The most common neurodegenerative diseases are Parkinson's disease (PD) and Alzheimer's disease (AD). It has been well reported that a small percentage of cases develop as a result of known genetic mutations, which has contributed to scientific knowledge on the pathophysiology of PD and AD. However, the vast majority of cases are attributed to the action and interaction of a host of genetic and environmental influences acting as susceptibility factors or triggers. Numerous epidemiological studies have linked a range of environmental factors to lower or higher levels of risk for both diseases. The epidemiological studies addressed are largely heterozygous, with result more or less consistent depending on the factor examined and on study design. Nonetheless, the following outlines potential environmental factors that may contribute to increased risk.
Interest in the link between pesticides and PD was awakened in the 1980's when parkinsonism was observed among users of a synthetic opioid bearing traces of MPTP. Pesticides destroy dopaminergic (DA) neurons, which is why they are used in animal models of PD. Several case control studies have linked exposure to pesticides in general with a higher risk of PD while others have found no correlation. Herbicides and insecticides, examined separately, showed either elevated risk or no association. Moreover, a number of studies have linked risk of PD to agricultural work, living in rural environments, and consumption of well water. However, it is important to note, the foregoing factors cannot be shown to be independent since they are frequently associated not only with each other, but also with pesticide use.
A systematic review of 21 case control studies and 3 cohort studies also revealed a consistent association between pesticide exposure and AD. Robust evidence points to an association between pesticide exposure and elevated risk of PD and AD. This risk cannot be explained by chance or biases alone, even though levels of pesticide exposure are often low and difficult to measure, with multiple variables or confounders presenting. Moreover, these are observational studies and therefore the relationship cannot be demonstrated as causal. It is also acknowledged that the mechanism of action is not well understood, despite availability of animal models, conditions are not comparable due to differences in dose and routes of administration in human cases of exposure.
Parkinsonism has been described in cases of high exposure to manganese or to lead. Researchers have found higher levels of iron, copper and zinc in the substantia nigra of PD patients than in controls, and these metals are also present in amyloid deposits. Interestingly, metals participate in the formation of senile plaques and tangles, as well as in the processes of oxidation, calcium homeostasis, and neuronal death. Aluminum is particularly important because it has been linked to AD epidemiology. Epidemiological studies, many of which have been carried out using surveys on occupational exposure to metals, generally do not show any associations between PD and occupational exposure to lead, copper, iron, mercury, zinc or manganese. Although quality epidemiological studies have not detected any links between AD and lead or aluminium exposure, 9 out of the 13 studies have established an association with consuming drinking water with high levels of aluminium. This association was also confirmed by a 15 year prospective study. Nonetheless, there is no convincing evidence that exposure to metals causes PD or AD, and, thus, only consumption of water with elevated aluminium levels have been associated with a higher risk of AD.
Statins have anti-inflammatory and antioxidant properties, decrease amyloid beta (AB) deposition, and exert a protective effect on DA neurons in animal models. Studies consistently show an association between AD and elevated cholesterol in middle-aged, yet not elderly individuals, according to an systematic review of 18 prospective studies. However, it has been demonstrated that cholesterol lowering medication (statins) does not reduce risk of AD. Regarding PD, three case control studies have shown a slight association between high cholesterol and lower risk of PD (NB: specific sub-groups were examined: women, men between the ages of 71 and 75). Interestingly, a recent retrospective study has shown a lower PD incidence among individuals treated with statins.
Coffee and Tea:
Adenosine A2A receptor antagonists lessen parkinsonism in animal models and randomised control trials. Caffeine, an adenosine A2A receptor antagonist, is considered to have a neuroprotective effect since it has been shown to inhibit MPTP toxicity in animal models of PD and reduce production of AB in AD models. Of the studies undertaken on coffee and PD, 95.3 percent have shown that coffee offers a protective effect. Moreover, recent findings have also found that consumption of black tea is associated with lower risk of PD. It is important to note that other compounds may be responsible for this effect, with previous findings indicating this anomaly.
Evidence is less robust for AD, and data regarding tea consumption is scarce. A systematic review that included two case control studies and 2 cohort studies showed a lower risk of AD among coffee drinkers, noting that 3 to 5 cups daily (middle-aged subjects) was associated with a 64 percent decrease in the risk of dementia or AD in old age.
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