Project #154695 - Parkinson's disease

Science Tutors

Subject Science
Due By (Pacific Time) 11/18/2016 12:00 am

second most common neurodegenerative disease after Alzheimer’s disease. Population prevalence of PD increases from about 1% at age 60 to 4% by age 80. Early symptoms of PD include tremor, rigidity, and difficulty walking; cognitive decline is common at later stages. The underlying pathology of PD is selective death of dopamine-generating cells in the substantia nigra, a part of the brain involved in movement, reward, and addiction. Treatment of PD with levodopa temporarily controls motor symptoms but does not slow disease progression. Like other common diseases, PD is thought to arise from complex interactions between genetic and environmental factors, which remain mostly unknown.

Many epidemiologic studies have found that PD is less common in people who drink coffee, as well as in those who smoke cigarettes. These findings are remarkably consistent and they have survived an exhaustive search for non-causal explanations. No one would suggest taking up smoking (or even coffee drinking) to prevent PD; however, understanding their “protective effects” could shed light on its molecular pathology. Such insights could suggest new treatments that not only treat symptoms but can slow or halt disease progression.

Parkinson's disease (PD), like most common disorders, involves interactions between genetic make-up and environmental exposures that are unique to each individual. Caffeinated-coffee consumption may protect some people from developing PD, although not all benefit equally. In a genome-wide search, we discovered that variations in the glutamate-receptor gene GRIN2A modulate the risk of developing PD in heavy coffee drinkers. The study was hypothesis-free, that is, we cast a net across the entire genome allowing statistical significance to point us to a genetic variant, regardless of whether it fell in a genomic desert or an important gene. Fortuitously, the most significant finding was in a well-known gene, GRIN2A, which regulates brain signals that control movement and behavior. Our finding is important for three reasons: First, it is a proof of concept that studying genes and environment on the whole-genome scale is feasible, and this approach can identify important genes that are missed when environmental exposures are ignored. Second, the knowledge of interaction between GRIN2A, which is involved in neurotransmission in the brain, and caffeine, which is an adenosine-A2A-receptor antagonist, will stimulate new research towards understanding the cause and progression of PD. Third, the results may lead to personalized prevention of and treatment for PD.

 

 

Question 1: Several case-control studies of PD have examined interactions of coffee consumption with candidate genes that were selected because of their associations with PD (e.g., SNCA), with caffeine metabolism (e.g., CYP1A2), or with caffeine’s CNS effects (e.g., ADORA2A). Although these studies have often confirmed previously observed main effects, they have not found statistically significant gene-environment interactions. Suggest two possible reasons why such studies have been unsuccessful in identifying interactions.

 

 

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