Biogerontology 

About: Biogerontology is an academic journal published by Springer Science+Business Media. The journal publishes majorly in the area(s): Senescence & Oxidative stress. It has an ISSN identifier of 1389-5729. Over the lifetime, 1298 publications have been published receiving 45834 citations. The journal is also known as: Biogerontology (London) & Biogerontology (Boston).

Adipocyte tissue volume in bone marrow is increased with aging and in patients with osteoporosis.

Abstract: Aging of the human skeleton is characterized by decreased boneformation and bone mass and these changes are more pronounced inpatients with osteoporosis. As osteoblasts and adipocytes share a commonprecursor cell in the bone marrow, we hypothesized that decreased boneformation observed during aging and in patients with osteoporosis is theresult of enhanced adipognesis versus osteoblastogenesis from precursorcells in the bone marrow. Thus, we examined iliac crest bone biopsiesobtained from 53 healthy normal individuals (age 30–100) and 26patients with osteoporosis (age 52–92). Adipose tissue volumefraction (AV), hematopoietic tissue volume fraction (HV) and trabecularbone volume fraction (BV) were quantitated as a percentage of totaltissue volume fraction (TV) (calculated as BV + AV + HV) usingthe point-counting method. We found an age-related increase in AV/TV(r = 0.53, p < 0.001, n =53) and an age-related decline in BV/TV (r =−0.46, p < 0.001, n = 53) as well asin the HV/TV (r = −0.318, p <0.05, n = 53). There was an age-related inversecorrelation between BV/TV and AV/TV (r =−0.58, p < 0.001). No significant correlation betweenthe AV/TV and the body mass index (r = 0.06, n.s.,n = 52) was detectable. Compared with age-matchedcontrols, patients with osteoporosis exhibited an increased AV/TV(P < 0.05) and decreased BV/TV (P < 0.05)but no statistically significant difference in HV/TV. Our datasupport the hypothesis that with aging and in osteoporosis an enhancedadipogenesis is observed in the bone marrow and that these changes areinversely correlated to decreased trabecular bone volume. The cellularand molecular mechanisms mediating these changes remain to bedetermined.

Physical activity in older age: perspectives for healthy ageing and frailty.

Abstract: Regular physical activity helps to improve physical and mental functions as well as reverse some effects of chronic disease to keep older people mobile and independent. Despite the highly publicised benefits of physical activity, the overwhelming majority of older people in the United Kingdom do not meet the minimum physical activity levels needed to maintain health. The sedentary lifestyles that predominate in older age results in premature onset of ill health, disease and frailty. Local authorities have a responsibility to promote physical activity amongst older people, but knowing how to stimulate regular activity at the population-level is challenging. The physiological rationale for physical activity, risks of adverse events, societal and psychological factors are discussed with a view to inform public health initiatives for the relatively healthy older person as well as those with physical frailty. The evidence shows that regular physical activity is safe for healthy and for frail older people and the risks of developing major cardiovascular and metabolic diseases, obesity, falls, cognitive impairments, osteoporosis and muscular weakness are decreased by regularly completing activities ranging from low intensity walking through to more vigorous sports and resistance exercises. Yet, participation in physical activities remains low amongst older adults, particularly those living in less affluent areas. Older people may be encouraged to increase their activities if influenced by clinicians, family or friends, keeping costs low and enjoyment high, facilitating group-based activities and raising self-efficacy for exercise.

Aging, frailty and age-related diseases

Abstract: The concept of frailty as a medically distinct syndrome has evolved based on the clinical experience of geriatricians and is clinically well recognizable. Frailty is a nonspecific state of vulnerability, which reflects multisystem physiological change. These changes underlying frailty do not always achieve disease status, so some people, usually very elderly, are frail without a specific life threatening illness. Current thinking is that not only physical but also psychological, cognitive and social factors contribute to this syndrome and need to be taken into account in its definition and treatment. Together, these signs and symptoms seem to reflect a reduced functional reserve and consequent decrease in adaptation (resilience) to any sort of stressor and perhaps even in the absence of extrinsic stressors. The overall consequence is that frail elderly are at higher risk for accelerated physical and cognitive decline, disability and death. All these characteristics associated with frailty can easily be applied to the definition and characterization of the aging process per se and there is little consensus in the literature concerning the physiological/biological pathways associated with or determining frailty. It is probably true to say that a consensus view would implicate heightened chronic systemic inflammation as a major contributor to frailty. This review will focus on the relationship between aging, frailty and age-related diseases, and will highlight possible interventions to reduce the occurrence and effects of frailty in elderly people.

Cellular and molecular mechanisms underlying age-related skeletal muscle wasting and weakness.

Abstract: Some of the most serious consequences of ageing are its effects on skeletal muscle. The term 'sarcopenia' describes the slow but progressive loss of muscle mass with advancing age and is characterised by a deterioration of muscle quantity and quality leading to a gradual slowing of movement and a decline in strength. The loss of muscle mass and strength is thought to be attributed to the progressive atrophy and loss of individual muscle fibres associated with the loss of motor units, and a concomitant reduction in muscle 'quality' due to the infiltration of fat and other non-contractile material. These age-related changes in skeletal muscle can be largely attributed to the complex interaction of factors affecting neuromuscular transmission, muscle architecture, fibre composition, excitation-contraction coupling, and metabolism. Given the magnitude of the growing public health problems associated with sarcopenia, there is considerable interest in the development and evaluation of therapeutic strategies to attenuate, prevent, or ultimately reverse age-related muscle wasting and weakness. The aim is to review our current understanding of some of the cellular and molecular mechanisms responsible for age-related changes in skeletal muscle.

Aging, articular cartilage chondrocyte senescence and osteoarthritis

Abstract: The incidence of osteoarthritis (OA), the disease characterized by joint pain and loss of joint form and function due to articular cartilage degeneration, is directly correlated with age. The strong association between age and increasing incidence of osteoarthritis (OA) marks OA as an age related disease. Yet, like many other age related diseases, OA is not an inevitable consequence of aging; instead, aging increases the risk of OA. Articular cartilage aging changes that may lead to articular cartilage degeneration include fraying and softening of the articular surface, decreased size and aggregation of proteoglycan aggrecans and loss of matrix tensile strength and stiffness. These changes most likely are the result of an age related decrease in the ability of chondrocytes to maintain and repair the tissue manifested by decreased mitotic and synthetic activity, decreased responsiveness to anabolic growth factors and synthesis of smaller less uniform aggrecans and less functional link proteins. Our recent work suggests that progressive chondrocyte senescence marked by expression of the senescence associated enzyme beta-galactosidase, erosion of chondrocyte telomere length and mitochondrial degeneration due to oxidative damage causes the age related loss of chondrocyte function. New efforts to prevent the development and progression of OA might include strategies that slow the progression of chondrocyte senescence or replace senescent cells.