Various definitions of aging are discussed. The term successful aging is criticized and some of the criteria of normal aging are discussed. The relevance of a good definition of biological aging and aging processes is outlined and it is stressed that aging process parameters should discriminate between individuals who are at higher and lower risk in terms of specific harmful consequences.

The maximum lifespan (MLS) of Homo sapiens is substantially greater than that of our closest relatives, the non-human primates. Since evolutionary divergence from a common primate ancestor occurred relatively recently, the genetic changes affecting MLS must have occurred quickly. The evolution of MLS is generally explainable as a pleiotropic effect of genetic material that speeds or postpones cellular damage. However, in humans it can be argued that direct selection for longevity is plausible: through mechanisms of personal fitness among males and inclusive fitness among females. A flaw to such an explanatory approach is that it is non-falsifiable.

There has been considerable speculation relating the neuroanatomic changes during normal aging with corresponding neuropsychological sequelae. This paper examines the empirical support for the hypothesis that the greatest structural changes in normal aging occur in the frontal-subcortical axis, and that these produce a similar pattern of neuropsychological performance to that seen in younger individuals with subcortical damage. In this study, 14 normal elderly, 12 younger patients with HIV encephalopathy, and 14 young neurologically intact control subjects were studied with a neuropsychological test battery. The results demonstrated that the normal elderly and HIV encephalopathy patients evidenced a strong similarity in both level and pattern of neuropsychological performance despite their considerable age disparity. These results support the notion that normal aging differentially affects functions subserved by frontal-subcortical brain regions.

This study investigated the speed of short-term memory scanning in two groups of patients: patients with Parkinson's disease (PD) (primarily subcortical pathology) and patients with a presumptive diagnosis of dementia of the Alzheimer type (DAT) (primarily cortical pathology). Non-demented PD patients (M age = 58.3), mildly demented DAT patients (M age = 67.0), and normal control (NC) subjects (M age = 58.9) were compared to one another in order to determine whether the presence of slowed scanning differentiates subcortical from cortical pathology. The three groups did not differ significantly on the memory scanning task. Slowed scanning speed does appear to occur in some patients with PD, however. This may relate to age, duration of disease, or an interaction between these two. Despite normal scanning speed, most DAT patients required highly structured instructions to be able to carry out the item-recognition task, and many remainedunable to perform this task even with additional instructions.

There is currently a scientific debate over the question of the existence of profiles of cognitive decline in old age which would be independent of social, health, generational factors and psychometric artefacts. This essay is a critical literature review which comes to the conclusion that evidence from neurology and neuropsychology strongly suggests the existence of such profiles. In addition, it is shown that the currently dominant neuropsychological model of aging postulates a decline of executive and mnemonic functions as a direct result of deterioration of frontal and temporal brain systems with advancing age.

Cultured Type II Diabetic Fibroblasts displayed no in vitro age-related changes in insulin - or serum-stimulated hexose transport. Additionally, the use of a dexamethasone amplified response protocol allowing use of near physiological concentrations of insulin (6.7 nM) also showed no in vitro age-related change in insulin-stimulated hexose transport in these cultured Type II Diabetic fibroblasts. The data indicate that Type II Diabetic fibroblasts express no differential in response to insulin or serum during aging in vitro.

Controversy continues over the relationship between calcium intake and bone density in women. Epidemiological evidence does not strongly support the conclusion that high levels of dietary calcium during the postmenopausal years influence the extent or rate of bone loss. Dietary calcium in the growing years may be a determinant of peak adult bone density attained at maturity. Experimental trials do not appear to support the contention that calcium supplementation will restore lost bone in healthy or osteoporotic postmenopausal women. However, an increased calcium intake to an optimal individual level may slow the rate of bone loss in postmenopausal women. The cross-sectional and controlled investigations regarding the relationship between calcium intake and bone density will be discussed in this review.

When cells are allowed to age in vitro, or are taken from aged normal donors or subjects with features of accelerated aging (progeria or Werner syndrome), they may be considered 'old'. Such old cells have reduced growth rates in culture compared to early or mid-passage cells from young normal donors. During exponential growth the rate constants for protein synthesis were not significantly different between young and old cells (0.023±0.002 h1 vs. 0.021±0.002 h1, respectively), yet growth rates (i.e. protein accretion) were only 0.013±0.003 h1 in old cells compared to 0.022±0.002 h1 in young cells. Thus, the reduced rate of protein accumulation during growth of old cells compared to young cells was associated with increased protein degradation (0.01+0.002 h1 vs. 0.001±0.002 h1; P<0.05) rather than reduced rates of protein synthesis. When cells entered quiescence from density dependent inhibition of growth, protein synthetic rates decreased in both young and old cells to comparable levels (0.013±0.002 h1) with the result that rates of growth (0.003±0.0003 h1) and degradation (0.01±0.003h1) were not significantly different between the two groups. Thus, a difference in protein turnover between young and old cells was only seen during exponential growth, where degradation was increased in old cells. The causal relationship between increased protein degradation and decreased growth rates in old cells is not known.

The possibility of measuring human activity patterns is discussed in terms of data obtained by attitude assessment, activity questionnaires, personal monitoring devices and fitness assessment. Specific problems are noted in applying these several techniques to elderly populations. Attitude assessments indicate the intention to exercise, and practical barriers may limit the translation of intention into overt behaviour. Questionnaires are open to exaggeration, but nevertheless remain the most practical method of evaluating large populations. Personal monitors can only be applied to small samples, but may nevertheless be helpful in improving questionnaire design. Fitness tests raise concerns of safety, and seem likely to bias population sampling towards the active elderly; scores are also influenced more by inherited factors than by current activity. Activity measurements seem unlikely to yield more than a crude estimate of total dietary needs in a population, but they may nevertheless help to identify a subset of old people where detailed nutritional examination is particularly cost-effective. The accurate determination of activity patterns will also have value as a means of encouraging the elderly to adopt an active lifestyle, maximizing their physical potential.

The purpose of the study was to compare passive joint stiffness in ankles of young and elderly men (21–39, and 64–87 years, respectively). A torque motor system was used to record angular displacement and resistive torque during a slow 6 degree/second ankle rotation from 10 degrees of plantarflexion to 10 degrees of dorsiflexion (DF). Passive torque (Nm) and passive elastic stiffness (Nm/degree) were measured at neutral, 5 and 10 degrees of DF. Passive torque increased nonlinearly as the ankle was rotated into DF. The elderly men had significantly lower passive torque values (p < .05), but there was no age-related difference in passive elastic stiffness. Variability of the two measures was greater in the older group. We concluded that within the range of motion tested, there was no evidence of increased stiffness in the elderly ankle joints.