O1.1 Biological ageing
O1.1 Biological ageing
Chair: Hilde Heimli
O1.1.1 Bone mineral density of the distal forearm as a predictor of all-cause mortality.
The Tromsø Study
Annette Vogt Hauger1, Bjørn Heine Strand2, Astrid Bergland1, Kristin Holvik2, Agneta Ståhle3
1 OsloMet – Oslo Metropolitan University (formerly Oslo and Akershus University College of Applied Sciences), Norway
Norway, 2 Norwegian Institute of Public Health, Norway, 3 Karolinska institutet, Sweden
Low bone mineral density (BMD) is a strong risk factor for fractures. Among fragility fractures, hip fractures are associated with the largest mortality while excess mortality is lower or non-signiﬁcant after distal forearm fractures. We aimed to investigate if BMD of the distal forearm can predict all-cause mortality and if grip strength is an effect modifier.
The study population constituted 50-79 year-old men and women participating in the Tromsø 4-study conducted in 1994-5. Forearm BMD measured by SXA was categorized as “normal”, “osteopenia” or “osteoporosis” following WHO’s definition. Cox regression with all-cause mortality as the outcome over up to 22 years of follow-up was performed for men and women separately and adjusting for lifestyle- and health-related factors, as well as BMD by grip strength interaction.
Included in the analyses were 2 775 men and 3 849 women. During follow-up, 1 552 men and 1 459 women died. Those categorized as osteoporotic had higher mortality hazard ratio (HR) compared to those with normal BMD; Men HR=1.41 (95% CI 1.23, 1.63) and women HR=1.32 (1.14, 1.52), adjusted for age, body mass index, physical activity, smoking habits, education and grip strength. Men categorized as osteopenic also had significant higher mortality HR=1.13 (1.01, 1.27), but not women; HR=1.15 (0.99, 1.32). Grip strength was a significant effect modifier in men only.
Men and women with distal forearm BMD-values consistent with osteoporosis had an increased risk of all-cause mortality compared with people with normal BMD-values.
O1.1.2 A 30-years longitudinal study of malaria and telomere length dynamics in
Muhammad Asghar1, A.
Miglar1, M. Vafa-Homann1, S.
Babiker1, L. Mhoja1, M.
Johansson2, S. Jesaja2, I. Rooth1, A. Färnert1
1 Karolinska Institutet, Sweden, 2 Nyamisati Malaria Research Unit, Tanzania
Aging may be the cause of diseases but infectious diseases can also act as exogenous drivers of aging and the underlying mechanisms may include enhanced inflammation, pathogen-dependent tissue destruction, or accelerated cellular aging through increased cell turnover. We have shown that chronic asymptomatic malaria infections in birds resulted in reduced lifespan, mediated through faster telomere shortening, which occurs in multiple body tissues. In a recent study in Swedish travellers. Here, we have analysed how multiple malaria episodes affect telomere length dynamics in disease endemic area.
The study is based on repeated cross-sectional annual surveys in a population living in malaria endemic area in Nyamisati village in Tanzania. Samples were collected at the start of the long rain season, together with a general health assessment. Parasite prevalence declined from 90% in 1993 to 10% in 2010. We analysed the telomere length in peripheral blood samples (n = 2900) by real time quantitative PCR, from 1000 individuals longitudinally followed from 1986-2016.
We found a significant negative effect of age (p < 0.001) and parasite prevalence (p = 0.001) on telomere length in a longitudinal follow up in this population. Furthermore, there was a significant interaction of age x gender (p = 0.014), indicating that male and female have different pattern of telomere length dynamics. During early childhood (0-12 year), there was no gender specific telomere length difference. However, after puberty women showed significantly longer telomere length than men (p = 0.001). Malaria parasite prevalence at time of blood sampling was significantly negatively correlate
O1.1.3 Functional biological age as marker of systemic aging processes
Finkel1, Ola Sternäng2, Nancy Pedersen3
1 Indiana University Southeast, USA, 2 Jönköping University, Sweden, 3Karolinska institutet, Sweden
Background: Chronological age does not capture individual differences in the aging process, thus researchers have developed various mean to tap biological aging. Many studies have developed physiological measures of aging that require sophisticated measurements. Functional biological age (fBioAge) uses measures accessible from most epidemiological studies of aging to capture age changes in functioning of four body systems: sensory (vision and hearing), pulmonary (lung function), strength (grip strength), and movement/balance (gait).
Method: The Swedish Adoption/Twin Study of Aging provides longitudinal data from 8 waves covering up to 23 years from 740 individuals ranging in age from 47 to 87 at wave 1. Measures in the 4 domains are standardized, combined, and transformed to T-scores to create fBioAge. A two-slope age-based latent growth curve model (LGCM) was applied to the data.
Results: Results indicated an inflection point in rates of change at age 75: the rate of increase in fBioAge was twice as fast after age 75, compared with prior to age 75. Analysis of the impact of several covariates on the LGCM parameters indicated that most impacted the intercept, only. Thus, on average higher (i.e., older) fBioAge was indicated for women, individuals with less education, smokers, drinkers, individuals who reported more illnesses, and individuals who reported poorer subjective health. In a survival model, fBioAge predicted mortality outcomes.
Conclusions: fBioAge functions well as a measure of systemic age changes and can be used in studies that may not have the means to collect more physiological measures, such as telomere length or frailty.
O1.1.4 Parental age and sex affects mitochondrial DNA copy number in human blood
and in Drosophila melanoga
Anne-Marie Svane1, Cino
Pertoldi2, Torsten Nygård Kristensen2, Volker Loeschcke3, Axel Skytte1, Kaare Christensen1, Jacob
Hjelmborg1, Lene Christiansen1
1 University of Southern Denmark, 2 Aalborg University, Denmark, 3 Aarhus University, Denmark
The mitochondrion is a key energy supply and central in metabolism. The peripheral blood cell mitochondria content measure, mitochondria DNA copy number (mtDNA CN), correlates positively with better general health in humans, e.g. it declines with age in elderly individuals, and elevated mtDNA CN is observed in long lived individuals in population based cohorts. We have estimated the within-pair correlation of mtDNA CN in twin pairs from a middle-aged twin cohort (N=591 pairs) and an elderly twins cohort (N=291 pairs). The heritability was estimated to be 0.16 (95% CI (0.05, 0.27) for middle-aged twins. A very similar low heritability (0.18 (95% CI (0.03, 0.32)) was observed for elderly twins, and no effect of common environment was observed for either of the cohorts. However, monozygotic twins born to younger mothers (<30 years of age) were more identical in mtDNA CN than those born to older mothers (30+ years of age). Overall women had higher mtDNA CN than men, but unexpectedly the sex difference was larger for twins born to older mothers (40+ years of age) than those born to younger mothers (<40 years of age). We tested our results using the model species Drosophila melanogaster. Here we found that females generally had higher mtDNA CN than males, but that paternal age effected mtDNA CN of offspring in a highly sex and age specific pattern. In conclusion, both parental age and sex influence mtDNA CN in aging individuals.
O1.1.5 Poor sleep is associated with CSF-markers of Alzheimer’s disease in 70-year-olds
Johan Skoog, Kern Silke, Kaj Blennow, Henrik
Zetterberg, Boo Johansson, Thorvaldsson Valgeir, Ingmar Skoog
University of Gothenburg, Sweden
Background: It may be possible to detect changes in cerebrospinal fluid (CSF) markers decades before onset of Alzheimer’s disease (AD). In order to find possible targets for treatment and prevention there is a need to know more about the clinical correlates of this preclinical phase. The aim of this study was to study the associations between subjective sleep disturbance and CSF-markers of Alzheimer’s Disease in a population-based sample of 70-year-olds without dementia.
Methods: A population-based representative sample of 70-year-olds (N=1203, response rate=72%) were examined between year 2014-2016 with comprehensive neuropsychiatric examinations. A subsample of 322 individuals (26%) consented to a lumbar puncture. Seven individuals were excluded due to dementia, leaving 315 for the analyses. Sleep disturbance was assessed with two questions regarding a subjective experience of decreased or increased sleep during the past month. CSF-markers included Amyloid β (Aβ38, Aβ40, Aβ42, Aβ42/Aβ40), total-tau (t-tau), phospho-tau (p-tau), neurofilament light (NFL), and neurogranin. CSF-markers were analyzed in ratio to Aβ42. Multiple regression was used to study the associations between subjective sleep disturbance and CSF-markers while controlling for several factors.
Research results: Individuals with sleep disturbance had lower levels of Aβ42, Aβ42/Aβ40, and higher levels of t-tau/Aβ42, p-tau/Aβ42 and neurogranin/Aβ42 than those without. There were no significant associations between sleep disturbance and Aβ38, Aβ40 or NFL/Aβ42 levels.
Conclusions: Our findings provide evidence that poor sleep is associated with CSF-markers of preclinical Alzheimer’s disease. Future research need to elucidate whether sleep disturbance is a consequence or cause of preclinical Alzheimer’s disease