Objective: We aimed to investigate the associations of the triglyceride-glucose index, which measures insulin resistance, and the incidence of Parkinson’s disease. Methods: Our study used the Health Screening Cohort database of the National Health Insurance Service of South Korea (2002–2019). We included 310,021 participants who had no previous history of Parkinson’s disease and for whom more than 3 triglyceride-glucose index measurements were available. A diagnosis of Parkinson’s disease was determined via the International Classification of Diseases Tenth edition (G20) with a specific reimbursement code for rare intractable diseases and a history of prescriptions for anti-Parkinsonism drugs. Results: During a median of 9.64 years (interquartile range 8.72–10.53), 4,587 individuals (1.5%) had Parkinson’s disease. Based on a multivariable time-dependent Cox proportional hazards model, a per-unit increase in triglyceride-glucose index score was associated with a significantly increased risk of Parkinson’s disease (hazard ratio [HR]: 1.062; 95% confidence interval [CI] 1.007–1.119). In a sensitivity analysis, the triglyceride-glucose index was associated with the incidence of Parkinson’s disease in a non–diabetes mellitus cohort (HR: 1.093; 95% CI 1.025–1.165), but not in the diabetes mellitus cohort (HR: 0.990; 95% CI 0.902–1.087). In a restricted cubic spline analysis, the association between the triglyceride-glucose index and the incidence risk of Parkinson’s disease showed a nonlinear increasing (J-shaped) trend. Conclusion Our study demonstrated that higher triglyceride-glucose index scores were associated with the incidence of Parkinson’s disease in the general population, particularly in a nondiabetic mellitus cohort.

Objective: We aimed to investigate the associations of the triglyceride-glucose index, which measures insulin resistance, and the incidence of Parkinson’s disease. Methods: Our study used the Health Screening Cohort database of the National Health Insurance Service of South Korea (2002–2019). We included 310,021 participants who had no previous history of Parkinson’s disease and for whom more than 3 triglyceride-glucose index measurements were available. A diagnosis of Parkinson’s disease was determined via the International Classification of Diseases Tenth edition (G20) with a specific reimbursement code for rare intractable diseases and a history of prescriptions for anti-Parkinsonism drugs. Results: During a median of 9.64 years (interquartile range 8.72–10.53), 4,587 individuals (1.5%) had Parkinson’s disease. Based on a multivariable time-dependent Cox proportional hazards model, a per-unit increase in triglyceride-glucose index score was associated with a significantly increased risk of Parkinson’s disease (hazard ratio [HR]: 1.062; 95% confidence interval [CI] 1.007–1.119). In a sensitivity analysis, the triglyceride-glucose index was associated with the incidence of Parkinson’s disease in a non–diabetes mellitus cohort (HR: 1.093; 95% CI 1.025–1.165), but not in the diabetes mellitus cohort (HR: 0.990; 95% CI 0.902–1.087). In a restricted cubic spline analysis, the association between the triglyceride-glucose index and the incidence risk of Parkinson’s disease showed a nonlinear increasing (J-shaped) trend. Conclusion Our study demonstrated that higher triglyceride-glucose index scores were associated with the incidence of Parkinson’s disease in the general population, particularly in a nondiabetic mellitus cohort.

Objective: We aimed to investigate the associations of the triglyceride-glucose index, which measures insulin resistance, and the incidence of Parkinson’s disease. Methods: Our study used the Health Screening Cohort database of the National Health Insurance Service of South Korea (2002–2019). We included 310,021 participants who had no previous history of Parkinson’s disease and for whom more than 3 triglyceride-glucose index measurements were available. A diagnosis of Parkinson’s disease was determined via the International Classification of Diseases Tenth edition (G20) with a specific reimbursement code for rare intractable diseases and a history of prescriptions for anti-Parkinsonism drugs. Results: During a median of 9.64 years (interquartile range 8.72–10.53), 4,587 individuals (1.5%) had Parkinson’s disease. Based on a multivariable time-dependent Cox proportional hazards model, a per-unit increase in triglyceride-glucose index score was associated with a significantly increased risk of Parkinson’s disease (hazard ratio [HR]: 1.062; 95% confidence interval [CI] 1.007–1.119). In a sensitivity analysis, the triglyceride-glucose index was associated with the incidence of Parkinson’s disease in a non–diabetes mellitus cohort (HR: 1.093; 95% CI 1.025–1.165), but not in the diabetes mellitus cohort (HR: 0.990; 95% CI 0.902–1.087). In a restricted cubic spline analysis, the association between the triglyceride-glucose index and the incidence risk of Parkinson’s disease showed a nonlinear increasing (J-shaped) trend. Conclusion Our study demonstrated that higher triglyceride-glucose index scores were associated with the incidence of Parkinson’s disease in the general population, particularly in a nondiabetic mellitus cohort.

Purpose: Repeated transcranial direct current stimulation (tDCS) is expected to have the potential to improve cognitive function in patients with mild cognitive impairment (MCI). We aimed to evaluate the efficacy and safety of at-home tDCS for elderly patients with MCI. Materials and Methods: Patients aged 60–80 years, who maintained normal daily living but reported objective memory impairments, were enrolled. Active or sham stimulations were applied to the dorsal frontal cortex (left: anode; right: cathode) at home for 2 weeks. Changes in cognitive function were assessed using visual recognition tasks and the Mini-Mental State Exam (MMSE), and safety and efficacy were assessed using self-reports and a remote monitoring application. Results: Of the 19 participants enrolled, 12 participants were included in the efficacy analysis. Response times and MMSE scores significantly improved after active stimulation compared to the sham stimulation; however, there were no significant differences in the proportion of correct responses. The mean compliance of the efficacy group was 97.5%±4.1%. Three participants experienced burns, but no permanent sequelae remained. Conclusion This preliminary result suggests that home-based tDCS may be a promising treatment option for MCI patients; however, it requires more attention and technological development to address safety concerns.

BACKGROUND: AND PURPOSE: Fibroblast growth factor 23 (FGF23) is associated with atherosclerosis via nitric-oxide-associated endothelial dysfunction and calcium-phosphate-related bone mineralization. This study aimed to determine the association of the plasma FGF23 concentration with intracranial cerebral atherosclerosis (ICAS) and extracranial cerebral atherosclerosis (ECAS). METHODS: We prospectively enrolled 262 first-ever ischemic stroke patients in whom brain magnetic resonance was performed and a blood sample acquired within 24 h after admission. Plasma FGF23 concentrations were measured using an enzyme-linked immunosorbent assay. The presence of ICAS or ECAS was defined as a ≥50% decrease in arterial diameter in magnetic resonance angiography. The burden of cerebral atherosclerosis was calculated by adding the total number of vessels defined as ICAS or ECAS. RESULTS: Our study population included 152 (58.0%) males. The mean age was 64.7 years, and the plasma FGF23 concentration was 347.5±549.6 pg/mL (mean±SD). ICAS only, ECAS only, and both ICAS and ECAS were present in 31.2% (n=82), 4.9% (n=13), and 6.8% (n=18) of the subjects, respectively. In multivariate binary and ordinal logistic analyses, after adjusting for sex, age, and variables for which p < 0.1 in the univariate analysis, the plasma FGF23 concentration (per 100 pg/mL) was positively correlated with the presence of ICAS [odds ratio (OR)=1.07, 95% CI=1.00–1.15, p=0.039], burden of ICAS (OR=1.09, 95% CI=1.04–1.15, p=0.001), and burden of ECAS (OR=1.06, 95% CI=1.00–1.12, p=0.038), but it was not significantly related to the presence of ECAS (OR=1.05, 95% CI=0.99–1.12, p=0.073). CONCLUSIONS The plasma FGF23 may be a potential biomarker for cerebral atherosclerosis, particularly the presence and burden of ICAS in stroke patients.

No abstract available.
Aorta, Thoracic ; Cerebral Infarction ; Humans ; Infarction

In brain death state, bilateral pupil light reflexes are disappeared, and pupils are fixed with dilated. However, spontaneous movements such as ocular microtremor or bilateral cyclical constriction-dilatation of pupils have been rarely reported in brain death patients. We present a brain death patient whose right pupil displayed spontaneously repetitive constriction and dilatation regardless of external stimuli such as light and pain. Early recognition of this phenomenon may prohibit the delay in the diagnosis of brain death and organ transplantation.
Brain Death ; Brain ; Coma ; Constriction ; Diagnosis ; Dilatation ; Humans ; Organ Transplantation ; Pupil ; Reflex ; Transplants

BACKGROUND AND PURPOSE: Elevated postprandial blood glucose is a critical risk factor for stroke. The dietary glycemic load (GL) and glycemic index (GI) are frequently used as markers of the postprandial blood glucose response to estimate the overall glycemic effect of diets. We hypothesized that high dietary GL, GI, or total carbohydrate intake is associated with a poor functional outcome in patients with acute ischemic stroke. METHODS: We prospectively included 263 first-ever ischemic stroke patients who completed a semiquantitative food-frequency questionnaire. The dietary GL, GI, and total carbohydrate intake were investigated by examining the average frequency of intake during the previous year based on reference amounts for various food items. Poor functional outcome was defined as a score on the modified Rankin Scale (mRS) of ≥3 at 3 months after stroke. RESULTS: The patients were aged 65.4±11.7 years (mean±standard deviation), and 58.2% of them were male. A multivariate analysis adjusted for age, sex, marital status, prestroke mRS score, diabetes mellitus, hyperlipidemia, body mass index, triglycerides, low-density lipoprotein, hemoglobin A1c, stroke classification, and National Institutes of Health Stroke Scale score, early neurological deterioration, and high-grade white-matter hyperintensities revealed that the dietary GL and total carbohydrate intake were associated with a poor functional outcome, with odds ratios for the top quartile relative to the bottom quartile of 28.93 (95% confidence interval=2.82–296.04) and 36.84 (95% confidence interval=2.99–453.42), respectively (p for trend=0.002 and 0.002, respectively). In contrast, high dietary GI was not associated with a poor functional outcome (p for trend=0.481). CONCLUSIONS: Increased dietary GL and carbohydrate intake were associated with a poor short-term functional outcome after an acute ischemic stroke.
Blood Glucose ; Body Mass Index ; Cerebral Infarction* ; Classification ; Diabetes Mellitus ; Diet ; Glycemic Index ; Glycemic Load* ; Humans ; Hyperlipidemias ; Lipoproteins ; Male ; Marital Status ; Multivariate Analysis ; National Institutes of Health (U.S.) ; Odds Ratio ; Prospective Studies ; Risk Factors ; Stroke ; Triglycerides

PURPOSE: Abnormalities in hemostasis and coagulation have been suggested in chronic renal failure (CRF). In this study, we compared processes of thrombus formation between rats with CRF and those with normal kidney function. MATERIALS AND METHODS: CRF was induced by 5/6 ablation/infarction of the kidneys in Sprague-Dawley rats, and surviving rats after 4 weeks were used. Ferric chloride (FeCl3)-induced thrombosis in the carotid artery was induced to assess thrombus formation. Whole blood clot formation was evaluated using rotational thromboelastometry (ROTEM). Platelet aggregation was assessed with impedance platelet aggregometry. RESULTS: FeCl3-induced thrombus formation was initiated faster in the CRF group than in the control group (13.2±1.1 sec vs. 17.8±1.0 sec, p=0.027). On histological examination, the maximal diameters of thrombi were larger in the CRF group than in the control group (394.2±201.1 µm vs. 114.0±145.1 µm, p=0.039). In extrinsic pathway ROTEM, the CRF group showed faster clot initiation (clotting time, 59.0±7.3 sec vs. 72.8±5.0 sec, p=0.032) and increased clot growth kinetics (α angle, 84.8±0.2° vs. 82.0±0.6°, p=0.008), compared to the control group. Maximal platelet aggregation rate was higher in the CRF group than in the control group (58.2±0.2% vs. 44.6±1.2%, p=0.006). CONCLUSION: Our study demonstrated that thrombogenicity is increased in rats with CRF. An activated extrinsic coagulation pathway may play an important role in increasing thrombogenicity in CRF.
Animals ; Blood Platelets ; Carotid Arteries ; Electric Impedance ; Hemostasis ; Kidney ; Kidney Failure, Chronic* ; Kinetics ; Models, Animal* ; Platelet Aggregation ; Rats* ; Rats, Sprague-Dawley ; Thrombelastography ; Thrombosis

Disease modeling of Alzheimer's disease (AD) has been hampered by the lack of suitable cellular models while animal models are mainly based on the overexpression of AD-related genes which often results in an overemphasis of certain pathways and is also confounded by aging. In this study, we therefore developed and used induced pluripotent stem cell (iPSC) lines from a middle-aged AD patient with a known presenilin 1 (PSEN1) mutation (Glu120Lys; PS1-E120K) and as a control, an elderly normal subject. Using this approach, we demonstrated that the extracellular accumulation of Aβ was dramatically increased in PS1-E120K iPSC-derived neurons compared with the control iPSC line. PS1-E120K iPSC-derived neurons also exhibited high levels of phosphorylated tau, as well as mitochondrial abnormalities and defective autophagy. Given that the effect of aging is lost with iPSC generation, these abnormal cellular features are therefore indicative of PSEN1-associated AD pathogenesis rather than primary changes associated with aging. Taken together, this iPSC-based approach of AD modeling can now be used to better understand AD pathogenesis as well as a tool for drug discovery.
Aged ; Aging ; Alzheimer Disease* ; Autophagy ; Cerebellar Ataxia* ; Drug Discovery ; Humans ; Models, Animal ; Neurons ; Pluripotent Stem Cells ; Presenilin-1 ; Stem Cells