Epidemiology & Etiology of PD

PD was first established as a medical condition in 1817 by James Parkinson in his landmark manuscript, “An Essay on the Shaking Palsy.”9 In this manuscript, Parkinson described six cases of “Shaking Palsy.” He distinguished the disease from other diseases, reflected on symptoms that should be examined, discussed potential cures, and encouraged others to study this disease. In 1861 the French neurologist Jean Martin Charcot distinguished the disease from other neurodegenerative disorders and named it “Parkinson’s disease.”10

In the current century, PD is the second most common adult-onset neurodegenerative disease lagging only behind Alzheimer’s disease.11 Worldwide, it is estimated that four to six million individuals endure this disorder. In the United States (U.S.) it is estimated that one million individuals experience this disorder.2 The American Parkinson Disease Association reports the disease prevalence rate is 329 per 100,000. Worldwide, the U.S. ranks third in PD prevalence. In North America the U.S. ranks first.12 The prevalence of PD is steadily increasing as an additional 50,000 to 60,000 cases are diagnosed each year.2 It is expected to double by 2030.13

There is ongoing debate about the etiology of PD and whether the disease is from genetic factors, environment toxins or injury, an illness, or some other event. Many experts think it is a combination of factors. Scientific advances point towards genetic mutations as the most likely etiology of the disease.14-16 Genetic and biochemical analyses have shown that DNA mutations and alterations in mitochondrial proteins may also play a role in neurodegeneration.17 The majority of PD cases are not directly inherited; however, in a small number of families, gene mutations that play a role in dopamine cell function have been shown to cause the disease directly.3,11,18,19 PD is more common in people who have a close relative diagnosed with the disease.3,11,18 In large population studies, individuals with an affected first-degree relative (parent or sibling) have a slightly higher chance of developing PD, as compared to the general population.19

Environmental and lifestyle factors have been shown to play a causative role in developing PD. PD is more common in developed countries.11 Studies have revealed rural living, well water, and exposure to lead and manganese are environmental factors linked to PD.11,19 Several studies have demonstrated that prolonged exposure to environmental toxins such as pesticides, herbicides, and/or fungicide may elevate the risk of developing PD.6,11,18 High consumption of dairy products and hormonal influences, have also shown a positive correlation with PD.11,18 Although the factors described above clearly play a role in developing PD, there is no evidence to substantiate that these factors can singlehandedly cause the disease.

Environmental and lifestyle factors have also been shown to play a protective role in developing PD. An extensive review of PD epidemiology and etiology research revealed sufficient evidence to support the notion that nicotine in cigarettes, caffeine in coffee, and uric acid are neuroprotective factors that decrease the likelihood of developing PD.11 Alcohol, estrogens, and physical activity appear to also reduce PD risk; though, the evidence to support this is not as strong.11,20 The physiology of these associations is not yet understood.

PD occurs more commonly in men and those who have a history of head trauma that resulted in concussion.11,21 As age increases, the risk for developing PD also increases.3,11,18 The average age of disease onset is 60 years; however, “early-onset,” before the age of 50, occurs in 5-10% of individuals diagnosed with PD.3 Although uncommon, Juvenile Parkinsonism disease may develop before the age of 20. Evidence suggests this form of the disease is from a gene mutation.3,11,18