This web page was produced as an assignment for Genetics 564, an undergraduate capstone course at UW-Madison.
What is Parkinson's Disease?
Parkinson's Disease (PD) is the second most common neurodegenerative disease. PD affects 1-2% of the population; about 1 million people in the United States. [1] Parkinson's Disease is a movement disorder caused by the degeneration of dopaminergic neurons in the substantia nigra. The average age of onset is 60 years old. If an individual is diagnosed between ages 20-40, it is considered early-onset Parkinson's Disease. [1]
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Signs and SymptomsParkinson's Disease is a movement disorder characterized by resting tremor, bradykinesia, rigidity, and postural instability, but it is also marked by cognitive decline and dementia. [2, 3]
Early signs of PD include:
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Risk Factors for Parkinson's Disease [4]
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The exact cause of PD is unknown, but it is believed to be a complex combination of both genetics and environmental factors. [4]
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Dopamine and the Brain [6] |
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PINK1 and Early-Onset PD [5]
Mutations in PINK1 are associated with early-onset PD.
A normally-functioning PINK1 protein is involved in monitoring mitochondrial dysfunction. It acts with another gene/protein product, Parkin.
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Treatment Options [4]
There is no known cure for Parkinson's or strong evidence for slowing the progression of the disease. Current treatment options only include symptomatic relief.
In cases of early-onset PD, dopamine agonists are often used as initial treatment. Dopamine agonists stimulate dopamine receptors, allowing for greater uptake of dopamine at synapses. The effectiveness of dopamine agonists on early-onset PD patients wears off after about 10 years and they transition to levodopa treatments. Levodopa is metabolized into dopamine, increasing its availability in the brain. |
Different treatment options are currently being researched.
Patient Resources and Societies
References
1. de Rijk MC, Breteler MM, Graveland GA, Ott A, Grobbee DE, van der Meche FG, Hofman A. Prevalence of Parkinson's disease in the elderly: the Rotterdam Study. Neurology. 1995;45:2143–2146. https://www.ncbi.nlm.nih.gov/pubmed/8848182
2. Lang AE, Lozano AM. Parkinson's disease. First of two parts. N Engl J Med. 1998a;339:1044–1053. https://www.ncbi.nlm.nih.gov/pubmed/9761807
3. Aarsland, D., Creese, B., Politis, M., Chaudhuri, K. R., Ffytche, D. H., Weintraub, D., & Ballard, C. (2017). Cognitive decline in Parkinson disease. Nature reviews. Neurology, 13(4), 217-231. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5643027/
4. Rizek, Philippe et al. “An update on the diagnosis and treatment of Parkinson disease” CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne vol. 188,16 (2016): 1157-1165.
5. Pickrell, A. M., & Youle, R. J. (2015). The roles of PINK1, parkin, and mitochondrial fidelity in Parkinson's disease. Neuron, 85(2), 257-73.
6. Langston JW, Ballard P, Tetrud JW, Irwin I. Chronic Parkinsonism in humans due to a product of meperidine-analog synthesis. Science. 1983;219:979–980. https://www.ncbi.nlm.nih.gov/pubmed/6823561
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