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Age-related Loss (age-related + loss)
Selected AbstractsModelling the Influence of Age, Body Size and Sex on Maximum Oxygen Uptake in Older HumansEXPERIMENTAL PHYSIOLOGY, Issue 2 2000Patrick 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] Evidence of a hypermineralised calcified fibrocartilage on the human femoral neck and lesser trochanterJOURNAL OF ANATOMY, Issue 2 2001J. E. SHEA Femoral neck fractures are a major cause of morbidity and mortality in elderly humans. In addition to the age-related loss of cancellous bone, changes to the microstructure and morphology of the metaphyseal cortex may be a contributing factor in osteoporotic hip fractures. Recent investigations have identified a hypermineralised tissue on the neck of the femur and trochanteric region that increases in fractional area with advancing age in both males (Boyce & Bloebaum, 1993) and females (Vajda & Bloebaum, 1999). The aim of this study was to determine if the hypermineralised tissue previously observed on the proximal femur is calcified fibrocartilage. Regional variations in the fractional area of hypermineralised tissue, cortical bone, and porosity of the cortical bone along the neck of the femur and lesser trochanter were also quantified. Comparison of back scattered electron and light microscope images of the same area show that regions of hypermineralised tissue correlate with the regions of calcified fibrocartilage from tendon and capsular insertions. The hypermineralised tissue and calcified fibrocartilage had similar morphological features such as the interdigitations of the calcified fibrocartilage into the bone, lacunar spaces, and distinctly shaped pores adjacent to the 2 tissues. Regions of the neck that did not contain insertions were covered with periosteum. There were no regional differences (P > 0.05) on the superior and inferior femoral neck in terms of the percentage area of hypermineralised calcified fibrocartilage, cortical bone, or cortical bone porosity. The lesser trochanter exhibited regional differences in the fractional area of hypermineralised calcified fibrocartilage (P = 0.007) and cortical bone (P = 0.007) but not porosity of the cortical bone (P > 0.05). The effects of calcified fibrocartilage on femoral neck periosteal expansion, repair, and mechanics are unknown, but may play a role in osteoporotic fractures and intracapsular fracture healing. [source] Reduced EBF expression underlies loss of B-cell potential of hematopoietic progenitors with ageAGING CELL, Issue 3 2010Chloé Lescale Summary Aging is accompanied by a reduction in the generation of B lymphocytes leading to impaired immune responses. In this study, we have investigated whether the decline in B lymphopoiesis is due to age-related defects in the hematopoietic stem cell compartment. The ability of hematopoietic stem cells from old mice to generate B cells, as measured in vitro, is decreased 2,5-fold, while myeloid potential remains unchanged. This age-related decrease in B-cell potential is more marked in common lymphoid progenitors (CLP) and was associated with reduced expression of the B-lineage specifying factors, EBF and Pax5. Notably, retrovirus-mediated expression of EBF complemented the age-related loss of B-cell potential in CLP isolated from old mice. Furthermore, transduction of CLP from old mice with a constitutively active form of STAT5 restored both EBF and Pax5 expression and increased B-cell potential. These results are consistent with a mechanism, whereby reduced expression of EBF with age decreases the frequency with which multipotent hematopoietic progenitors commit to a B-cell fate, without altering their potential to generate myeloid cells. [source] Stem Cell Review Series: Regulating highly potent stem cells in aging: environmental influences on plasticityAGING CELL, Issue 4 2008Jay M. Edelberg Summary Significant advances in the past decade have revealed that a large number of highly plastic stem cells are maintained in humans through adulthood and are present even in older adults. These findings are notable in light of the reduced capacity for repair and regeneration in older tissues. The apparent dichotomy can be reconciled through an appreciation of the age-associated changes in the microenvironmental pathways that govern adult stem cell plasticity and differentiation patterns. Specifically, the recent identification of the age-related loss of the local platelet-derived growth factor signals that promote the induction of cardiac myocytes from Oct-3/4+ bone marrow stem cells, rather than impairment in the stem cells themselves, provides a template for understanding and targeting the environmental pathways underlying the regenerative capacity of older tissues and organs. It is projected that this paradigm extends to the overall regulation of adult stem cell biology, shifting the balance from tissue generation during development and maturation to the prevention of untoward stem cell differentiation with aging. [source] Mitochondrial DNA mutations as a fundamental mechanism in physiological declines associated with agingAGING CELL, Issue 1 2003Jeong W. Pak Summary The hypothesis that mitochondrial DNA damage accumulates and contributes to aging was proposed decades ago. Only recently have technological advancements, which facilitate microanalysis of single cells or portions of cells, revealed that mtDNA deletion mutations and, perhaps, single nucleotide mutations accumulate to physiologically relevant levels in the tissues of various species with age. Although a link between single nucleotide mutations and physiological consequences in aging tissue has not been established, the accumulation of deletion mutations in skeletal muscle fibres has been associated with sarcopenia. Different, and apparently random, deletion mutations are specific to individual fibres. However, the mtDNA deletion mutation within a phenotypically abnormal region of a fibre is the same, suggesting a selection, amplification and clonal expansion of the initial deletion mutation. mtDNA deletion mutations within a muscle fibre are associated with specific electron transport system abnormalities, muscle fibre atrophy and fibre breakage. These data point to a causal relationship between mitochondrial DNA mutations and the age-related loss of muscle mass. [source] Demyelination Induces the Decline of the Myelinated Fiber Length in Aged Rat White MatterTHE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 4 2009Chen Li Abstract To determine the exact reason for the age-related decline of the myelinated fiber length in white matter, we performed this study. In middle-aged rats, there was age-related loss of the unmyelinated fibers with large diameters. The demyelination of the myelinated fibers with small diameters in middle-aged rat white matter might make the age-related decrease of the unmyelinated fibers with small diameters in the white matter unnoticeable. However, in old-aged female rats, the unmyelinated fibers with large and small diameters significantly degenerated together and that the unmyelinated fibers formed from the demyelination of the myelinated fibers could not replenish the age-related loss of the unmyelinated fibers in the white matter. In conclusion, this study suggested that demyelination of myelinated fibers with small diameters in aged white matter might be the key mechanism of the significant decline of the myelinated fiber length in aged white matter. Anat Rec, 292:528,535, 2009. © 2009 Wiley-Liss, Inc. [source] Sarcopenia of aging: Underlying cellular mechanisms and protection by calorie restrictionBIOFACTORS, Issue 1 2009Emanuele Marzetti Abstract Sarcopenia, the loss of muscle mass and function, is a common feature of aging and impacts on individual health and quality of life. Several cellular mechanisms have been involved in the pathogenesis of this syndrome, including mitochondrial dysfunction, altered apoptotic and autophagic signaling, and, more recently, trace metal dyshomeostasis. Calorie restriction (CR) without malnutrition has been shown to ameliorate the age-related loss of muscle mass in a variety a species. Mechanisms of protection span from preservation of mitochondrial functional and structural integrity to mitochondrial biogenesis, reduction of oxidative stress, and favorable modulation of apoptotic and autophagic signaling pathways. Importantly, preliminary evidence indicates that moderate CR may promote muscle mitochondrial biogenesis in middle-aged human subjects. Further research is warranted to investigate whether CR may represent a safe and efficient strategy to delay the onset and mitigate the progression of sarcopenia in older adults. © 2009 International Union of Biochemistry and Molecular Biology, Inc. [source] | ||||||||||