Increasing social concern surrounds the potential adverse health effects of precarious employment (PE). In this study, we explored the association between PE and the onset of depressive symptoms.

A total of 11,555 Korean waged workers (5700 females) contributed 62,217 observations from 2009 to 2022. PE was operationalized as a multidimensional construct, including employment insecurity, income inadequacy and lack of rights and protection. Depressive symptoms were evaluated using the Center for Epidemiological Studies-Depression Scale (11-item version). The association between PE and the onset of depressive symptoms in the subsequent year was estimated using generalized estimating equations. Effect sizes were reported as odds ratio (OR) and 95% confidence interval (CI).

The overall incidence of depressive symptoms was 8.3% during the study period. In cross-sectional analysis, daily employment, disguised employment, lower monthly wages and lack of social insurance coverage were associated with concurrent depressive symptoms in both men and women. Longitudinally, fixed-term employment (OR: 1.17, 95% CI: 1.07–1.29), daily employment (OR: 1.64, 95% CI: 1.45–1.85) and disguised employment (OR: 1.36, 95% CI: 1.17–1.57) were associated with the onset of depressive symptoms among the overall sample. Among men, the lowest quartiles of wage were associated with the onset of depressive symptoms (OR: 1.34, 95% CI: 1.13–1.60), while the absence of a trade union was associated among women (OR: 1.18, 95% CI: 1.01–1.39).

Employment insecurity, inadequate income and lack of rights and protection may contribute to depressive symptoms. Therefore, PE serves as a significant social determinant of mental health among workers in Korea. Active policy efforts are warranted to improve the overall quality of employment in the workforce.

Cerebral white matter hyperintensities (WMH) are prevalent incident findings on brain MRI scans among elderly people and have been consistently implicated in cognitive dysfunction. However, differential roles of WMH by region in cognitive function are still unclear. The aim of this study was to ascertain the differential role of regional WMH in predicting progression from mild cognitive impairment (MCI) to different subtypes of dementia.

Participants were recruited from the Clinical Research Center for Dementia of South Korea (CREDOS) study. A total of 622 participants with MCI diagnoses at baseline and follow-up evaluations were included for the analysis. Initial MRI scans were rated for WMH on a visual rating scale developed for the CREDOS. Differential effects of regional WMH in predicting incident dementia were evaluated using the Cox proportional hazards model.

Of the 622 participants with MCI at baseline, 139 patients (22.3%) converted to all-cause dementia over a median of 14.3 (range 6.0–36.5) months. Severe periventricular WMH (PWMH) predicted incident all-cause dementia (Hazard ratio (HR) 2.22; 95% confidence interval (CI) 1.43–3.43) and Alzheimer's disease (AD) (HR 1.86; 95% CI 1.12–3.07). Subcortical vascular dementia (SVD) was predicted by both PWMH (HR 16.14; 95% CI 1.97–132.06) and DWMH (HR 8.77; 95% CI 1.77–43.49) in more severe form (≥ 10 mm).

WMH differentially predict dementia by region and severity. Our findings suggest that PWMH may play an independent role in the pathogenesis of dementia, especially in AD.

Decreased hemoglobin levels increase the risk of developing dementia among the elderly. However, the underlying mechanisms that link decreased hemoglobin levels to incident dementia still remain unclear, possibly due to the fact that few studies have reported on the relationship between low hemoglobin levels and neuroimaging markers. We, therefore, investigated the relationships between decreased hemoglobin levels, cerebral small-vessel disease (CSVD), and cortical atrophy in cognitively healthy women and men.

Cognitively normal women (n = 1,022) and men (n = 1,018) who underwent medical check-ups and magnetic resonance imaging (MRI) were enrolled at a health promotion center. We measured hemoglobin levels, white matter hyperintensities (WMH) scales, lacunes, and microbleeds. Cortical thickness was automatically measured using surface based methods. Multivariate regression analyses were performed after controlling for possible confounders.

Decreased hemoglobin levels were not associated with the presence of WMH, lacunes, or microbleeds in women and men. Among women, decreased hemoglobin levels were associated with decreased cortical thickness in the frontal (Estimates, 95% confidence interval, −0.007, (−0.013, −0.001)), temporal (−0.010, (−0.018, −0.002)), parietal (−0.009, (−0.015, −0.003)), and occipital regions (−0.011, (−0.019, −0.003)). Among men, however, no associations were observed between hemoglobin levels and cortical thickness.

Our findings suggested that decreased hemoglobin levels affected cortical atrophy, but not increased CSVD, among women, although the association is modest. Given the paucity of modifiable risk factors for age-related cognitive decline, our results have important public health implications.

There is increasing evidence of a relationship between underweight or obesity and dementia risk. Several studies have investigated the relationship between body weight and brain atrophy, a pathological change preceding dementia, but their results are inconsistent. Therefore, we aimed to evaluate the relationship between body mass index (BMI) and cortical atrophy among cognitively normal participants.

We recruited cognitively normal participants (n = 1,111) who underwent medical checkups and detailed neurologic screening, including magnetic resonance imaging (MRI) in the health screening visits between September 2008 and December 2011. The main outcome was cortical thickness measured using MRI. The number of subjects with five BMI groups in men/women was 9/9, 148/258, 185/128, 149/111, and 64/50 in underweight, normal, overweight, mild obesity, and moderate to severe obesity, respectively. Linear and non-linear relationships between BMI and cortical thickness were examined using multiple linear regression analysis and generalized additive models after adjustment for potential confounders.

Among men, underweight participants showed significant cortical thinning in the frontal and temporal regions compared to normal weight participants, while overweight and mildly obese participants had greater cortical thicknesses in the frontal region and the frontal, temporal, and occipital regions, respectively. However, cortical thickness in each brain region was not significantly different in normal weight and moderate to severe obesity groups. Among women, the association between BMI and cortical thickness was not statistically significant.

Our findings suggested that underweight might be an important risk factor for pathological changes in the brain, while overweight or mild obesity may be inversely associated with cortical atrophy in cognitively normal elderly males.

Epidemiological studies have reported that higher education (HE) is associated with a reduced risk of incident Alzheimer's disease (AD). However, after the clinical onset of AD, patients with HE levels show more rapid cognitive decline than patients with lower education (LE) levels. Although education level and cognition have been linked, there have been few longitudinal studies investigating the relationship between education level and cortical decline in patients with AD. The aim of this study was to compare the topography of cortical atrophy longitudinally between AD patients with HE (HE-AD) and AD patients with LE (LE-AD).

We prospectively recruited 36 patients with early-stage AD and 14 normal controls. The patients were classified into two groups according to educational level, 23 HE-AD (>9 years) and 13 LE-AD (≤9 years).

As AD progressed over the 5-year longitudinal follow-ups, the HE-AD showed a significant group-by-time interaction in the right dorsolateral frontal and precuneus, and the left parahippocampal regions compared to the LE-AD.

Our study reveals that the preliminary longitudinal effect of HE accelerates cortical atrophy in AD patients over time, which underlines the importance of education level for predicting prognosis.

This study aimed to investigate the influences of age, education, and gender on the two total scores (TS-I and TS-II) of the Consortium to Establish a Registry for Alzheimer's Disease Neuropsychological assessment battery (CERAD-NP) and to provide normative information based on an analysis for a large number of elderly persons with a wide range of educational levels.

In the study, 1,987 community-dwelling healthy volunteers (620 males and 1,367 females; 50–90 years of age; and zero to 25 years of education) were included. People with serious neurological, medical, and psychiatric disorders (including dementia) were excluded. All participants underwent the CERAD-NP assessment. TS-I was generated by summing raw scores from the CERAD-NP subtests, excluding Mini-Mental State Examination and Constructional Praxis (CP) recall subtests. TS-II was calculated by adding CP recall score to TS-I.

Both TS-I and TS-II were significantly influenced by demographic variables. Education accounted for the greatest proportion of score variance. Interaction effect between age and gender was found. Based on the results obtained, normative data of the CERAD-NP total scores were stratified by age (six overlapping tables), education (four strata), and gender.

The normative information will be very useful for better interpretation of the CERAD-NP total scores in various clinical and research settings and for comparing individuals’ performance of the battery across countries.

Major depressive disorder (MDD) is closely related to stress reactions and serotonin probably underpins the pathophysiology of MDD. Alterations of the hypothalamic-pituitary-adrenal axis at the gene level have reciprocal consequences on serotonin neurotransmission. Glucocorticoid receptor (GR) polymorphisms affect glucocorticoid sensitivity, which is associated with cortisol feedback effects. Therefore, we hypothesised that GR polymorphisms are associated with the susceptibility to MDD and predict the treatment response.

Ninety-six subjects with a minimum score of 17 on the 21-item Hamilton Depression Scale (HAMD) at baseline were enrolled into the present study. The genotypes of GR (N363S, ER22/23EK, Bcl1, and TthIII1 polymorphisms) were analysed. The HAMD score was again measured after 1, 2, 4 and 8 weeks of antidepressant treatment to detect whether the therapeutic effects differed with the GR genotype.

Our subjects carried no N363S or ER22/23EK genetic polymorphisms and three types of Bcl1 and TthIII1 genetic polymorphisms. The C/C genotype and C allele at Bcl1 polymorphism were more frequent in MDD patients than in normal controls (p < 0.01 and p = 0.01, respectively). The genotype distributions did not differ significantly between responders and non-responders.

These results suggest that GR polymorphism cannot predict the therapeutic response after antidepressant administration. However, GR polymorphism (Bcl1) might play a role in the pathophysiology of MDD. Future studies should check this finding in larger populations with different characteristics.