Peripheral high levels of CRP predict progression from normal cognition to dementia: A systematic review and meta-analysis.

OBJECTIVE: Several cross-sectional studies have demonstrated a relationship between inflammation and dementia. Uncertainty exists over the ability of C-reactive protein (CRP), one of the most investigated markers of inflammation, to predict the progression of normal cognition to dementia. A systematic review and meta-analysis were performed to assess whether high peripheral levels of CRP are associated with cognitive impairment and whether CRP is a risk factor for predicting progression from normal cognition to cognitive decline or dementia. METHODS: Literature published before November 2022 was retrieved from PubMed, Embase, and Web of Science. Prospective cohort studies that employed recognized evaluation instruments to assess global cognitive function or used accepted diagnostic criteria to ascertain dementia were selected. Subgroup analysis was conducted on specific cognitive domains and causes of dementia (i.e., Alzheimer's disease and vascular dementia). Odds ratios (ORs) and hazard ratios (HRs) were extracted and merged to facilitate data analysis. A random-effects model was used for the meta-analysis and a descriptive analysis of the data that could not be merged was conducted. RESULTS: A total of 13 articles (14 cohort studies) were included for meta-analysis and six articles were included for descriptive analysis. The results showed that high CRP levels were not related to future cognitive decline (OR = 1.115; 95 % CI: 0.830-1.497; p = 0.469) but were associated with an increased risk of conversion to dementia. (HR = 1.473; 95 % CI: 1.037-2.090; p = 0.0394). This association persisted after full adjustment for potential covariates, with an OR of 1.044 (95 % CI:0.767-1.421, p = 0.785) for cognitive decline and an HR of 1.429 (95 % CI:1.088-1.876, p = 0.010) for dementia. The subgroup analysis showed that a higher level of CRP was related to a decline in visual-spatial ability (OR = 1.402, 95 % CI: 1.045-1.882, p = 0.024) and the risk of conversion to vascular dementia (total effect size of OR and HR = 2.769, 95 % CI: 1.586-4.83, p = 0.000). CONCLUSIONS: Higher CRP levels as an indicator of chronic systemic inflammation cannot predict future cognitive decline but may indicate a higher risk of conversion to dementia.

Plasma ß-amyloid, tau, neurodegeneration biomarkers and inflammatory factors of probable Alzheimer's disease dementia in Chinese individuals.

Background: Plasma-derived ß-amyloid, tau, and neurodegeneration (ATN) biomarkers can accurately diagnose Alzheimer's disease (AD) and predict its progression. Few studies have investigated the relationship between plasma biomarkers and changes in plasma inflammatory markers in clinically diagnosed AD. Methods: Seventy-four participants were recruited, including 30 mild-to-moderate AD dementia patients and 44 normal controls (NC). All participants underwent neuropsychological testing and blood sampling for biomarker testing. AD was clinically diagnosed according to the National Institute on Aging-Alzheimer's Association (NIA-AA) core criteria and required age-mismatched hippocampal atrophy. We performed Single Molecule Array (Simoa), an ultra-sensitive enzyme-linked immunosorbent assay (ELISA), to examine plasma ATN markers, including ß-amyloid (Aß) 40, Aß42, p-tau181, total (t)-tau, neurofilament protein light chain (NfL), and inflammatory factors (TNF-α, IL-1ß, IL-6, and IL-8). Results: The level of the plasma Aß42/Aß40 ratio was significantly declined and the levels of the plasma p-tau181, NfL and TNF-α were significantly higher in the AD group than the NC group, but there was no significant difference in the levels of plasma t-tau, IL-1ß, IL-6, and IL-8 between the AD and NC groups. The levels of plasma p-tau181, NfL, Aß42/Aß40 ratio, and TNF-α were all associated with impairments in multiple cognitive domains. Among them, the plasma Aß42/Aß40 ratio, and the p-tau181 and TNF-α levels were associated with impairments in global cognition, memory, and visuospatial abilities, but not with executive function, only plasma NfL level was associated with executive function. Plasma NfL showed higher diagnostic performance in AD than in NC individuals (AUC = 0.833). A combined diagnostic prediction model of plasma Aß42/Aß40 ratio, p-tau 181, and NfL had the highest value than each factor alone (AUC = 0.902),with a sensitivity and specificity of 0.867 and 0.886, respectively. Conclusion: The levels of plasma ATN biomarkers (Aß42/Aß40 ratio, p-tua181, and NfL) were significantly changed in clinically diagnosed AD patients and they all associated with different domains of cognitive impairment. Plasma ATN biomarkers better differentiate mild-to-moderate AD dementia from NC when they are incorporated into diagnostic models together rather than individually. Plasma ATN biomarkers have the potential to be a screening tool for AD. However, the expression of inflammatory factors in AD patients requires further research.

A novel versatile instrument for combined studies of persistent luminescence, thermoluminescence, and mechanoluminescence in micro-scale.

This paper presents a new method for combined measurements of persistent luminescence (PersL), thermoluminescence (TL), and mechanoluminescence (ML) of luminescent materials in the micrometer scale. Both the hardware and software designs have been illustrated in detail, and the experimental procedures to execute the emission map, PersL, TL, and ML measurements have been demonstrated. The PersL, TL, and ML properties of the SrAl2O4:Eu2+, Dy3+ micropowder, as well as the corresponding temperature variable emission spectra, have been measured. The results show good agreement with published investigations, indicating the accomplishment of designed functions. The instrument would be a powerful tool for exploring phosphorescent materials in the micrometer and smaller scales.

Temperature-Dependent and Threshold Behavior of Sm3+ Ions on Fluorescence Properties of Lithium Niobate Single Crystals.

Temperature-dependent and threshold behavior of Sm3+ ions on fluorescence properties of lithium niobate (LiNbO3, LN) single crystals were systematically investigated. The test materials, congruent LiNbO3 single crystals (Sm:LN), with various concentrations of doped Sm3+ ions from 0.2 to 2.0 mol.%, were grown using the Czochralski technique. Absorption spectra were obtained at room temperature, and photoluminescence spectra were measured at various temperatures in the range from 73 K to 423 K. Judd⁻Ofelt theory was applied to calculate the intensity parameters Ωt (t = 2, 4, 6) for 1.0 mol.% Sm3+-doped LiNbO3, as well as the radiative transition rate, Ar, branching ratio, ß, and radiative lifetime, τr, of the fluorescent 4G5/2 level. Under 409 nm laser excitation, the photoluminescence spectra of the visible fluorescence of Sm3+ mainly contains 568, 610, and 651 nm emission spectra, corresponding to the energy level transitions of 4G5/2→6H5/2, 4G5/2→6H7/2, and 4G5/2→6H9/2, respectively. The concentration of Sm3+ ions has great impact on the fluorescence intensity. The luminescence intensity of Sm (1.0 mol.%):LN is about ten times as against Sm (0.2 mol.%):LN at 610 nm. The intensity of the fluorescence spectra were found to be highly depend on temperature, as well as the concentration of Sm3+ ions in LiNbO3 single crystals, as predicted; however, the lifetime changed little with the temperature, indicating that the temperature has little effect on it, in Sm:LN single crystals. Sm:LN single crystals, with orange-red emission spectra, can be used as the active material in new light sources, fluorescent display devices, UV-sensors, and visible lasers.

A feasible strategy for focal cerebral ischemia-reperfusion injury: remote ischemic postconditioning.

It is difficult to control the degree of ischemic postconditioning in the brain and other ischemia-sensitive organs. Remote ischemic postconditioning could protect some ischemia-sensitive organs through measures on terminal organs. In this study, a focal cerebral ischemia-reperfusion injury model was established using three cycles of remote ischemic postconditioning, each cycle consisted of 10-minute occlusion of the femoral artery and 10-minute opening. The results showed that, remote ischemic postconditioning significantly decreased the percentage of the infarct area and attenuated brain edema. In addition, inflammatory nuclear factor-κB expression was significantly lower, while anti-apoptotic Bcl-2 expression was significantly elevated in the cerebral cortex on the ischemic side. Our findings indicate that remote ischemic postconditioning attenuates focal cerebral ischemia/reperfusion injury, and that the neuroprotective mechanism is mediated by an anti-apoptotic effect and reduction of the inflammatory response.