Association of Coffee and Caffeine Intake With the Risk of Parkinson Disease

Gw, Ross; Abbott, R D; Petrovitch, Helen; Dm, Morens; Grandinetti, Andrew; Kh, Tung; Cm, Tanner; Kh, Masaki; Pl, Blanchette; Jd, Curb; Js, Popper; Lr, White

doi:10.1001/jama.283.20.2674

Cited by 703 publications

(505 citation statements)

References 31 publications

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“…Taken together, these results indicate that there is a functional antagonism between A 2A and D 2 receptors (Ferré et al, 1997). In line with these experimental data, both retrospective epidemiological evidence Benedetti et al, 2000 and references therein) as well as prospective cohort studies (Ross et al, 2000;Ascherio et al, 2001) indicate that blockage of A 2A receptors by caffeine intake reduces the risk of people to develop Parkinson's disease. Similarly, the adenosine uptake inhibitor dipyridamol enhances the antipsychotic activity of the D 2 antagonist haloperidol (Akhondzadeh et al, 2000).…”

Section: Introductionsupporting

confidence: 62%

The Human D2 Dopamine Receptor Synergizes with the A2A Adenosine Receptor to Stimulate Adenylyl Cyclase in PC12 Cells

Kudlacek

Just

Korkhov

et al. 2003

Neuropsychopharmacol

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The adenosine A 2A receptor and the dopamine D 2 receptor are prototypically coupled to G s and G i /G o , respectively. In striatal intermediate spiny neurons, these receptors are colocalized in dendritic spines and act as mutual antagonists. This antagonism has been proposed to occur at the level of the receptors or of receptor-G protein coupling. We tested this model in PC12 cells which endogenously express A 2A receptors. The human D 2 receptor was introduced into PC12 cells by stable transfection. A 2A -agonistmediated inhibition of D 2 agonist binding was absent in PC12 cell membranes but present in HEK293 cells transfected as a control. However, in the resulting PC12 cell lines, the action of the D 2 agonist quinpirole depended on the expression level of the D 2 receptor: at low and high receptor levels, the A 2A -agonist-induced elevation of cAMP was enhanced and inhibited, respectively. Forskolin-stimulated cAMP formation was invariably inhibited by quinpirole. The effects of quinpirole were abolished by pretreatment with pertussis toxin. A 2A -receptor-mediated cAMP formation was inhibited by other G i /G o -coupled receptors that were either endogenously present (P 2y12 -like receptor for ADP) or stably expressed after transfection (A 1 adenosine, metabotropic glutamate receptor-7A). Similarly, voltage activated Ca 2+ channels were inhibited by the endogenous P 2Y receptor and by the heterologously expressed A 1 receptor but not by the D 2 receptor. These data indicate functional segregation of signaling components. Our observations are thus compatible with the proposed model that D 2 and A 2A receptors are closely associated, but they highlight the fact that this interaction can also support synergism.

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Section: Introductionsupporting

confidence: 62%

The Human D2 Dopamine Receptor Synergizes with the A2A Adenosine Receptor to Stimulate Adenylyl Cyclase in PC12 Cells

Kudlacek

Just

Korkhov

et al. 2003

Neuropsychopharmacol

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“…For example, strong data from a number of prospective studies show that both caffeine and coffee reduce the risk of Type 2 Diabetes Mellitus by 35-79% [28]. Both retrospective and prospective studies report a reduced risk of Parkinson's disease with habitual caffeine/coffee intake [29,30]. Risk of liver cirrhosis is significantly reduced by both caffeine and coffee [31].…”

Section: Discussionmentioning

confidence: 99%

Caffeine and Coffee as Therapeutics Against Alzheimer's Disease

Arendash

Cao

2010

JAD

163

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Abstract. Epidemiologic studies have increasingly suggested that caffeine/coffee could be an effective therapeutic against Alzheimer's disease (AD). We have utilized a transgenic mouse model for AD in well-controlled studies to determine if caffeine and/or coffee have beneficial actions to protect against or reverse AD-like cognitive impairment and AD pathology. AD mice given caffeine in their drinking water from young adulthood into older age showed protection against memory impairment and lower brain levels of the abnormal protein (amyloid-β; Aβ) thought to be central to AD pathogenesis. Moreover, "aged" cognitively-impaired AD mice exhibited memory restoration and lower brain Aβ levels following only 1-2 months of caffeine treatment. We believe that the cognitive benefits of chronic caffeine administration in AD mice are due to caffeine itself, and not metabolites of caffeine; this, because our long-term administration of theophylline to AD mice provided no cognitive benefits. In acute studies involving AD mice, one oral caffeine treatment quickly reduced both brain and plasma Aβ levels -similarly rapid alterations in plasma Aβ levels were seen in humans following acute caffeine administration. "Caffeinated" coffee provided to AD mice also quickly decreased plasma Aβ levels, but not "decaffeinated" coffee, suggesting that caffeine is critical to decreasing blood Aβ levels. Caffeine appears to provide its disease-modifying effects through multiple mechanisms, including a direct reduction of Aβ production through suppression of both β-and γ-secretase levels. These results indicate a surprising ability of moderate caffeine intake (the human equivalent of 500 mg caffeine or 5 cups of coffee per day) to protect against or treat AD in a mouse model for the disease and a therapeutic potential for caffeine against AD in humans.

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Section: Coffee and Teamentioning

confidence: 93%

“…However, with longer follow-up and more incident cases detected, an inverse association was seen following adjustment for age and smoking (RR for coffee non-drinkers versus drinkers 2.2, 95% CI 1.4-3.3) [477]. Risk estimates were similar for total amount of caffeine [477]. Similarly, a strong inverse relationship of PD with coffee and total caffeine intake was reported in the Health Professionals Follow-up Study, a cohort of men (RR 0.42, 95% CI 0.23-0.78 for highest versus lowest quintile, p for trend <0.001) [478].…”

Section: Coffee and Teamentioning

confidence: 98%