Prevalence and possible factors of cognitive frailty in the elderly with hypertension and diabetes.

Background: Cognitive frailty is the coexistence of physical frailty and mild cognitive impairment. Research shows that cognitive frailty is related to an increased risk of hospitalization, mortality, disability, and dementia. Diabetes and hypertension are common risk factors for physical frailty and cognitive impairment. However, the factors influencing cognitive frailty in the elderly with hypertension and diabetes are still unclear. This study aimed to investigate the possible factors influencing cognitive frailty in the elderly with hypertension and diabetes. Methods: A cross-sectional study was conducted. We evaluated people over 60 years with hypertension and diabetes who underwent physical examination in Wuxi Xin'an Community Health Service Center. Frail scale, Montreal Cognitive Assessment-Basic and clinical dementia rating were used to assess cognitive frailty. We collected demographic characteristics, hypertension and diabetes-related laboratory indicators of the participants. We also used various scales to assess the overall health status of the elderly. Results: Approximately 20.8% of the participants were determined to have cognitive frailty in elderly adults with hypertension and diabetes. These participants were older, had a lower monthly income, and included a higher proportion of peasants. They also had a higher level of depression (p = 0.037), higher risk of falls (p = 0.000), higher risk of malnutrition (p = 0.002), poorer ability to perform activities of daily living (ADL) (p = 0.000), and less social support (p = 0.030). Multivariate regression analysis was used to further assess the factors for cognitive frailty. After adjusting for possible confounders, age and ADL score emerged as risk factors, whereas high monthly income decreased the risk of cognitive frailty. Conclusion: Cognitive frailty is correlated with age, income, and ability to perform daily living activities in the elderly with diabetes and hypertension. Closer attention to the elderly who have low income and poor self-care ability may play an important role in the early prevention of cognitive frailty and even dementia.

Wogonoside preserves against ischemia/reperfusion-induced myocardial injury by suppression of apoptosis, inflammation, and fibrosis via modulating Nrf2/HO-1 pathway.

OBJECTIVE: Myocardial ischemia/reperfusion (I/R) injury occurs after restoring blood supply, which brings about extra damage to heart tissue. Thus, exploring protection measures and underlying mechanisms appear to be particularly important. In this study, we investigated the cardioprotection of wogonoside against I/R injury in mice and further uncovered its mechanism. METHODS: Mice model of myocardial I/R injury was established by left anterior descending coronary artery (LAD). Before modeling, mice were administered the wogonoside (10, 20, and 40 mg/kg) for 7 d. To evaluate the effect of wogonoside through nuclear factor E2-associated factor 2/heme oxygenase-1 (Nrf2/HO-1) pathway, sh-Nrf2 was transfected into wogonoside-treated I/R mice. Subsequently, echocardiography detection, HE staining, western blotting, ELISA, TUNEL assay, and MASSON assay were utilized to evaluate the degree of myocardial injury. RESULTS: In I/R group, mice had severe myocardial injury, however, pretreatment of wogonoside at doses of 20 and 40 mg/kg ameliorated the cardiac function, as evidenced by improving hemodynamic parameters. Besides, wogonoside could relieved the abnormality of cardiomyocytes structure, inflammatory reaction, apoptosis, and myocardial fibrosis. Importantly, wogonoside activated the Nrf2/HO-1 pathway, as demonstrated by increasing Nrf2 expression in nucleus and its downstream genes including HO-1 and NADPH quinone oxidoreductase-1 (NQO1). However, effects of wogonoside on cardioprotection were abolished by sh-Nrf2. CONCLUSIONS: Wogonoside exerted the protective role against I/R-induced myocardial injury by suppression of apoptosis, inflammation, and fibrosis via activating Nrf2/HO-1 pathway.

Gut Microbiota and Targeted Biomarkers Analysis in Patients With Cognitive Impairment.

Gut microbial alteration is closely associated with brain disorders including cognitive impairment (CI). Gut microbes have the potential to predicate the development of diseases. However, the gut microbial markers for CI remain to be elucidated. In this study, the gut microbial alterations were assessed using16S rRNA sequencing, and identified the gut microbial markers using a random forest model. The results showed that there were significant gut microbial differences between the control and CI groups based on beta diversity (p < 0.002). Patients with CI had higher abundances of Actinobacteria and Proteobacteria but lower proportions of Bcateroidetes and Firmicutes vs. that in the control group. Patients had 39 special genera and the control subjects had 11 special genera. Furthermore, 11 genera such as Blautia, Roseburia, and Lactococcus and 18 genera such as Lactobacillus, Ruminococcus 2, and Akkermansia were the differential taxa in the control and CI groups, respectively. Gene functions related to nutrient metabolisms were upregulated in patients with CI. This suggested that the huge differences in gut microbes between the two groups and gut microbiota had the potential to predicate the development of CI. Based on machine learning results, 15 genera such as Lactobacillus, Bifidobacterium, and Akkermansia were selected as the optimal marker set to predicate CI with an area under curve (AUC) value of 78.4%. The results revealed the gut microbial markers for CI and provided a potential diagnosis tool to prevent the development of CI in the elderly.

Predictive Value of Gut Microbiome for Cognitive Impairment in Patients with Hypertension.

A connection exists between hypertension (HTN) and cognitive impairment (CI) or gut microbiota (GM) and neuropsychiatric disease. However, the link between GM and HTNCI has not been illustrated. This study endeavoured to profile the landscape of GM in HTNCI patients and evaluate the value of GM as HTNCI biomarkers. We recruited 128 patients with hypertension and assigned them to two groups of different MoCA scores. Clinical and biological data were recorded. GM composition was illustrated with 16S ribosomal RNA sequencing, and the dominant species were identified by linear discriminant analysis Effect Size (LEfSe). It showed higher abundance of TM7 and lower abundances of Veillonella and Peptoniphilus in the HTNCI group than in the HTN without cognitive impairment (HTNnCI) group. We next clarified the link between GM and MoCA scores or HTNCI factors. KEGG analysis revealed the involvement of decreased bile secretion. An evident correlation showed up between HTNCI and Veillonella abundance (P = 0.0340). We concluded that some representative GM species, especially Veillonella, could predict cognitive impairment in hypertension patients, making them potential benchmarks of HTNCI.

The diversity of gut microbiota in type 2 diabetes with or without cognitive impairment.

BACKGROUND: Diabetes is associated with a high risk of developing cognitive impairment, but the underlying mechanism remains unclear. Recent studies have found that gut microbiota may be involved in the progression of diabetes-associated cognitive impairment. AIMS: To analyze the diversity of gut microbiota in type 2 diabetes with or without cognitive impairment METHODS: 16S rRNA sequencing was used to detect the gut microbiota composition in 154 type 2 diabetes (T2DM) subjects RESULTS: Among 154 elderly T2DM participants included in our study, 73 with normal and 81 with impaired cognition. Lower levels of hemoglobin and HDL were observed in subjects with cognitive impairment. Patients with cognitive impairment had a lower abundance of Tenericutes. Comparison at the genus level revealed that T2DM patients with cognitive impairment had a decreased abundance of Bifidobacterium and unranked-RF39 and an increased abundance of Peptococcus and unranked-Leuconostocaceae. Additionally, the relative abundance of Veillonella and Pediococcus were decreased in subjects with cognitive impairment. Furthermore, the relative abundance of 7 sub-functions was significantly changed in the group with cognitive impairment. Calcium signaling pathways and the Renin-angiotensin system were upregulated in the cognitive impairment group while GnRH signaling, Fc gamma R-mediated phagocytosis, endocytosis, isoflavonoid biosynthesis, and cytochrome P450 were deregulated. CONCLUSION: Bifidobacterium may be associated with cognition in T2DM. Calcium signaling and renin-angiotensin system were shown to be associated with diabetes-associated cognitive impairment through gut microbiota.

[Curcumin attenuates left ventricular dysfunction and remodeling in rabbits with chronic heart failure.].

OBJECTIVE: To investigate the effects of Curcumin on rabbits with chronic heart failure. METHODS: Heart failure was induced by combined aortic regurgitation and aortic stenosis in 20 New Zealand rabbits and treated with placebo (HF, n = 10) and Curcumin (Cur, 100 mgxkg(-1)xd(-1), n = 10) for 8 weeks, 10 sham operated rabbits served as controls (Con). Echocardiography was performed in all rabbits at baseline and 8 weeks later. Aortic diameter (AO), left ventricular ejection fraction (LVEF), left ventricular fractional shortening (LVFS), left ventricular end-systolic dimension (LVDs), left ventricular end-diastolic dimension (LVDd), left ventricular posterior wall thickness (LVPW) and interventricular septum thickness (IVS) were measured. Myocardial matrix metalloproteinase (MMP)-2 and MMP-9 expressions and fibrosis were determined by immunohistochemistry and Masson staining respectively. RESULTS: Compared to baseline, LVEF and LVFS were significantly decreased, AO, LVDs, LVDd, LVPW, and IVS significantly increased at 8 weeks after operation in HF group while these changes could be significantly attenuated in Curcumin treated rabbits. The protein expressions of MMP-2 and MMP-9 were significantly down-regulated in HF group and could be significantly up-regulated by Curcumin treatment. The increased collagen deposition in HF group was also significantly reduced by Curcumin treatment. CONCLUSION: Curcumin attenuated left ventricular dysfunction and remodeling by up-regulating MMPs expressions and reducing myocardial fibrosis.