Case-control study of hypertension and Parkinson's disease.
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ABSTRACT:
SUBMITTER: Ng YF
PROVIDER: S-EPMC8295270 | biostudies-literature |
REPOSITORIES: biostudies-literature
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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.
| S-EPMC5794149 | biostudies-literature
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.
| S-EPMC2095589 | biostudies-literature
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: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 drinking and we studied two genes: ADORA2A, which encodes the major receptor activity of caffeine in the brain (variants rs5751876 and rs3032740), and CYP1A2, which encodes the major rate-limiting step of caffeine metabolism (variants rs35694136 and rs762551). We did not observe significant associations of coffee drinking or of the genetic variants with PD susceptibility, either independently or jointly, in the sample overall and in most strata. Our study neither supports the hypothesis that coffee protects against PD nor provides evidence for a pharmacogenetic effect.
| S-EPMC4554698 | biostudies-literature
Project description:WTCCC genome-wide case-control association study for Hypertension (HT) using the 1958 British Birth Cohort and the UK National Blood Service collections as controls.
| EGAS00000000009 | EGA
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.
| S-EPMC5509109 | biostudies-literature
Project description:Aggregation and fibrillization of the alpha-synuclein protein, which is the main component of Lewy bodies, may represent important processes in the pathogenesis of Parkinson's disease (PD). Several in vivo and in vitro studies suggest that beta-synuclein may be a natural negative regulator of alpha-synuclein aggregation and fibrillization. The goal of the present study was to investigate the association of two polymorphisms (rs35035889 and rs1352303) in the beta-synuclein (SNCB) gene with PD. Our case-control study included a total of 370 case-unaffected sibling pairs and 168 case-unrelated control pairs (538 pairs total). The subjects were recruited from an ongoing study of the molecular epidemiology of PD in the Upper Midwest (USA). We employed a liberalization of the sibling transmission disequilibrium test to study the main effects of the gene variants for subjects overall and for strata defined by age at study, gender, ethnicity, clinical diagnostic certainty, dementia, and family history of PD (adjusted for age at study and gender as appropriate). The analyses were conducted for each SNCB variant separately, and also for two-locus haplotypes using score tests. Neither of the SNCB SNPs examined were associated with PD overall or in strata, and haplotype analyses were negative as well. However, one of the two SNPs (rs1352303) was associated with a delayed age at onset of PD in women. The results of this preliminary study suggest that the SNCB locus, though not a susceptibility gene for PD, might modify the age at onset of PD.
| S-EPMC1978171 | biostudies-literature
Project description:BackgroundThe analysis of the procedural memory is particularly relevant in neurodegenerative disorders like Parkinson's disease, due to the central role of the basal ganglia in procedural memory. It has been shown that anterograde procedural memory, the ability to learn a new skill, is impaired in Parkinson's disease. However, retrograde procedural memory, the long-term retention and execution of skills learned in earlier life stages, has not yet been systematically investigated in Parkinson's disease.ObjectiveThis study aims to investigate retrograde procedural memory in people with Parkinson's disease. We hypothesized that retrograde procedural memory is impaired in people with Parkinson's disease compared to an age- and gender-matched control group.MethodsFirst, we developed the CUPRO evaluation system, an extended evaluation system based on the Cube Copying Test, to distinguish the cube copying procedure, representing functioning of retrograde procedural memory, and the final result, representing the visuo-constructive abilities. Development of the evaluation system included tests of discriminant validity.ResultsComparing people with typical Parkinson's disease (n = 201) with age- and gender-matched control subjects (n = 201), we identified cube copying performance to be significantly impaired in people with Parkinson's disease (p = 0.008). No significant correlation was observed between retrograde procedural memory and disease duration.ConclusionWe demonstrated lower cube copying performance in people with Parkinson's disease compared to control subjects, which suggests an impaired functioning of retrograde procedural memory in Parkinson's disease.
| S-EPMC9108589 | biostudies-literature
Project description:Background: Parkinson's disease (PD) is the most common neurodegenerative movement disorder that is known to be related to neuro-inflammation. Chemokines participate in this process usually through upregulation of expression levels, which are closely related to the polymorphisms in their genes. Recent studies have further revealed the association between these polymorphisms and the risk of PD in multiple populations, but not the Chinese Han population. Methods:The promoter region of CCL2 was sequenced in 411 PD patients and 422 gender-age matched control from a Chinese Han population using PCR-RFLP method. Their genotype frequencies were analyzed statistically. Dual-luciferase reporter assays were conducted in neuroblastoma cells to assess the promoter transcriptional activity of the rs1024611 variants (T>C) and the GRCh38.p12chr17:34252593 G>C alleles in CCL2. Results:We found that the frequency of the CCL2 genotype of rs1024611 was significantly different between the PD and control groups (p = 0.021), while the C allele was associated with a significantly increased risk in the PD group (p = 0.004). Moreover, C allele of this newly identified alteration in CCL2 (GRCh38.p12chr17:34252593 G>C) was also found to be associated with an increased risk of PD (P genotype = 0.006, P allele = 0.006). Dual-luciferase reporter assay results indicated that rs1024611 C allele and GRCh38.p12chr17:.34252593 C allele increased the transcriptional activity of the CCL2 promoter. Conclusions: We, for the first time, report a risk polymorphism (rs1024611) and a new locus (GRCh38.p12chr17:.34252593 G>C) on CCL2, both of which are suggested as risk factors for PD in a Chinese Han population.
| S-EPMC6362632 | biostudies-literature