of research in understanding the nature of the disease as the data in previous research show that dopamine neurons in the brains of Parkinson’s disease patients have higher levels of the inflammatory enzyme called COX-2.
Furthermore, some researches focus on the MPTP model of Parkinson’s disease on animals which allows researchers to study the mechanisms of the disease and helps in the development of new treatments while others focus on the biomarkers of the disease to help doctors detect the disease before the onset of symptoms and improve its diagnosis. Conclusion Parkinson’s disease is a neurodegenerative disease characterized by tremors, rigidity, bradykinesia and postural instability.
It usually manifests itself during the later stage of life, typically around the age of 60, and may be caused by genetic and environmental factors, or a combination of both. Researchers have identified a number of genetic mutations and environmental toxins associated with an increased risk of acquiring Parkinson’s disease. Surprisingly, other environmental factors that cause other health risks such as nicotine intake from cigarette smoking and caffeine can help reduce the risk of the disease. There is no currently known cure for the disease.
However, medical treatments are available to help reduce the effects of the disease. Researches are continuously being performed to help prevent, minimize the effect and cure Parkinson’s disease. Bibliography GAO, H. M. , LIU, B. , ZHANG, W. , & HONG, J. S. Synergistic dopaminergic neurotoxicity of MPTP and inflammogen lipopolysaccharide: Relevance to the etiology of Parkinson’s disease. The FASEB Journal August 2003 doi: 10. 1096/fj. 03-0203fje. National Institute of Neurological Disorders and Stroke (NINDS). Parkinson’s disease: Hope through research. National Institutes of Health NINDS, January 2006.
Retrieved 6 April 2009. <http://www. ninds. nih. gov/disorders/parkinsons_disease/detail_parkinsons_disease. htm> TAN, L. C. et al. Differential effects of black versus green tea on risk of Parkinson’s disease in the Singapore Chinese health study. American Journal of Epidemiology 167(5) December 2007, 553-560. TANG, S. , ZHANG, Z. , KAVITHA, G. , TAN, E. K. , & NG, S. K. MDPD: An integrated genetic information resource for Parkinson’s disease. Nucleic Acids Research 37, 2009: D858-DD562. UITTI, R. J. Surgical treatments for Parkinson’s disease. Canadian Family Physician 46(2) February 2000, 368-373.