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Background: The impact of gestational diabetes mellitus (GDM) on incident dementia is unknown. Our aim was to evaluate the relationship between GDM and all‐cause dementia and the mediating effects of chronic diseases on this relationship. Methods: This prospective cohort study included women from the UK Biobank who were grouped based on GDM history. Multivariate Cox proportional hazard models were used to explore the associations between GDM and dementia. We further analysed the mediating effects of chronic diseases on this relationship and the interactions of covariates. Results: A total of 1292 women with and 204,171 women without a history of GDM were included. During a median follow‐up period of 45 years after first birth, 2921 women were diagnosed with dementia. Women with a GDM history had a 67% increased risk of incident dementia (hazard ratio 1.67, 95% confidence interval: 1.03–2.69) compared with those without a GDM history. According to mediation analyses, type 2 diabetes, coronary heart disease, chronic kidney disease and comorbidities (diagnosed with any two of the three diseases) explained 34.5%, 8.4%, 5.2% and 18.8% of the mediating effect on the relationship. Subgroup analyses revealed that physical activity modified the association between GDM history and dementia (p for interaction = 0.030). Among physically inactive women, GDM was significantly associated with incident dementia; however, this association was not observed among physically active women. Conclusions: A history of GDM was associated with a greater risk of incident dementia. Type 2 diabetes partially mediated this relationship. Strategies for dementia prevention might be considered for women with a history of GDM. [ABSTRACT FROM AUTHOR]

Background: Blood pressure (BP) is a dynamic measure that fluctuates over time. However, conventional BP control indicators may not adequately reflect the variability of BP during a period of time. Methods: We performed a secondary analysis of the Systolic Blood Pressure Intervention Trial (SPRINT), which compared systolic blood pressure (SBP) targets of <120 mmHg (intensive) and <140 mmHg (standard) among patients with hypertension and high cardiac risks. The target ranges were defined as 110 to 130 mmHg in intensive treatment arm and 120 to 140 mmHg in standard treatment arm, respectively. Time in target range (TTR) was calculated based on SBP measurements recorded during the first 3‐month follow‐up using linear interpolation method. The Fine‐Gray competing risk regression models were used to evaluate the association between TTR and cognitive outcomes. Results: A total of 7965 patients with the mean (SD) age of 68.0 (9.2) years were included, and 35% were female. Patients with higher TTR were younger, more likely to be male and take <3 BP‐lowering agents. Compared to the last quartile, the first quartile of TTR was significantly associated with a higher risk of probable dementia (HR: 1.74; 95% CI: 1.22–2.46; p = 0.002) and the composite of probable dementia or mild cognitive impairment (HR: 1.26; 95% CI: 1.03–1.55; p = 0.025). The risk of probable dementia and the composite outcome increased with per quartile decrease of TTR (HR: 1.18; 95% CI: 1.06–1.30; p = 0.002 and HR: 1.07; 95% CI: 1.00–1.14; p = 0.036). Sensitivity analyses showed similar results after adjusting mean SBP during the first 3‐month follow‐up. Conclusions: In this secondary analysis of SPRINT data, TTR was independently associated with probable dementia among patients with hypertension, suggesting that TTR could be used as a practical metric of BP control to evaluate the risk of dementia in older adults. Registration: URL: https://www.clinicaltrials.gov; Identifier: NCT01206062. [ABSTRACT FROM AUTHOR]

Background: The longitudinal association between persistent moderate to severe pain and subsequent long‐term cognitive decline remains inconclusive. Methods: Study population came from the English Longitudinal Study of Ageing, an ongoing prospective and nationally representative cohort of community‐dwelling adults aged ≥50 years in England. At waves 1 (2002/2003) and 2 (2004/2005) of the study, pain severity was measured based on pain intensity scores ranged from 0 to 10. We defined moderate to severe pain as pain intensity scores ≥5 points. Persistent moderate to severe pain was defined as participants reported moderate to severe pain at both waves 1 and 2. Standardized global cognitive Z scores derived from verbal memory, temporal orientation and semantic fluency were used as the primary outcome. Results: A total of 6,869 individuals (3,896 women; mean age: 63.9 ± 9.5 years) who have accepted twice measurements of pain at waves 1 and 2 (baseline), and at least one reassessment of cognitive function at waves 3 (2006/2007) to 8 (2016/2017), were included in this study. Each 5‐point increase in the sum of pain intensity scores was associated with a faster rate of –0.009 (95% CI: –0.013 to –0.006, p <.001) in global cognitive Z scores. Compared with no pain group, persistent moderate to severe pain group was associated with a significantly faster decline rate of –0.031 SD/year (95% CI: –0.043 to –0.018), in global cognitive Z scores. The relationships of persistent moderate to severe pain with verbal memory, temporal orientation and semantic fluency were similar. Conclusion: Cognitive function should be monitored in individuals with persistent moderate to severe pain. Significance: Persistent moderate to severe pain in adults age 50 and older was associated with accelerated cognitive decline over a median follow‐up of 12 years. More severe pain was associated with faster cognitive decline in a dose‐response pattern, and the relationship was demonstrated throughout multiple cognitive domains. While the overall effect was subtle, clinicians should be aware that older adults with persistent pain are at risk of faster cognitive decline. [ABSTRACT FROM AUTHOR]

Chiral phosphoric acids are incorporated into indium‐based metal–organic frameworks (In‐MOFs) by sterically preventing them from coordination. This concept leads to the synthesis of three chiral porous 3D In‐MOFs with different network topologies constructed from three enantiopure 1,1′‐biphenol‐phosphoric acid derived tetracarboxylate linkers. More importantly, all the uncoordinated phosphoric acid groups are periodically aligned within the channels and display significantly enhanced acidity compared to the non‐immobilized acids. This facilitates the Brønsted acid catalysis of asymmetric condensation/amine addition and imine reduction. The enantioselectivities can be tuned (up to >99 % ee) by varying the substituents to achieve a nearly linear correlation with the concentrations of steric bulky groups in the MOFs. DFT calculations suggest that the framework provides a chiral confined microenvironment that dictates both selectivity and reactivity of chiral MOFs. [ABSTRACT FROM AUTHOR]

Background: This study aimed to examine whether baseline atherosclerosis was associated with subsequent short-term domain-specific cognitive decline., Methods and Results: This research was based on the BRAVE (Beijing Research on Aging and Vessel) study, a population-based prospective cohort study of adults aged 40 to 80 years, free of dementia. At baseline (wave 1, 2019), cognitive assessments and atherosclerosis measures, including carotid intima-media thickness, carotid plaques, coronary artery calcification, and brachial-ankle pulse wave velocity were conducted. Cognitive function was reassessed in wave 2 (2022-2023) using linear mixed models for analysis. A total of 932 participants (63.7% women; mean age, 60.0±6.9 years) were included. Compared with the lowest tertile of carotid intima-media thickness, carotid plaques, and brachial-ankle pulse wave velocity, or a coronary artery calcification score=0, the highest tertile of carotid intima-media thickness (β=-0.065 SD/y [95% CI, -0.112 to -0.017]; P =0.008), carotid plaques (β=-0.070 SD/y [95% CI, -0.130 to -0.011]; P =0.021), and brachial-ankle pulse wave velocity (β=-0.057 SD/y [95% CI, -0.105 to -0.010]; P =0.018), and a coronary artery calcification score≥400 (β=-0.081 SD/y [95% CI, -0.153 to -0.008]; P =0.029) were significantly associated with a faster decline in semantic fluency after multivariable adjustment. Moreover, greater carotid intima-media thickness, coronary artery calcification, and brachial-ankle pulse wave velocity were significantly associated with a faster decline in global cognition., Conclusions: More significant atherosclerosis was associated with faster semantic fluency and global cognition declines.

Background: The association of age at coronary heart disease (CHD) onset with incident dementia remains unexplored. This study aimed to examine whether younger onset age of CHD is associated with a higher risk of incident dementia., Methods and Results: Data were obtained from the UK Biobank. Information on the diagnosis of CHD and dementia was collected at baseline and follow-ups. Propensity score matching method and Cox proportional hazards models were used to evaluate the association between different ages at CHD onset and incident dementia. A total of 432 667 adults (mean±SD age, 56.9±8.1 years) were included, of whom 11.7% had CHD. Compared with participants without CHD, participants with CHD exhibited higher risks of developing all-cause dementia, Alzheimer's disease, and vascular dementia. More importantly, younger age at CHD onset (per 10-year decrease) was significantly associated with elevated risks of all-cause dementia (hazard ratio [HR], 1.25 [95% CI, 1.20-1.30]; P <0.001), Alzheimer's disease (HR, 1.29 [95% CI, 1.20-1.38]; P <0.001), and vascular dementia (HR, 1.22 [95% CI, 1.13-1.31]; P <0.001). After propensity score matching, patients with CHD had significantly higher risks of all-cause dementia, Alzheimer's disease, and vascular dementia than matched controls among all onset age groups, and the HRs gradually elevated with decreasing age at CHD onset., Conclusions: Younger onset age of CHD is associated with higher risks of incident all-cause dementia, Alzheimer's disease, and vascular dementia, underscoring the necessity to pay attention to the neurocognitive status of individuals diagnosed with CHD at younger age to conduct timely interventions to attenuate subsequent risk of incident dementia.