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Published By Springer-Verlag

2509-2723, 2509-2715
Updated Sunday, 28 November 2021

GeroScience ◽  
2021 ◽  
Author(s):  
Lilla István ◽  
Cecilia Czakó ◽  
Fruzsina Benyó ◽  
Ágnes Élő ◽  
Zsuzsa Mihály ◽  
...  

AbstractCarotid artery stenosis (CAS) is among the leading causes of mortality and permanent disabilities in the Western world. CAS is a consequence of systemic atherosclerotic disease affecting the majority of the aging population. Optical coherence tomography angiography (OCTA) is a novel imaging technique for visualizing retinal blood flow. It is a noninvasive, fast method for qualitative and quantitative assessment of the microcirculation. Cerebral and retinal circulation share similar anatomy, physiology, and embryology; thus, retinal microvasculature provides a unique opportunity to study the pathogenesis of cerebral small vessel disease in vivo. In this study, we aimed to analyze the effect of systemic risk factors on retinal blood flow in the eyes of patients with significant carotid artery stenosis using OCT angiography. A total of 112 eyes of 56 patients with significant carotid stenosis were included in the study. We found that several systemic factors, such as decreased estimated glomerular filtration rate (eGFR), hypertension, and carotid occlusion have a significant negative effect on retinal blood flow, while statin use and carotid surgery substantially improve ocular microcirculation. Neither diabetes, clopidogrel or acetylsalicylic acid use, BMI, serum lipid level, nor thrombocyte count showed a significant effect on ocular blood flow. Our results demonstrate that a systematic connection does exist between certain systemic risk factors and retinal blood flow in this patient population. OCTA could help in the assessment of cerebral circulation of patients with CAS due to its ability to detect subtle changes in retinal microcirculation that is considered to represent changes in intracranial blood flow.


GeroScience ◽  
2021 ◽  
Author(s):  
Setor K. Kunutsor ◽  
Samuel Seidu ◽  
Jari A. Laukkanen

AbstractThe beneficial effects of regular physical activity in promoting health and preventing chronic diseases are well documented. The relationship between regular physical activity and the risk of pneumonia is uncertain. We aimed to evaluate the magnitude and specificity of the prospective association between regular physical activity and the risk of pneumonia using a systematic review and meta-analysis of published observational cohort studies in general populations. Relevant studies with at least 1 year of follow-up were sought from inception until 15 September 2021 in MEDLINE, Embase, Web of Science, and manual search of relevant articles. Relative risks (RRs) with 95% confidence intervals (CIs) for the maximum versus the minimal amount of physical activity groups were pooled using fixed effects meta-analysis. The quality of the evidence was evaluated using the GRADE tool. A total of 10 prospective cohort studies comprising 1,044,492 participants and 7681 events were eligible. The pooled multivariable-adjusted RR (95% CI) of pneumonia comparing the most versus the least physically active groups was 0.69 (0.64–0.74). This association was significantly modified by type of outcome (p-value for meta-regression = .002): 0.82 (0.72–0.93) for incident pneumonia and 0.64 (0.59–0.70) for pneumonia-related mortality. There was no evidence of heterogeneity and publication bias. The GRADE quality of the evidence ranged from moderate to low. Aggregate analysis of 10 cohort studies shows that regular physical activity is associated with lowered risk of incident pneumonia and pneumonia-related mortality in the general population. Physical activity types that are attractive to and feasible for high-risk populations need to be identified and encouraged. Systematic review registration: PROSPERO 2021: CRD42021277514.


GeroScience ◽  
2021 ◽  
Author(s):  
Marco Raffaele ◽  
Kristina Kovacovicova ◽  
Tommaso Biagini ◽  
Oriana Lo Re ◽  
Jan Frohlich ◽  
...  

GeroScience ◽  
2021 ◽  
Author(s):  
Maud van Dinther ◽  
Miranda T. Schram ◽  
Jacobus F. A. Jansen ◽  
Walter H. Backes ◽  
Alfons J. H. M. Houben ◽  
...  

Abstract Background Cerebral small vessel disease (cSVD) is a late consequence of cerebral microvascular dysfunction (MVD). MVD is hard to measure in the brain due to its limited accessibility. Extracerebral MVD (eMVD) measures can give insights in the etiology of cerebral MVD, as MVD may be a systemic process. We aim to investigate whether a compound score consisting of several eMVD measures is associated with structural cSVD MRI markers. Methods Cross-sectional data of the population-based Maastricht Study was used (n = 1872, mean age 59 ± 8 years, 49% women). Measures of eMVD included flicker light-induced retinal arteriolar and venular dilation response (retina), albuminuria and glomerular filtration rate (kidney), heat-induced skin hyperemia (skin), and plasma biomarkers of endothelial dysfunction (sICAM-1, sVCAM-1, sE-selectin, and von Willebrand factor). These measures were standardized into z scores and summarized into a compound score. Linear and logistic regression analyses were used to investigate the associations between the compound score and white matter hyperintensity (WMH) volume, and the presence of lacunes and microbleeds, as measured by brain MRI. Results The eMVD compound score was associated with WMH volume independent of age, sex, and cardiovascular risk factors (St β 0.057 [95% CI 0.010–0.081], p value 0.01), but not with the presence of lacunes (OR 1.011 [95% CI 0.803–1.273], p value 0.92) or microbleeds (OR 1.055 [95% CI 0.896–1.242], p value 0.52). Conclusion A compound score of eMVD is associated with WMH volume. Further research is needed to expand the knowledge about the role of systemic MVD in the pathophysiology of cSVD.


GeroScience ◽  
2021 ◽  
Author(s):  
Ana Stojiljković ◽  
Véronique Gaschen ◽  
Franck Forterre ◽  
Ulrich Rytz ◽  
Michael H. Stoffel ◽  
...  

GeroScience ◽  
2021 ◽  
Author(s):  
Nadine Bahour ◽  
Briana Cortez ◽  
Hui Pan ◽  
Hetal Shah ◽  
Alessandro Doria ◽  
...  

AbstractChronological age (CA) is determined by time of birth, whereas biological age (BA) is based on changes on a cellular level and strongly correlates with morbidity, mortality, and longevity. Type 2 diabetes (T2D) associates with increased morbidity and mortality; thus, we hypothesized that BA would be increased and calculated it from biomarkers collected at routine clinical visits. Deidentified data was obtained from three cohorts of patients (20–80 years old)—T2D, type 1 diabetes (T1D), and prediabetes—and compared to gender- and age-matched non-diabetics. Eight clinical biomarkers that correlated with CA in people without diabetes were used to calculate BA using the Klemera and Doubal method 1 (KDM1) and multiple linear regression (MLR). The phenotypic age (PhAge) formula was used with its predetermined biomarkers. BA of people with T2D was, on average, 12.02 years higher than people without diabetes (p < 0.0001), while BA in T1D was 16.32 years higher (p < 0.0001). Results were corroborated using MLR and PhAge. The biomarkers with the strongest correlation to increased BA in T2D using KDM were A1c (R2 = 0.23, p < 0.0001) and systolic blood pressure (R2 = 0.21, p < 0.0001). BMI had a positive correlation to BA in non-diabetes subjects but disappeared in those with diabetes. Mortality data using the ACCORD trial was used to validate our results and showed a significant correlation between higher BA and decreased survival. In conclusion, BA is increased in people with diabetes, irrespective of pathophysiology, and to a lesser extent in prediabetes.


GeroScience ◽  
2021 ◽  
Author(s):  
Andrea Ágnes Molnár ◽  
György László Nádasy ◽  
Gabriella Dörnyei ◽  
Bernadett Bettina Patai ◽  
Jordan Delfavero ◽  
...  

Abstract Aging-induced pathological alterations of the circulatory system play a critical role in morbidity and mortality of older adults. While the importance of cellular and molecular mechanisms of arterial aging for increased cardiovascular risk in older adults is increasingly appreciated, aging processes of veins are much less studied and understood than those of arteries. In this review, age-related cellular and morphological alterations in the venous system are presented. Similarities and dissimilarities between arterial and venous aging are highlighted, and shared molecular mechanisms of arterial and venous aging are considered. The pathogenesis of venous diseases affecting older adults, including varicose veins, chronic venous insufficiency, and deep vein thrombosis, is discussed, and the potential contribution of venous pathologies to the onset of vascular cognitive impairment and neurodegenerative diseases is emphasized. It is our hope that a greater appreciation of the cellular and molecular processes of vascular aging will stimulate further investigation into strategies aimed at preventing or retarding age-related venous pathologies.


GeroScience ◽  
2021 ◽  
Author(s):  
Johannes T. Neumann ◽  
Le T. P. Thao ◽  
Emily Callander ◽  
Enayet Chowdhury ◽  
Jeff D. Williamson ◽  
...  

AbstractIdentification of individuals with increased risk of major adverse cardiovascular events (MACE) is important. However, algorithms specific to the elderly are lacking. Data were analysed from a randomised trial involving 18,548 participants ≥ 70 years old (mean age 75.4 years), without prior cardiovascular disease events, dementia or physical disability. MACE included coronary heart disease death, fatal or nonfatal ischaemic stroke or myocardial infarction. Potential predictors tested were based on prior evidence and using a machine-learning approach. Cox regression analyses were used to calculate 5-year predicted risk, and discrimination evaluated from receiver operating characteristic curves. Calibration was also assessed, and the findings internally validated using bootstrapping. External validation was performed in 25,138 healthy, elderly individuals in the primary care environment. During median follow-up of 4.7 years, 594 MACE occurred. Predictors in the final model included age, sex, smoking, systolic blood pressure, high-density lipoprotein cholesterol (HDL-c), non-HDL-c, serum creatinine, diabetes and intake of antihypertensive agents. With variable selection based on machine-learning, age, sex and creatinine were the most important predictors. The final model resulted in an area under the curve (AUC) of 68.1 (95% confidence intervals 65.9; 70.4). The model had an AUC of 67.5 in internal and 64.2 in external validation. The model rank-ordered risk well but underestimated absolute risk in the external validation cohort. A model predicting incident MACE in healthy, elderly individuals includes well-recognised, potentially reversible risk factors and notably, renal function. Calibration would be necessary when used in other populations.


GeroScience ◽  
2021 ◽  
Author(s):  
Danut-Adrian Dumbrava ◽  
Roxana Surugiu ◽  
Verena Börger ◽  
Mihai Ruscu ◽  
Tobias Tertel ◽  
...  

AbstractSmall extracellular vesicles (sEVs) obtained from mesenchymal stromal cells (MSCs) promote neurological recovery after middle cerebral artery occlusion (MCAO) in young rodents. Ischemic stroke mainly affects aged humans. MSC-sEV effects on stroke recovery in aged rodents had not been assessed. In a head-to-head comparison, we exposed young (4–5 months) and aged (19–20 months) male Sprague–Dawley rats to permanent distal MCAO. At 24 h, 3 and 7 days post-stroke, vehicle or MSC-sEVs (2 × 106 or 2 × 107 MSC equivalents/kg) were intravenously administered. Neurological deficits, ischemic injury, brain inflammatory responses, post-ischemic angiogenesis, and endogenous neurogenesis were evaluated over 28 days. Post-MCAO, aged vehicle-treated rats exhibited more severe motor-coordination deficits evaluated by rotating pole and cylinder tests and larger brain infarcts than young vehicle-treated rats. Although infarct volume was not influenced by MSC-sEVs, sEVs at both doses effectively reduced motor-coordination deficits in young and aged rats. Brain macrophage infiltrates in periinfarct tissue, which were evaluated as marker of a recovery-aversive inflammatory environment, were significantly stronger in aged than young vehicle-treated rats. sEVs reduced brain macrophage infiltrates in aged, but not young rats. The tolerogenic shift in immune balance paved the way for structural brain tissue remodeling. Hence, sEVs at both doses increased periinfarct angiogenesis evaluated by CD31/BrdU immunohistochemistry in young and aged rats, and low-dose sEVs increased neurogenesis in the subventricular zone examined by DCX/BrdU immunohistochemistry. Our study provides robust evidence that MSC-sEVs promote functional neurological recovery and brain tissue remodeling in aged rats post-stroke. This study encourages further proof-of-concept studies in clinic-relevant stroke settings.


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