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Background: Altered thyroid hormone levels have been associated with increased risk of Alzheimer's disease (AD) dementia and related cognitive decline. However, the neuropathological substrates underlying the link between thyroid hormones and AD dementia are not yet fully understood. We first investigated the association between serum thyroid hormone levels and in vivo AD pathologies including both beta-amyloid (Aβ) and tau deposition measured by positron emission tomography (PET). Given the well-known relationship between Aβ and tau pathology in AD, we additionally examined the moderating effects of thyroid hormone levels on the association between Aβ and tau deposition. Methods: This cross-sectional study was conducted as part of the Korean Brain Aging Study for Early Diagnosis and Prediction of Alzheimer's Disease (KBASE) cohort. This study included a total of 291 cognitively normal adults aged 55 to 90. All participants received comprehensive clinical assessments, measurements for serum total triiodothyronine (T3), free triiodothyronine (fT3), free thyroxine (fT4), and thyroid-stimulating hormone (TSH), and brain imaging evaluations including [11C]-Pittsburgh compound B (PiB)- PET and [18F] AV-1451 PET. Results: No associations were found between either thyroid hormones or TSH and Aβ and tau deposition on PET. However, fT4 (p = 0.002) and fT3 (p = 0.001) exhibited significant interactions with Aβ on tau deposition: The sensitivity analyses conducted after the removal of an outlier showed that the interaction effect between fT4 and Aβ deposition was not significant, whereas the interaction between fT3 and Aβ deposition remained significant. However, further subgroup analyses demonstrated a more pronounced positive relationship between Aβ and tau in both the higher fT4 and fT3 groups compared to the lower group, irrespective of outlier removal. Meanwhile, neither T3 nor TSH had any interaction with Aβ on tau deposition. Conclusion: Our findings suggest that serum thyroid hormones may moderate the relationship between cerebral Aβ and tau pathology. Higher levels of serum thyroid hormones could potentially accelerate the Aβ-dependent tau deposition in the brain. Further replication studies in independent samples are needed to verify the current results. [ABSTRACT FROM AUTHOR]

In water splitting, anode catalysts for the oxygen evolution reaction (OER), which is the rate‐determining step, are more critical than cathode catalysts. Herein, the authors prepare Ni‐IrOx composite catalysts consisting of NiO and IrO2 for the OER by a solid‐state reaction with different ratios of NiO to IrO2 and reaction temperatures. In particular, Ni‐IrOx‐400 with a molar ratio of NiO/IrO2 = 1:1 heated at 400 °C shows the best OER performance. In the overall water splitting test using an anion exchange membrane (AEM) water electrolyzer, the single cell with Ni‐IrOx‐400 as the anode catalyst shows current densities of 1454.8 mA cm−2, respectively, measured at 1.8 V. Furthermore, the stability tests of the AEM single cells are carried out at 50 °C under a constant current density of 500 mA cm−2. The single cell with Ni‐IrOx‐400 shows only a slight increase in the overpotential (rate: 2.0 mV h−1) for 100 h owing to the enhanced stability of Ni‐IrOx‐400 compared to IrO2 (12.5 mV h−1). The improved OER performance of the Ni‐IrOx‐400 may be attributed to a composite structure that can prevent particle agglomeration and thus preserve the active sites during the OER. [ABSTRACT FROM AUTHOR]