Although there is a consensus on the reduced levels of Aβ1-42 in the CSF of patients with AD, studies of plasma Aβ levels were inconsistent and have limited clinical value. We developed an immunomagnetic reduction assay (IMR) to determine the plasma levels of Aβ. We surveyed patients with varying AD severity (CDR = 0.5, n=16; CDR ≥ 1, n=18) and controls (n=26). Significant group differences were apparent in the levels of Aβ1-42 (F = 5.54, p = 0.002) and the Aβ1-42/Aβ1-40 ratio (F = 24.198, p < 0.001). Post-hoc analyses showed significant differences in the Aβ1-42 levels of controls and AD patients (p = 0.001) and in the Aβ1-42/Aβ1-40 ratio of control, MCI and AD subjects (all p ≤ 0.001). Regression analysis of Aβ1-42/Aβ1-40 ratios on dementia severity showed an adjusted R2 of 0.553 (p = 0.001). We identified a cut-off of 16.1 pg/ml for Aβ1-42 to differentiate control subjects from patients (both AD and MCI) with 85.3% sensitivity and 88.5% specificity. We also obtained a cut-off value of 0.303 for Aβ1-42/Aβ1-40 ratios with 85.3% sensitivity and 96.2% specificity. APOE 4 carriers had significantly higher Aβ1-42/Aβ1-40 ratios than the non-carriers (F = 4.839, p = 0.015). An independent group of case-control subjects validated both cut-off values for Aβ1-42/Aβ1-40 (100% sensitivity and 83.3% specificity) and for Aβ1-42 (100% sensitivity and 75.3% specificity). In a subgroup of longitudinal follow- up study, we found that the plasma Aβ was relatively stable with an interval of approximately 3 months. In conclusion, we found that the plasma Aβ1-42 is a useful biomarker for AD. The Aβ1-42/Aβ1-40 ratio improves the diagnostic power of the plasma Aβ biomarkers. The iron nanoparticles and IMR provides a novel method to measure plasma Aβ and could serve as an important clinical tool for the diagnosis of neurodegenerative diseases.
Objectives The objective of this study was to evaluate whether melatonin could ameliorate cognitive function in Ab 1-42 -induced mouse model and its underlying mechanisms. Methods Series behaviour tests were performed to demonstrate the amelioration of cognitive function of the Alzheimer's disease (AD) mice induced by Ab 1-42 . Additionally, enzyme-linked immunosorbent assay was applied to detect the expression of Ab 1-42 , BACE1 and p-tau protein in the brain of the AD mice. JC-1 was performed to investigate the role in alleviating mitochondrial damage by melatonin in vitro. Western blot was used to detect the expression of melatonin on apoptosis-related factors caspase-3 and Bcl-2, as well as the expressions of GSK-3b and PP2A to further determine the mechanisms of melatonin on the expression of p-tau protein.Key findings Melatonin significantly ameliorated the cognitive function and mitochondrial damage in AD mice, reduced the expression levels of GSK-3b, caspase-3, Ab 1-42 , BACE1, p-tau protein and increased the expressions of PP2A and Bcl-2. Conclusion From the overall results, we concluded that melatonin alleviated the mitochondrial damage effectively and decreased the expressions of the p-tau and some key proteins of apoptosis, leading to the improvement of cognitive function of the mice induced by Ab 1-42 .
Aim: Alumina nanoparticles (AlNPs) exert toxic effects in several organs. This study aimed to investigate the toxicity of AlNPs to the immune system. Materials & methods: AlNPs distribution was assessed using CRi in vivo fluorescence imaging. Inductively coupled plasma atomic emission spectrometry was used to detect the content of aluminum in the spleen. Cytokines expression was detected in the immune organs and blood of mice. Results & conclusion: AlNPs can accumulate in mice spleen. Superoxide dismutase and glutathione levels decreased, whereas the level of malondialdehyde increased with decreasing particle size. AlNPs exposure caused cytokine level changes in the spleen, thymus and serum, besides causing damage to immune organs and dysfunction of immune cells, leading to abnormal immune-related cytokine expression.
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