Age and Ageing

BackgroundImmunity and inflammation may be essential to the pathogenesis of dementia. However, the association of immune-mediated diseases with the risk of incident dementia has not been well characterised.ObjectivesWe aimed to investigate the prospective association of 27 immune-mediated diseases and incident dementia risk and to explore the underlying mechanisms driven by brain structures.MethodsWe included 487 459 UK Biobank participants aged 37–73 years without dementia at enrolment. Immune-mediated diseases and dementia cases were ascertained according to the International Classification of Diseases codes. Time-varying Cox proportional hazards regression and general linear regression models were used to examine the association of immune-mediated disease with incident dementia risk and brain morphometric measures, respectively.ResultsOver a median follow-up of 12.3 years, 1654 cases of incident dementia were documented in 86 243 patients with immune-mediated diseases. Overall, immune-mediated diseases were associated with a higher all-cause dementia risk (hazard ratio [HR], 1.24; 95% confidence interval, 1.17–1.32). Five out of 27 immune-mediated diseases were associated with an increased risk of dementia individually. Comorbidity of multiple immune-mediated diseases further increased the risk. Moreover, the immune-mediated disease was associated with smaller total surface areas of both left (β, −286.51; SE, 102.58; P = .014) and right hemispheres (β, −298.56; SE, 103.96; P = .016), greater white matter hyperintensities volume (β, 1.02; SE, 0.13; P < .001) and less healthy white matter microstructures.ConclusionsImmune-mediated diseases were associated with an increased risk of incident dementia, and the association of those diseases with brain structural abnormalities might provide clues to the underlying mechanisms.

doi: 10.1093/ageing/afae263pmid: 39656763

BackgroundFrailty, malnutrition and low socioeconomic status may mutually perpetuate each other in a self-reinforcing and interdependent manner. The intertwined nature of these factors may be overlooked when investigating impacts on perioperative outcomes. This study aimed to investigate the impact of frailty, malnutrition and socioeconomic status on perioperative outcomes.MethodsA multicentre cohort study involving six Australian tertiary hospitals was undertaken. All consecutive surgical patients who underwent an operation were included. Frailty was defined by the Hospital Frailty Risk Score, malnutrition by the Malnutrition Universal Screening Tool (MUST) and low socioeconomic status by the Index of Relative Socioeconomic Disadvantage. Linear mixed-effects and binary logistic generalised estimated equation models were performed for the outcomes: inpatient mortality, length of stay, 30-day readmission and re-operation.ResultsA total of 21 976 patients were included. After controlling for confounders, malnutrition and socioeconomic status, patients at high risk of frailty have a mean hospital length of stay 3.46 times longer (mean ratio = 3.46; 95% confidence interval (CI): 3.20, 3.73; P value < .001), odds of 30-day readmission 2.4 times higher (odds ratio = 2.40; 95% CI: 2.19, 2.63; P value < .001) and odds of in-hospital mortality 12.89 times greater than patients with low risk of frailty (odds ratio = 12.89; 95% CI: 4.51, 36.69; P value < .001). Elevated MUST scores were also significantly associated with worse outcomes, but to a lesser extent. Socioeconomic status had no association with outcomes.ConclusionPerioperative risk evaluation should consider both frailty and malnutrition as separate, significant risk factors. Despite strong causal links with frailty and malnutrition, socioeconomic disadvantage is not associated with worse postoperative outcomes. Additional studies regarding the prospective identification of these patients with implementation of strategies to mitigate frailty and malnutrition and assessment of perioperative risk are required.

ObjectivesTo investigate the effects of non-pharmacological treatments on sarcopenic obesity (SO).MethodsA search for randomized controlled trials (RCTs) on SO was conducted in PubMed, Web of Science, CINAHL, CENTRAL, SPORTDiscus, CNKI, Wanfang and VIP. A meta-analysis was conducted using random-effects models for MDs.ResultsThe meta-analysis on 21 RCTs showed that exercise improved PBF (MD: −1.67%, p < .01, I2 = 35%), grip strength (MD: 2.2 kg, p = .03, I2 = 61%), GS (MD: 0.08 m/s, p = .02, I2 = 0%), TCR (MD: 2.22 repetitions, p < .01, I2 = 0%), TUG (MD: −1.48 s, p < .01, I2 = 61%), UE strength (MD: 1.88 kg/kg, p < .01, I2 = 0%) and LE strength (MD: 2.19 kg/kg, p < .01, I2 = 0%). Nutritional interventions improved grip strength (MD: 1.52 kg, p < .01, I2 = 0%). Combine interventions improved PBF (MD: −1.97%, p < .01, I2 = 38%), ASMM (MD: 0.4 kg, p < .01, I2 = 6%), grip strength (MD: 1.83 kg, p < .01, I2 = 38%) and GS (MD: 0.04 m/s, p < .01, I2 = 0%). Combined interventions were more effective than nutrition alone for reducing PBF (MD: −0.8%, p = .05, I2 = 0%).ConclusionThe effects of exercise and nutrition interventions on SO are limited individually, especially regarding muscle mass, but their combination can yield optimal results. Additionally, physical therapy also demonstrated some potential.