Aging affects most living organisms and includes the processes that reduce health and survival. The chronological and the biological age of individuals can differ remarkably, and there is a lack of reliable biomarkers to monitor the consequences of aging. In this review we give an overview of commonly mentioned and frequently used potential aging-related biomarkers. We were interested in biomarkers of aging in general and in biomarkers related to cellular senescence in particular. To answer the question whether a biological feature is relevant as a potential biomarker of aging or senescence in the scientific community we used the PICO strategy known from evidence-based medicine. We introduced two scoring systems, aimed at reflecting biomarker relevance and measurement effort, which can be used to support study designs in both clinical and research settings.

Aging is a significant factor influencing the course of multiple sclerosis (MS). Accelerated telomere attrition is an indicator of premature biological aging and a potential contributor to various chronic diseases, including neurological disorders. However, there is currently a lack of studies focusing on telomere lengths in patients with MS. We measured the average leukocyte telomere length (LTL) in biobanked DNA samples of 40 relapsing-remitting MS patients (RRMS), 20 primary progressive MS patients (PPMS), and 60 healthy controls using a multiplex quantitative polymerase chain reaction method. Changes in LTL over a period of >10 years were evaluated in a subset of 10 patients. Association analyses of baseline LTL with the long-term clinical profiles of the patients were performed using inferential statistical tests and regression models adjusted for age and sex. The cross-sectional analysis revealed that the RRMS group was characterized by a significantly shorter relative LTL, on average, as compared to the PPMS group and controls. Shorter telomeres at baseline were also associated with a higher conversion rate from RRMS to secondary progressive MS (SPMS) in the 10-year follow-up. The LTL decrease over time was similar in RRMS patients and PPMS patients in the longitudinal analysis. Our data suggest a possible contributory role of accelerated telomere shortening in the pathobiology of MS. The interplay between disease-related immune system alterations, immunosenescence, and telomere dynamics deserves further investigation. New insights into the mechanisms of disease might be obtained, e.g., by exploring the distribution of telomere lengths in specific blood cell populations.

Telomerase can overcome replicative senescence by elongation of telomeres but is also a specific element in most cancer cells. It is expressed more vastly than any other tumor marker. Telomerase as a tumor target inducing replicative immortality can be overcome by only one other mechanism: alternative lengthening of telomeres (ALT). This limits the probability to develop resistance to treatments. Moreover, telomerase inhibition offers some degree of specificity with a low risk of toxicity in normal cells. Nevertheless, only one telomerase antagonist reached late preclinical studies. The underlying causes, the pitfalls of telomerase-based therapies, and future chances based on recent technical advancements are summarized in this review. Based on new findings and approaches, we propose a concept how long-term survival in telomerase-based cancer therapies can be significantly improved: the TICCA (Transient Immediate Complete and Combinatory Attack) strategy.

Short bowel syndrome results from extensive small bowel resection and induces adaptation of the remaining intestine. Ileocecal resection (ICR) is the most frequent situation in humans. Villus hypertrophy is one hallmark of mucosal adaptation, but the functional mechanisms of mucosal adaptation are incompletely understood.

Patients undergoing cardiac surgery are at increased cardiovascular risk, which includes altered lipid status. However, data on the effect of cardiac surgery and cardiopulmonary bypass (CPB) on plasma levels of key lipids are scarce. We investigated potential effects of CPB on plasma lipid levels and associations with early postoperative clinical outcomes. This is a prospective bio-bank study of patients undergoing elective cardiac surgery at our center January to December 2019. The follow-up period was 1 year after surgery. Blood sampling was performed before induction of general anesthesia, upon weaning from cardiopulmonary bypass (CPB), and on the first day after surgery. Clinical end points included the incidence of postoperative stroke, myocardial infarction, and death of any cause at 30 days after surgery as well as 1-year all-cause mortality. A total of 192 cardiac surgery patients (75% male, median age 67.0 years (interquartile range 60.0–73.0), median BMI 26.1 kg/m² (23.7–30.4)) were included. A significant intraoperative decrease in plasma levels compared with preoperative levels (all p < 0.0001) was observed for total cholesterol (TC) (Cliff’s delta d: 0.75 (0.68–0.82; 95% CI)), LDL-Cholesterol (LDL-C) (d: 0.66 (0.57–0.73)) and HDL-Cholesterol (HDL-C) (d: 0.72 (0.64–0.79)). At 24h after surgery, the plasma levels of LDL-C (d: 0.73 (0.650.79)) and TC (d: 0.77 (0.69–0.82)) continued to decrease compared to preoperative levels, while the plasma levels of HDL-C (d: 0.46 (0.36–0.55)) and TG (d: 0.40 (0.29–0.50)) rebounded, but all remained below the preoperative levels (p < 0.001). Mortality at 30 days was 1.0% (N = 2/192), and 1-year mortality was 3.8% (N = 7/186). Postoperative myocardial infarction occurred in 3.1% of patients (N = 6/192) and postoperative stroke in 5.8% (N = 11/190). Adjusting for age, sex, BMI, and statin therapy, we noted a protective effect of postoperative occurrence of stroke for pre-to-post-operative changes in TC (adjusted odds ratio (OR) 0.29 (0.07–0.90), p = 0.047), in LDL-C (aOR 0.19 (0.03–0.88), p = 0.045), and in HDL-C (aOR 0.01 (0.00–0.78), p = 0.039). No associations were observed between lipid levels and 1-year mortality. In conclusion, cardiac surgery induces a significant sudden drop in levels of key plasma lipids. This effect was pronounced during the operation, and levels remained significantly lowered at 24 h after surgery. The intraoperative drops in LDL-C, TC, and HDL-C were associated with a protective effect against occurrence of postoperative stroke in adjusted models. We demonstrate that the changes in key plasma lipid levels during surgery are strongly correlated, which makes attributing the impact of each lipid to the clinical end points, such as postoperative stroke, a challenging task. Large-scale analyses should investigate additional clinical outcome measures.