Coffee, caffeine-related genes, and Parkinson's disease: a case-control study.
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ABSTRACT:
SUBMITTER: Facheris MF
PROVIDER: S-EPMC4554698 | biostudies-literature | 2008 Oct
REPOSITORIES: biostudies-literature
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Coffee, caffeine-related genes, and Parkinson's disease: a case-control study.
Facheris Maurizio F MF Schneider Nicole K NK Lesnick Timothy G TG de Andrade Mariza M Cunningham Julie M JM Rocca Walter A WA Maraganore Demetrius M DM
Movement disorders : official journal of the Movement Disorder Society 20081001 14
An inverse association between coffee and Parkinson's disease (PD) has been reported. However, it remains uncertain why some but not all coffee drinkers are less susceptible to PD. We considered the possibility of a pharmacogenetic effect. In our study, we included 1,208 subjects (446 case-unaffected sibling pairs and 158 case-unrelated control pairs) recruited from an ongoing study of the molecular epidemiology of PD in the Upper Midwest (USA). We collected information on lifetime coffee drinki ...[more]
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Project description:BACKGROUND AND PURPOSE:In 1-methyl-4-phenyl 1,2,3,6-tetrahydropyridine animal models of Parkinson's disease (PD), caffeine protects neurons by blocking the adenosine receptor A2A (ADORA2A). Caffeine is primarily metabolized by cytochrome P450 1A2 (CYP1A2). Our objective was to examine whether ADORA2A and CYP1A2 polymorphisms are associated with PD risk or modify the caffeine-PD association. METHODS:Parkinson's Epidemiology and Genetic Associations Studies in the United States (PEGASUS) included five population-based case-control studies. One laboratory genotyped four ADORA2A and three CYP1A2 polymorphisms in 1325 PD cases and 1735 age- and sex-matched controls. Information regarding caffeine (coffee) consumption and other lifestyle factors came from structured in-person or telephone interviews. Odds ratios (OR) and 95% confidence intervals (CI) were estimated using logistic regression. RESULTS:Two ADORA2A polymorphisms were inversely associated with PD risk - rs71651683, a 5' variant (adjusted allelic OR = 0.51, 95% CI 0.33-0.80, permutation-adjusted P = 0.015) and rs5996696, a promoter region variant (adjusted OR for AC and CC genotypes compared with the AA wild-type genotype were 0.76 (95% CI 0.57-1.02) and 0.37 (95% CI 0.13-1.01), respectively (permutation-adjusted P for trend = 0.04). CYP1A2 polymorphisms were not associated with PD risk; however, the coffee-PD association was strongest among subjects homozygous for either variant allele rs762551 (P(interaction) = 0.05) or rs2470890 (P(interaction) = 0.04). CONCLUSION:In this consortium study, two ADORA2A polymorphisms were inversely associated with PD risk, but there was weak evidence of interaction with coffee consumption. In contrast, the coffee-PD association was strongest among slow metabolizers of caffeine who were homozygous carriers of the CYP1A2 polymorphisms.
| S-EPMC3556904 | biostudies-literature
Project description:We evaluate the association of hypertension with PD in an Asian population and performed a meta-analysis on similar studies to address the effect of hypertension on PD risk. A matched case-control study involving 1342 Chinese subjects (671 PD and 671 age and gender-matched controls (with a mean age of 63.9 ± 9.7 and 63.5 ± 9.8 years, and identical proportion of gender distribution) was conducted. Hypertension increases PD risk by 1.9 times [OR 1.86 (1.46-2.38)]. The literature search identified 618 studies initially; however, only three matched case-control studies (all in Caucasians) met the inclusion criteria for meta-analysis. Overall analysis showed that hypertension decreases PD risk by 0.2 times [OR 0.80 (0.66-0.96)]. Hypertension increases PD risk by 1.9 times in our Asian population. However, a meta-analysis comprising of Caucasian populations showed a protective effect of hypertension suggesting that ethnic differences or other genetic or environmental factors may contribute to the divergent observation. Early diagnosis and treatment of hypertension may potentially reduce the risk of PD, at least in our population.
| S-EPMC8295270 | biostudies-literature
Project description:BackgroundTo evaluate the association between Parkinson's disease (PD) prognosis and the patient's onset of depression.MethodsA total of 353 patients with newly-diagnosed PD and a history of depression were enrolled. On the basis of the onset of depression before or after PD diagnosis, we divided participants into PD patients with pre- or post-diagnostic depression. Cox's regression analysis was used to detect risks between the onset of depression and outcomes (including death, accidental injury, dementia, and aspiration pneumonia). The association between the onset of depression and levodopa equivalent dosage (LED) and cumulative equivalent dosage of antidepressants were assessed.ResultsPD patients with post-diagnostic depression were associated with significantly higher risks of dementia (adjusted HR = 2·01, p = 0·015), and were older (58·5 ± 17·7 vs. 53·7 ± 18·6, p = 0·020) at the time of PD diagnosis than PD patients with pre-diagnostic depression. The higher incident rate of accidental injury was also noted in PD patients with post-diagnostic depression (48·1 vs. 31·3/1000 person-years, HR = 1·60, p = 0·041), but no statistical significance was observed in the adjusted hazard ratio (HR) (HR = 1·52, p = 0·069). Otherwise, mortality, motor condition and severity of depression revealed no significant difference between PD patients with pre-diagnostic and post-diagnostic depression.ConclusionPD patients with post-diagnostic depression had higher incidence of dementia, implying different onset time of depression could be associated with different subtypes and spreading routes which should be examined in follow-up studies.
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Project description:Hyperphosphorylated ?-synuclein in Lewy bodies and Lewy neurites is a characteristic neuropathological feature of Parkinson's disease (PD) and Dementia with Lewy bodies (DLB). The catalytic subunit of the specific phosphatase, protein phosphatase 2A (PP2A) that dephosphorylates ?-synuclein, is hypomethylated in these brains, thereby impeding the assembly of the active trimeric holoenzyme and reducing phosphatase activity. This phosphatase deficiency contributes to the accumulation of hyperphosphorylated ?-synuclein, which tends to fibrillize more than unmodified ?-synuclein. Eicosanoyl-5-hydroxytryptamide (EHT), a fatty acid derivative of serotonin found in coffee, inhibits the PP2A methylesterase so as to maintain PP2A in a highly active methylated state and mitigates the phenotype of ?-synuclein transgenic (SynTg) mice. Considering epidemiologic and experimental evidence suggesting protective effects of caffeine in PD, we sought, in the present study, to test whether there is synergy between EHT and caffeine in models of ?-synucleinopathy. Coadministration of these two compounds orally for 6 mo at doses that were individually ineffective in SynTg mice and in a striatal ?-synuclein preformed fibril inoculation model resulted in reduced accumulation of phosphorylated ?-synuclein, preserved neuronal integrity and function, diminished neuroinflammation, and improved behavioral performance. These indices were associated with increased levels of methylated PP2A in brain tissue. A similar profile of greater PP2A methylation and cytoprotection was found in SH-SY5Y cells cotreated with EHT and caffeine, but not with each compound alone. These findings suggest that these two components of coffee have synergistic effects in protecting the brain against ?-synuclein-mediated toxicity through maintenance of PP2A in an active state.
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Project description:Circadian disruptions may result in sleep problems, oxidative stress and an altered inflammatory response. These symptoms may contribute to PD pathogenesis, despite a lack of direct experimental evidence supporting this relationship. Clock genes are essential to drive and maintain circadian rhythm. To elucidate the possible role of circadian disruptions in PD, we investigated 132 tag variants in eight clock genes. We genotyped these tags within 1,394 Chinese cases and 1,342 controls using Illumina GoldenGate chips. We discovered that SNPs in ARNTL (rs900147, P = 3.33 × 10(-5), OR = 0.80) and PER1 (rs2253820, P = 5.30 × 10(-6), OR = 1.31) genes are significantly associated with PD risk. Moreover, the positive association of the ARNTL rs900147 variant was more robust in tremor dominant (TD) (P = 3.44 × 10(-4)) than postural instability and gait difficulty (PIGD) cases (P = 6.06 × 10(-2)). The association of the PER1 rs2253820 variant was more robust in PIGD (P = 5.42 × 10(-5)) than TD cases (P = 4.2 × 10(-2)). Haplotype analysis also showed that ARNTL and PER1 were associated with PD. Imputation analysis identified more SNPs within ARNTL and PER1 associated with PD, some of which may affect gene expression through altering the transcription factor binding site. In summary, our findings suggest that genetic polymorphisms in ARNTL and PER1 genes, as well as circadian disruptions, may contribute to PD pathogenesis.
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Project description:Patients with Parkinson's disease experience debilitating motor symptoms as well as nonmotor symptoms, such as cognitive dysfunction and sleep disorders. This constellation of symptoms has the potential to negatively influence pedestrian safety. The objective of this study was to investigate the association of motor symptoms, daytime sleepiness, impaired vigilance, and cognitive dysfunction with pedestrian behavior in patients with Parkinson's disease and healthy older adults.Fifty Parkinson's disease and 25 control participants were evaluated within a virtual reality pedestrian environment and completed assessments of motor performance, daytime sleepiness (Epworth Sleepiness Scale), vigilance (psychomotor vigilance task), and visual processing speed (Useful Field of View) outside the virtual reality environment. The primary outcome measure was time to contact, defined as the time remaining until a participant would have been hit by an approaching vehicle while crossing the virtual street.The virtual reality pedestrian environment was feasible in all participants. Patients with Parkinson's disease demonstrated riskier pedestrian behavior compared with controls. Among Parkinson's disease participants, walking speed, objective measures of vigilance, and visual processing speed were correlated with pedestrian behavior, with walking speed the strongest predictor of time to contact, explaining 48% of the variance. Vigilance explained an additional 8% of the variance. In controls, vigilance was also important for street-crossing safety, but older age was the most robust predictor of pedestrian safety.Walking speed is associated with unsafe pedestrian behavior in patients with Parkinson's disease. In contrast, age was the strongest predictor of pedestrian safety in healthy older adults. © 2017 International Parkinson and Movement Disorder Society.
| S-EPMC5732050 | biostudies-other
Project description:BackgroundPreliminary work has shown that diffusion tensor MRI (DTI) may contribute to the diagnosis of Parkinson's disease (PD).ObjectivesWe conducted a large, prospective, case control study to determine: (1) if fractional anisotropy (FA) and apparent diffusion coefficient (ADC) values on DTI in the basal ganglia and substantia nigra are different between patients with PD and healthy controls; and (2) the predictive value of these parameters and their clinical utility.MethodsDTI imaging was carried out in patients with PD and controls. FA and ADC values were obtained from various brain structures on the DTI scan using the diffusion tensor taskcard. The structures studied were: caudate, putamen, globus pallidus, thalamus and substantia nigra.Results151 subjects (73 PD patients, 41 men, 32 women; mean age 63.6 years) and 78 age and sex matched control subjects were studied. The FA value of the substantia nigra in patients with PD was lower compared with controls (0.403 vs 0.415; p = 0.001). However, no significant differences were demonstrated for FA or ADC values of other structures. Multiple regression analysis revealed that the clinical severity of PD correlated inversely with the FA value in the substantia nigra in patients with PD (regression coefficient -0.019). No single FA value had both a high positive and negative predictive power for PD.ConclusionsWe demonstrated in a large, prospective, case control study that the FA value in the substantia nigra on DTI was lower in PD compared with healthy controls, and correlated inversely with the clinical severity of PD. Further longitudinal studies would be helpful to assess the clinical utility of serial FA measurements of the substantia nigra in objective quantification of disease progression and monitoring of the therapeutic response.
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Project description:BackgroundSleep disorders are common in Parkinson's disease (PD) and include alterations in sleep-related EEG oscillations.ObjectiveThis case-control study tested the hypothesis that patients with PD would have a lower density of Scalp-Slow Wave (SW) oscillations and higher slow-to-fast frequencies ratio in rapid eye movement (REM) sleep than non-PD controls. Other sleep-related quantitative EEG (qEEG) features were also examined, including SW morphology, sleep spindles, and Scalp-SW spindle phase-amplitude coupling.MethodsPolysomnography (PSG)-derived sleep EEG was compared between PD participants (n = 56) and non-PD controls (n = 30). Following artifact rejection, sleep qEEG analysis was performed in frontal and central leads. Measures included SW density and morphological features of SW and sleep spindles, SW-spindle phase-amplitude coupling, and spectral power analysis in Non-REM (NREM) and REM. Differences in qEEG features between PD and non-PD controls were compared using two-tailed Welch's t-tests, and correction for multiple comparisons was performed per the Benjamini-Hochberg method.ResultsSW density was lower in PD than in non-PD controls (F = 13.5, p' = 0.003). The PD group also exhibited higher ratio of slow REM EEG frequencies (F = 4.23, p' = 0.013), higher slow spindle peak frequency (F = 24.7, p' < 0.002), and greater SW-spindle coupling angle distribution non-uniformity (strength) (F = 7.30, p' = 0.034).ConclusionThis study comprehensively evaluates sleep qEEG including SW-spindle phase amplitude coupling in PD compared to non-PD controls. These findings provide novel insights into how neurodegenerative disease disrupts electrophysiological sleep rhythms. Considering the role of sleep oscillatory activity on neural plasticity, future studies should investigate the influence of these qEEG markers on cognition in PD.
| S-EPMC10200139 | biostudies-literature
Project description:Background:Acute administration of caffeine produces panic attacks in most Panic Disorder (PD) patients, but little is known about chronic caffeine use in these patients. Objective:To assess caffeine use in patients with PD and to ascertain if caffeine consumption is associated with sociodemographic or clinical features. Methods:65 adults with PD and 66 healthy controls were included in the current study. Their caffeine intake within the previous week was quantified with a questionnaire and compared. Harmful caffeine use was defined as consumption above 400 mg/day of caffeine. We tested for correlations between caffeine intake, demographic and clinical features. Results:Patients consumed significantly more caffeine than controls (P < 0.001). 14% (N = 9) of the PD patients made harmful use of caffeine. The use of caffeine-containing medications was observed in 40% (N = 26) of the PD patients and 6% (N = 4) of controls. Consumption of energy drinks was observed in 11% (N = 7) of PD patients and in none of the healthy subjects. Patients reported sleeping significantly less than controls (P < 0.001). In PD patients, caffeine consumption was not correlated with the presence of panic attacks or comorbidity with depression. The use of benzodiazepines or sedative medications was not correlated with caffeine intake. Conclusion:High caffeine consumption in PD patients could be explained by the development of tolerance with regular use of this substance. Subtypes of sensitive and non-sensitive PD patients could also explain why some of these patients are able to tolerate high doses of caffeine.
| S-EPMC6882139 | biostudies-literature
Project description:OBJECTIVE:To investigate whether Sjogren's syndrome would have an influence on the development of Parkinson's disease. METHODS:A population-based case-control study was conducted. Participants consisted of 7716 subjects with newly diagnosed Parkinson's disease and a population of 75129 matched control subjects between 2000 and 2010. We measured the risk of Parkinson's disease in association with Sjogren's syndrome by using adjusted odds ratios. RESULTS:A total of 143 Parkinson's disease subjects (1.9%) and 893 control subjects (1.2%) suffered from Sjogren's syndrome (p < 0.001). The crude odds ratio for Parkinson's disease among subjects with Sjogren's syndrome was 1.56 (95% CI 1.30-1.86; p < 0.01). After adjustment for potential confounders which have been proposed that would increase the risk of development of Parkinson's disease, Sjogren's syndrome was found to be significantly associated with the risk of Parkinson's disease with an odds ratio of 1.37 (95% CI 1.15-1.65; p < 0.01). CONCLUSION:This study preliminarily proposed that Sjogren's syndrome was significant associated with an increased risk of Parkinson's disease.
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