Age-associated Decline (age-associated + decline)

Distribution by Scientific Domains

Selected Abstracts

Modelling the Influence of Age, Body Size and Sex on Maximum Oxygen Uptake in Older Humans

Patrick J. Johnson
The purpose of this study was to describe the influence of body size and sex on the decline in maximum oxygen uptake (V,O2,max) in older men and women. A stratified random sample of 152 men and 146 women, aged 55-86 years, was drawn from the study population. Influence of age on V,O2,max, independent of differences in body mass (BM) or fat-free mass (FFM), was investigated using the following allometric model: V,O2,max= BMb (or FFMb) exp(a + (c age) + (d sex)) [epsilon]. The model was linearised and parameters identified using standard multiple regression. The BM model explained 68.8% of the variance in V,O2,max. The parameters ( s.e.e., standard error of the estimate) for lnBM (0.563 0.070), age (-0.0154 0.0012), sex (0.242 0.024) and the intercept (-1.09 0.32) were all significant (P < 0.001). The FFM model explained 69.3% of the variance in V,O2,max, and the parameters ( s.e.e) lnFFM (0.772 0.090), age (-0.0159 0.0012) and the intercept (-1.57 0.36) were significant (P < 0.001), while sex (0.077 +/, 0.038) was significant at P = 0.0497. Regardless of the model used, the age-associated decline was similar, with a relative decline of 15% per decade (0.984 exp(age)) in V,O2,max in older humans being estimated. The study has demonstrated that, for a randomly drawn sample, the age-related loss in V,O2,max is determined, in part, by the loss of fat-free body mass. When this factor is accounted for, the loss of V,O2,max across age is similar in older men and women. [source]

Trehalose extends longevity in the nematode Caenorhabditis elegans

AGING CELL, Issue 4 2010
Yoko Honda
Summary Trehalose is a disaccharide of glucose found in diverse organisms and is suggested to act as a stress protectant against heat, cold, desiccation, anoxia, and oxidation. Here, we demonstrate that treatment of Caenorhabditis elegans with trehalose starting from the young-adult stage extended the mean life span by over 30% without any side effects. Surprisingly, trehalose treatment starting even from the old-adult stage shortly thereafter retarded the age-associated decline in survivorship and extended the remaining life span by 60%. Demographic analyses of age-specific mortality rates revealed that trehalose extended the life span by lowering age-independent vulnerability. Moreover, trehalose increased the reproductive span and retarded the age-associated decrease in pharyngeal-pumping rate and the accumulation of lipofuscin autofluorescence. Trehalose also enhanced thermotolerance and reduced polyglutamine aggregation. These results suggest that trehalose suppressed aging by counteracting internal or external stresses that disrupt protein homeostasis. On the other hand, the life span-extending effect of trehalose was abolished in long-lived insulin/IGF-1-like receptor (daf-2) mutants. RNA interference-mediated inactivation of the trehalose-biosynthesis genes trehalose-6-phosphate synthase-1 (tps-1) and tps-2, which are known to be up-regulated in daf-2 mutants, decreased the daf-2 life span. These findings indicate that a reduction in insulin/IGF-1-like signaling extends life span, at least in part, through the aging-suppressor function of trehalose. Trehalose may be a lead compound for potential nutraceutical intervention of the aging process. [source]

The effect of caloric restriction interventions on growth hormone secretion in nonobese men and women

AGING CELL, Issue 1 2010
Leanne M. Redman
Summary Lifespan in rodents is prolonged by caloric restriction (CR) and by mutations affecting the somatotropic axis. It is not known if CR can alter the age-associated decline in growth hormone (GH), insulin-like growth factor (IGF)-1 and GH secretion. To evaluate the effect of CR on GH secretory dynamics; forty-three young (36.8 1.0 years), overweight (BMI 27.8 0.7) men (n = 20) and women (n = 23) were randomized into four groups; control = 100% of energy requirements; CR = 25% caloric restriction; CR + EX = 12.5% CR + 12.5% increase in energy expenditure by structured exercise; LCD = low calorie diet until 15% weight reduction followed by weight maintenance. At baseline and after 6 months, body composition (DXA), abdominal visceral fat (CT) 11 h GH secretion (blood sampling every 10 min for 11 h; 21:00,08:00 hours) and deconvolution analysis were measured. After 6 months, weight (control: ,1 1%, CR: ,10 1%, CR + EX: ,10 1%, LCD: ,14 1%), fat mass (control: ,2 3%, CR: ,24 3%, CR + EX: ,25 3%, LCD: ,31 2%) and visceral fat (control: ,2 4%, CR: ,28 4%, CR + EX: ,27 3%, LCD: ,36 2%) were significantly (P < 0.001) reduced in the three intervention groups compared to control. Mean 11 h GH concentrations were not changed in CR or control but increased in CR + EX (P < 0.0001) and LCD (P < 0.0001) because of increased secretory burst mass (CR + EX: 34 13%, LCD: 27 22%, P < 0.05) and amplitude (CR + EX: 34 14%, LCD: 30 20%, P < 0.05) but not to changes in secretory burst frequency or GH half-life. Fasting ghrelin was significantly increased from baseline in all three intervention groups; however, total IGF-1 concentrations were increased only in CR + EX (10 7%, P < 0.05) and LCD (19 4%, P < 0.001). A 25% CR diet for 6 months does not change GH, GH secretion or IGF-1 in nonobese men and women. [source]

Mild Parkinsonian signs: An overview of an emerging concept

Elan D. Louis MD
Abstract Mild Parkinsonian signs (MPS) include gait and balance changes, rigidity, bradykinesia, and tremor. MPS can occur commonly during the clinical examination of older people who do not have known neurological disease, with prevalence estimates for MPS as a whole ranging from 15% to 95%. MPS are generally progressive and they are coupled with functional difficulties, impaired gait and balance, and increased risks of mild cognitive impairment, dementia, and mortality. The mechanistic basis for these signs is unclear, but is likely to be multifactorial, with possible factors including an age-associated decline in dopaminergic nigrostriatal activity, the early development of neurodegenerative (Lewy body or Alzheimer's type) pathologies in the basal ganglia, or the accumulation of vascular pathology in the brain. It would be valuable to identify those individuals with MPS who are at increased risk for the development of future Alzheimer's disease, full-blown Parkinson's disease, or strokes, and to develop therapeutic strategies to intervene to lessen the likelihood of MPS-related morbidity and mortality. 2007 Movement Disorder Society [source]

The age-related decrease in CNS remyelination efficiency is caused by an impairment of both oligodendrocyte progenitor recruitment and differentiation

C. Zhao
Developing strategies to reverse the age-associated decline in CNS remyelination requires the identification of how the regenerative process is impaired. We have addressed whether remyelination becomes slower because of an impairment of recruitment of oligodendrocyte progenitors (OPs) or, an impairment of OP differentiation into remyelinating oligodendrocytes. The OP response during remyelination of focal, toxin-induced CNS demyelination in young and old rats was compared by in situ hybridization using probes to PGDF-,R, and the OP transcription factor, MyT1. The expression patterns for both OP markers are very similar and reveal a delay in the colonization of the demyelinated focus with OPs in the old animals compared to young. By comparing the mRNA expression pattern MyT1 with that of the myelin proteins MBP and Gtx, we have found that in the old animals there is also a delay in OP differentiation, which increases with longer survival times. These results indicate that the age-associated decrease in remyelination efficiency occurs because of an impairment of OP recruitment and their subsequent differentiation into remyelinating oligodendrocytes, and that strategies aimed at ameliorating the age-associated decline in remyelination efficiency will therefore need to promote both components of the regenerative process. [source]

Tracing thymic output in older individuals

W. A. Mitchell
Summary As a result of age-associated thymic atrophy, T cell production declines with age. Some studies suggest that production undergoes an exponential decline starting at birth, while others consider the decline to be in a biphasic manner with a rapid reduction in output occurring before middle age followed by a phase in which output declines at a regular, albeit much slower, rate. Both approaches provide estimations of the time of termination of thymic output, but on the basis of limited amounts of data. We have analysed blood from more than 200 individuals between the ages of 58 and 104 years to determine changes in thymic output using signal-joint T cell receptor excision circles (sjTREC)/T cells as our measure. To reduce any potential geographical or nutritional bias we have obtained samples from five different European countries. Our results reveal that while the absolute number of T cells per microlitre of blood does not change significantly across the age range we tested, the values of sjTREC per microlitre show wide variation and reveal an age-associated decline in thymic output. In addition we show gender differences, with notably higher thymic output in females than males at each decade. More importantly, we noted a significant decline in sjTREC/T cell levels in those more than 90 years of age in both males and females. Our results provide information about the potential end-point for thymic output and suggest that sjTREC analysis may be a biomarker of effective ageing. [source]

Prevalence of adrenal androgen excess in patients with the polycystic ovary syndrome (PCOS)

Ashim Kumar
Summary Objective, To determine the prevalence of adrenal androgen (AA) excess in the polycystic ovary syndrome (PCOS) using age- and race-specific normative values. Design, Cross-sectional observational study. Patients, One hundred and eight-two (88 Black and 94 White) age-matched healthy eumenorrhoeic nonhirsute women (controls) and 213 (27 Black and 186 White) women with PCOS were recruited. Measurements, Total testosterone (T), free T, androstenedione (A4), dehydroepiandrosterone sulfate (DHEAS) and SHBG, as well as fasting insulin and glucose, were measured in plasma. Results, The mean total T, free T, A4, DHEAS and body mass index (BMI) were higher in women with PCOS than in control women. DHEAS levels were significantly lower in Black controls than White controls, whereas fasting insulin and BMI were higher in Black controls. In control and Black PCOS women, DHEAS levels did not correlate with BMI, waist-to-hip ratio (WHR) or fasting insulin. Among White women with PCOS, DHEAS levels correlated negatively with BMI and fasting insulin. DHEAS levels decreased similarly with age in control and PCOS women of either race. For each race and age group the upper 95% normative values for log DHEAS was calculated, and the number of PCOS subjects with log DHEAS values above this level were assessed. The prevalence of supranormal DHEAS levels was 333% and 199%, respectively, among Black and White women with PCOS. Conclusions, The prevalence of DHEAS excess is approximately 20% among White and 30% among Black PCOS patients, when using age- and race-adjusted normative values. This study also indicates that the age-associated decline in DHEAS levels is observable and similar in both control and PCOS women, regardless of race. While BMI and fasting insulin had little impact on circulating DHEAS levels in healthy women, among White PCOS patients these parameters were negatively associated with circulating DHEAS levels. [source]