What genes are linked to Parkinson's Disease and what are the environmental factors that effect the development of the disease?

What genes are linked to Parkinson’s Disease and what are the environmental factors that effect the development of the disease?

CAPSTONE PROJECT TOPIC
Sibel Uzun
Summary
Parkinson’s Disease ailment is a neurological disorder that is characterized by tremor, slow movement, stiffness of arms and legs, and shaking arms, it is the most common neurodegenerative disease after Alzheimer’s. Research shows that three out of a thousand people aged above 50 years have the condition (Westenberger 2012).

Research Questions (Condense the 4 questions to 2 and then try to condense to 1 question.)
1. What genes are linked to Parkinson’s Disease and what are the environmental factors that effect the development of the disease?
2. Can gene mapping be used in the early diagnosis & treatment of Parkinson’s Disease? Condense to one question.
3. How accurate the results of genetic mapping will be?
4. Will genetic mapping answer the cause ( genetic/environmental) of the gene mutation and development of the disease? Condense to one question.

Study Variables The study variables should be bullet-points or a short list of independent and dependent variables you’ll be assessing.
The study indicated that about 10- 15% of people with Parkinson’s ailment have a family history of the disease. Family-linked cases are a result of genetic mutations in the gene category that includes; SNAC gene, it is responsible for making alpha-synuclein protein, in the brain of a patient with Parkinson’s ailment, this protein gather and form a clump called Lewy bodies. SNCA gene mutation transpires in early Parkinson’s disease. PARK2 gene that helps in making parkin protein that assists in breaking down of cells and protein recycling. PARK7 gene mutation may result in the formation of early Parkinson’s disease, it is responsible for making DJ-1 protein which protects mitochondria from stress. PINK1 protein makes kinase protein that also helps protect mitochondria’s inner structure from stress. PINK1 also occurs in the early stage of Parkinson’s disease. In the inherited instance of Parkston’s, the pattern of inheritance varies, this is because it depends on the involved gene (Lill 2016)
When SNAC and LRRK2 genes are involved, the likeliness of the inherited Parkinson’s is just from a single parent. This is known as an autosomal dominant pattern; this means that only a single gene is required for alteration of the gene hence disorder. If PINK1, PARK2, or PARK7 gene is involved, this state is known as autosomal recessive pattern. This is when two copies of the gene are required to alter for the disorder to be realized meaning that both parents are responsible for the passing of the altered gene but had no sign of the Parkinson’s ailment themselves (Schulzer 2004). Nonetheless, the interlinkage between mutations or generic changes and risk of individual developing the disorder has not been realized fully, the above gene mapping research assist in managing Parkinson’s disease. This is by gene editing, gene transfer, and transplant of stem cells-derived dopaminergic neuron (Duvoisin 1996).
Extensive research has also revealed that Parkinson’s disease can be caused by environmental and genetic factors. Interaction of environment can be complex; some environments lower the risk of Parkinson’s while other increase. Comparably, generic (genetic?) makeup in some people makes them vulnerable to toxic materials than others. Research reveals that a combination of the two factors may enhance biological changes resulting in Parkinson’s (Gasser 2001)
The environmental risk includes; a head injury that may alter the level of consciousness, traumatic head injury has been linked to the risk of developing Parkinson’s ailment however, the underlying mechanism is not clear. Polychlorinated Biphenyls has also been linked to the development of Parkinson’s; many industries use Trichloroethylene as a solvent yet it is known to be a common contaminant of groundwater, exposed to the mentioned chemical is connected to Parkinson’s disease. Also, herbicides and pesticides have been linked to Parkinson’s, one herbicide associated with Parkinson’s is Paraquat that was commonly used in the United States but was banned after the realization of its effect. Study shows that potential environmental causes of Parkinson’s can be managed by; consumption of caffeine in the coffee, Uric acid that occurs naturally in the blood and is associated with diets, taking anti-inflammatory drugs, and regular physical exercise (Logroscino 2005).

Study Design
Systematic literature review. Review the “Young student’s guide to performing a systematic review” in the Ancillary folder.
Instrumentation
Information on the paper has been collected through research from eBooks, scholarly journals, articles from magazines (please avoid infotainment/ads and similar non-peer-reviewed material), and search from the NU library. Be much more specific as to the key published resources and databases from which you’re gathering your information. A systematic review outlines a particular approach.

References (Correct the format for this section.)
I counted six (6) citations in your text but see many more listed here.

Polymeropoulos, M. H., Higgins, J. J., Golbe, L. I., Johnson, W. G., Ide, S. E., Di Iorio, G., … & Duvoisin, R. C. (1996). Mapping of a gene for Parkinson’s disease to chromosome 4q21-q23. Science, 274(5290), 1197-1199.
Klein, C., & Westenberger, A. (2012). Genetics of Parkinson’s disease. Cold Spring Harbor perspectives in medicine, 2(1), a008888.
Gasser, T. (2001). Genetics of Parkinson’s disease. Journal of neurology, 248(10), 833-840.
Lill, C. M. (2016). Genetics of Parkinson’s disease. Molecular and cellular probes, 30(6), 386-396.
Gasser, T. (2007). Update on the genetics of Parkinson’s disease. Movement disorders: official journal of the Movement Disorder Society, 22(S17), S343-S350.
Gasser, T. (1998). Genetics of Parkinson’s disease. Clinical genetics, 54(4), 259-265.
Siderowf, A., & Stern, M. (2003). Update on Parkinson disease. Annals of internal medicine, 138(8), 651-658.
Kumar, A., Calne, S. M., Schulzer, M., Mak, E., Wszolek, Z., Van Netten, C., … & Calne, D. B. (2004). Clustering of Parkinson disease: shared cause or coincidence?. Archives of neurology, 61(7), 1057-1060.
Logroscino, G. (2005). The role of early life environmental risk factors in Parkinson disease: what is the evidence?. Environmental health perspectives, 113(9), 1234-1238.
Warner, T. T., & Schapira, A. H. (2003). Genetic and environmental factors in the cause of Parkinson’s disease. Annals of Neurology: Official Journal of the American Neurological Association and the Child Neurology Society, 53(S3), S16-S25.
Willemsen, M. D., Grimbergen, Y. A., Slabbekoorn, M., & Bloem, B. R. (2000). Falling in Parkinson disease: more often due to postural instability than to environmental factors. Nederlands Tijdschrift voor Geneeskunde, 144(48), 2309-2314.
Koller, W., Vetere-Overfield, B., Gray, C., Alexander, C., Chin, T., Dolezal, J., … & Tanner, C. (1990). Environmental risk factors in Parkinson’s disease. Neurology, 40(8), 1218-1218.
Chin-Chan, M., Navarro-Yepes, J., & Quintanilla-Vega, B. (2015). Environmental pollutants as risk factors for neurodegenerative disorders: Alzheimer and Parkinson diseases. Frontiers in cellular neuroscience, 9, 124.
de Wit, S., Barker, R. A., Dickinson, A. D., & Cools, R. (2011). Habitual versus goal-directed action control in Parkinson disease. Journal of Cognitive Neuroscience, 23(5), 1218-1229.
Carpenter, M. G., & Bloem, B. R. (2011). Postural control in Parkinson patients: a proprioceptive problem?. Experimental neurology, 227(1), 26-30.
Pelykh, O., Klein, A. M., Bötzel, K., Kosutzka, Z., & Ilmberger, J. (2015). Dynamics of postural control in Parkinson patients with and without symptoms of freezing of gait. Gait & Posture, 42(3), 246-250.
Scott, W. K., Nance, M. A., Watts, R. L., Hubble, J. P., Koller, W. C., Lyons, K., … & Pericak-Vance, M. A. (2001). Complete genomic screen in Parkinson disease: evidence for multiple genes. Jama, 286(18), 2239-2244.
Dumitriu, A. (2012). Genome-wide expression and genomic data integration analyses in sporadic Parkinsons disease. Boston University.
Maraganore, D. M., De Andrade, M., Lesnick, T. G., Strain, K. J., Farrer, M. J., Rocca, W. A., … & Ballinger, D. G. (2005). High-resolution whole-genome association study of Parkinson disease. The American Journal of Human Genetics, 77(5), 685-693.
Pankratz, N., Nichols, W. C., Uniacke, S. K., Halter, C., Rudolph, A., Shults, C., … & Parkinson Study Group. (2002). Genome screen to identify susceptibility genes for Parkinson disease in a sample without parkin mutations. The American Journal of Human Genetics, 71(1), 124-135.
Ahmed, S. S., Santosh, W., Kumar, S., & Christlet, H. T. T. (2009). Metabolic profiling of Parkinson’s disease: evidence of biomarker from gene expression analysis and rapid neural network detection. Journal of biomedical science, 16(1), 1-12.

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