Background: Alzheimer's disease (AD) is a chronic and irreversible neurodegenerative disease. Oxidative stress emerges at the early AD stage. As a non-invasive therapy with few adverse reactions, transcutaneous electrical acupoint stimulation (TEAS) combines acupuncture points of traditional Chinese medicine (TCM) and electrical stimulation. This study aimed to investigate the amelioration effects of preventive TEAS treatment (P-TEAS) on cognitive impairment and oxidative stress in AD model rats. Methods: The AD model was established via subcutaneous injections of D-galactose (D-gal, 120 mg/kg/d) into the back of neck for 9 weeks in Sprague Dawley (SD) rats to simulate the oxidative stress in the early AD stage. On the first day of the 10th week, A beta(1-42) (1 mu g/mu l) was injected into the CA1 regions of the bilateral hippocampus. P-TEAS was synchronized from the first day of subcutaneous D-gal injections for 9 weeks. Results: Empirical measurements showed that P-TEAS can improve the spatial memory ability of AD model rats in the Morris water maze. Superoxide dismutase (SOD) was upregulated in the P-TEAS group. Through the detection of the anti-oxidative stress signaling pathway, namely, Kelch-like ECH-associated protein 1 (Keap1)/ NFE2-related factor 2 (Nrf2), it was found that P-TEAS could promote Nrf2 entering into the nucleus and upregulating the production of protective factors heme oxygenase 1 (HO-1) and NADPH quinone oxidoreductase 1 (NQO1). It was also found that P-TEAS could downregulate the expressions of BCL2-associated X-protein (Bax), caspase 3, and caspase 9 to inhibit neuronal apoptosis. Conclusions: P-TEAS has similar efficacy to electroacupuncture in preventing AD occurrence and development. P-TEAS is a new non-invasive intervention therapy for the prevention of AD. (c) 2023 Korea Institute of Oriental Medicine. Published by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/)

Background: Previous studies have shown that a diet with inflammatory and antioxidant properties can alter the risk of cognitive impairment. There are few studies using a large sample of the Chinese population. The specific relationship between inflammation, an antioxidant diet, and cognitive impairment remains unclear, and the potential impact of metabolic disorders remains to be determined. Methods: This is a cross-sectional study, with data from the China Health and Nutrition Survey (CHNS) in 2018. Individual and combined effects of the dietary inflammation index (DII) and composite dietary antioxidant index (CDAI) on cognitive impairment were assessed by binary logistic regression models. Nonlinear correlations and the inflection point were explored using restricted cubic splines (RCSs), and the mediation effects of triglyceride glucose–body mass index (TyG-BMI) were explored in greater depth using causal mediation analysis. Results: An increased CDAI was associated with a significantly decreased risk of cognitive impairment, at 0.68 (95%CI: 0.499–0.928). Contrary to this, the DII was positively associated with the risk of cognitive impairment, at 1.289 (95%CI: 1.03–1.613). The joint effects of the DII and CDAI indicated the minimal hazard effects on the risk of cognitive (0.787 (95%CI: 0.622–0.995)) impairment in subjects with low_DII + high_CDAI when compared with those with high_DII + low_CDAI. Furthermore, a significant nonlinear relationship was found between the CDAI and the risk of cognitive impairment, exhibiting an “L”-shaped curve (p-overall = 0.001, p-nonlinear = 0.007). However, no evidence was found for a nonlinear relationship between the DII and the risk of cognitive impairment. The mediation analysis did not reveal a mediating effect of TyG-BMI on the association between the CDAI and DII scores and the risk of cognitive impairment. Conclusions: Findings revealed that the CDAI could mitigate the adverse consequences of the DII on cognitive decline, which offers new insights into preventing early cognitive impairment through dietary intervention.

Assessing the predictive value of nutritional indices in trauma patients could provide a scientific basis for clinical nutritional interventions. Eight databases, including PubMed and Embase, were searched up to January 19, 2025. Case-control and cohort studies involving adult trauma patients were included, with low nutritional risk as the experimental group and high risk as the control group. Primary outcomes were mortality, hospital length of stay (LOS), and complications. Study quality was assessed using the NIH tool, and statistical analysis was performed using STATA 15.0. Effect models were selected based on the I² statistic, with results expressed as relative risk (RR) or weighted mean difference (WMD) with 95% confidence intervals (CI). Sensitivity analysis and publication bias assessment were conducted. Eighteen studies (11,275 patients) were included. Low nutritional indices were significantly associated with higher mortality (RR = 0.51; 95% CI: 0.36-0.72; P < 0.001), complications (RR = 0.68; 95% CI: 0.51-0.90; P = 0.008), and prolonged LOS (WMD = - 1.49; 95% CI: -2.20 to - 0.78; P < 0.001). Subgroup analysis showed the Mini Nutritional Assessment-Short Form (MNA-SF) had the strongest association with mortality, while the Prognostic Nutritional Index (PNI) was weakest. The Geriatric Nutritional Risk Index (GNRI) showed a non-significant trend for complications. Meta-regression indicated heterogeneity was not influenced by exposure type, sample size, or other factors. Sensitivity analysis confirmed robustness, with minimal publication bias. Nutritional indices effectively predict mortality, complications, and LOS in trauma patients, with higher scores linked to better outcomes, suggesting their utility as prognostic tools in trauma care.