Cohort- and age-related decline in elder's life satisfaction: is there really a paradox?
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ABSTRACT:
SUBMITTER: Schilling OK
PROVIDER: S-EPMC5546290 | biostudies-other | 2005 Dec
REPOSITORIES: biostudies-other
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Project description:A paradox is a seemingly absurd or impossible concept, proposition, or theory that is often difficult to understand or explain, sometimes apparently self-contradictory, and yet ultimately correct or true. How is it possible, for example, that oxygen "a toxic environmental poison" could be also indispensable for life (Beckman and Ames Physiol Rev 78(2):547-81, 1998; Stadtman and Berlett Chem Res Toxicol 10(5):485-94, 1997)?: the so-called Oxygen Paradox (Davies and Ursini 1995; Davies Biochem Soc Symp 61:1-31, 1995). How can French people apparently disregard the rule that high dietary intakes of cholesterol and saturated fats (e.g., cheese and paté) will result in an early death from cardiovascular diseases (Renaud and de Lorgeril Lancet 339(8808):1523-6, 1992; Catalgol et al. Front Pharmacol 3:141, 2012; Eisenberg et al. Nat Med 22(12):1428-1438, 2016)?: the so-called, French Paradox. Doubtless, the truth is not a duality and epistemological bias probably generates apparently self-contradictory conclusions. Perhaps nowhere in biology are there so many apparently contradictory views, and even experimental results, affecting human physiology and pathology as in the fields of free radicals and oxidative stress, antioxidants, foods and drinks, and dietary recommendations; this is particularly true when issues such as disease-susceptibility or avoidance, "healthspan," "lifespan," and ageing are involved. Consider, for example, the apparently paradoxical observation that treatment with low doses of a substance that is toxic at high concentrations may actually induce transient adaptations that protect against a subsequent exposure to the same (or similar) toxin. This particular paradox is now mechanistically explained as "Adaptive Homeostasis" (Davies Mol Asp Med 49:1-7, 2016; Pomatto et al. 2017a; Lomeli et al. Clin Sci (Lond) 131(21):2573-2599, 2017; Pomatto and Davies 2017); the non-damaging process by which an apparent toxicant can activate biological signal transduction pathways to increase expression of protective genes, by mechanisms that are completely different from those by which the same agent induces toxicity at high concentrations. In this review, we explore the influences and effects of paradoxes such as the Oxygen Paradox and the French Paradox on the etiology, progression, and outcomes of many of the major human age-related diseases, as well as the basic biological phenomenon of ageing itself.
| S-EPMC5745211 | biostudies-literature
Project description:Exercise has emerged as a powerful variable that can improve cognitive function and delay age-associated cognitive decline and Alzheimer’s disease (AD), however, the underlying mechanisms are poorly understood. To determine if protective mechanisms may occur at the transcriptional level, we used microarrays to investigate the relationship between physical activity levels and gene expression patterns in the cognitively-intact aged human hippocampus. In parallel, hippocampal gene expression patterns associated with Aging and AD were assessed using publicly available microarray data profiling hippocampus from young (20-59 yrs), cognitively-intact aging (73-95 yrs) and age-matched AD cases. To identify “anti-Aging/AD” transcription patterns associated with physical activity, probesets significantly associated with both physical activity and Aging/AD were identified and their directions of expression change in each condition were compared. Remarkably, of the 2138 probesets significant in both datasets, nearly 95% showed opposite transcription patterns with physical activity compared to Aging/AD. The majority (>70%) of these anti-Aging/AD genes showed increased expression with physical activity and decreased expression in Aging/AD. Enrichment analysis of the anti-Aging/AD genes showing increased expression in association with physical activity revealed strong overrepresentation of mitochondrial energy production and synaptic function, along with axonal function and myelin integrity. Synaptic genes were notably enriched for synaptic vesicle priming, release and recycling, glutamate and GABA signaling and synaptic spine plasticity. Anti-Aging/AD genes showing decreased expression in association with physical activity were enriched for transcription-related function. These data suggest that physical activity preserves a more youthful profile in the hippocampus across multiple biological processes, providing a potential molecular foundation for how physical activity can delay age- and AD-related decline of hippocampal function.
2018-12-31 | GSE110298 | GEO
Project description:The aim of the study was to assess the level of life and job satisfaction of Polish anesthesiologists and to explore the impact of extrinsic-hygiene and intrinsic-motivating determinants.A cross-sectional questionnaire study was conducted among consultant anesthesiologists in Lodz region. The questionnaire concerned patient care, burden, income, personal rewards, professional relations, job satisfaction in general, and life satisfaction. Respondents were asked to rate their level of satisfaction for each item on a seven-point Likert scale (1: extremely dissatisfied; 7: extremely satisfied).86.03% of anesthesiologists were satisfied with their economic status, 77.94% found their health status satisfactory, and 52.21% viewed their personal future optimistically. In general, 71.32% of anesthesiologists were satisfied with their current job situation. Among the less satisfying job aspects were work-related stress (2.49; SD = 1.23), administrative burden (2.85; SD = 1.47), workload (3.63; SD = 1.56), and leisure time (3.09; SD = 1.44).Considerable work-related stress leads to job dissatisfaction among anesthesiologists. There is an association between job satisfaction and health status, social life, and economic status. Working for long hours by anesthesiologists results in a high risk of burnout.
| S-EPMC4070397 | biostudies-other
Project description:Studies exploring age-related brain and cognitive change have identified substantial heterogeneity among individuals, but the underlying reasons for the differential trajectories remain largely unknown. We investigated cross-sectional and longitudinal associations between brain-imaging phenotypes (IDPs) and cognitive ability, and how these relations may be modified by common risk and protective factors. Participants were recruited from the 1953 Danish Male Birth Cohort (N=123), a longitudinal study of cognitive and brain ageing. Childhood IQ and socio-demographic factors are available for these participants who have been assessed regularly on multiple IDPs and behavioural factors in midlife. Using Pearson correlations and canonical correlation analysis (CCA), we explored the relation between 454 IDPs and 114 behavioural variables. CCA identified a single mode of population covariation coupling cross-subject longitudinal changes in brain structure to changes in cognitive performance and to a range of age-related covariates (r=0.92, Pcorrected < 0.001). Specifically, this CCA-mode indicated that; decreases in IQ and speed assessed tasks, higher rates of familial myocardial infarct, less physical activity, and poorer mental health are associated with larger decreases in whole brain grey matter and white matter. We found no evidence supporting the role of baseline scores as predictors of impending brain and behavioural change in late-midlife.
| S-EPMC7521526 | biostudies-literature
Project description:Nicotinamide adenine dinucleotide (NAD+) is an essential metabolite that is reported to decline in concentration in tissues of aged animals. Strategies to increase NAD+ availability have shown promise in treating many conditions in rodents, including age-related degeneration, which has in turn driven intense interest in the effects of supplements on human health. However, many aspects of NAD+ metabolism remain poorly understood, and human data are limited. Here, we discuss the state of the evidence for an age-related decline in NAD+, along with potential mechanistic explanations, including increased consumption or decreased synthesis of NAD+ and changes in the composition of cells or tissues with age. Key challenges for the field involve the development of better tools to resolve information on the NAD+ content of specific cells and subcellular compartments as well as determining the threshold levels at which NAD+ depletion triggers physiological consequences in different tissues. Understanding how NAD+ metabolism changes with age in humans may ultimately allow the design of more targeted strategies to maintain its availability, such as inhibition of key consumers in specific tissues or direct delivery of precursors to sites of deficiency. In the meantime, human clinical trials with oral supplements are poised to provide some of the first direct evidence as to whether increasing NAD+ availability can impact human physiology. Thus, it is an exciting time for NAD+ research, with much remaining to be learned in terms of both basic biology and potential therapeutic applications.
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Project description:BACKGROUND:Episodic memory (EM) declines with age and the rate of decline is variable across individuals. A single nucleotide polymorphism (rs17070145) in the WWC1 gene that encodes the KIBRA protein critical for long-term potentiation and memory consolidation has previously been associated with EM performance, as well as differences in hippocampal engagement during EM tasks using functional magnetic resonance imaging (fMRI). In the current study, we explore the effect of this polymorphism on EM-related activity and cognitive performance across the adult life span using fMRI. METHODS:Two hundred thirty-two healthy, Caucasian subjects (18-89 years) completed a battery of cognitive tests, as well as an EM task during an fMRI scan. RESULTS:WWC1 T carriers had significantly better delayed recall performance than CC individuals (p = .006). The relationship between increasing age and recall scores (immediate and delayed) was also significantly different between WWC1 genotype groups (p = .01). In addition to the age-related decline in hippocampal formation (HF) activation (p < .05; false discovery ratesmall volume correction-HF-region of interest), we observed an age by WWC1 genotype interaction on HF activation during encoding and retrieval. The CC group showed a significant negative association between HF activity and increasing age, while no such association was observed in the T carrier group (left HF p = .04; r-z correlation difference during encoding and retrieval; right HF p = .0008; r-z correlation difference during retrieval). CONCLUSIONS:Our results show a dynamic relationship between rs17070145 polymorphism and increasing age on neuronal activity in the hippocampal region.
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Project description:Comparison of hippocampal gene expression between normal young animals and older animals with good spatial memory and older animals with poor spatial memory
2009-01-15 | GSE13799 | GEO
Project description:Human older age ushers in functional decline across the majority of cognitive domains. A notable exception seems to be affective processing, with older people reporting higher levels of emotional well-being. Here we evaluated age-related changes in emotional reactivity and regulation in a representative subsample (N = 104; age range: 23-88 years) of the population-derived Cambridge Centre for Ageing and Neuroscience cohort. Performance on a film-based emotion reactivity and regulation task in the magnetic resonance imaging scanner showed an age-related decline in positive reactivity, alongside a similar decline in the capacity to down-regulate negative affect. Decreased positivity with age was associated with reduced activation in the middle frontal gyrus. These findings, from the largest neuroimaging investigation to-date, provide no support for age-related increases in positive emotional reactivity.
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Project description:An unfortunate result of the rapid rise in geriatric populations worldwide is the increasing prevalence of age-related cognitive disorders such as Alzheimer's disease (AD). AD is a devastating neurodegenerative illness that is characterized by a profound impairment of cognitive function, marked physical disability, and an enormous economic burden on the afflicted individual, caregivers, and society in general. The rise in elderly populations is also resulting in an increase in individuals with related (potentially treatable) conditions such as "Mild Cognitive Impairment" (MCI) which is characterized by a less severe (but abnormal) level of cognitive impairment and a high-risk for developing dementia. Even in the absence of a diagnosable disorder of cognition (e.g., AD and MCI), the perception of increased forgetfulness and declining mental function is a clear source of apprehension in the elderly. This is a valid concern given that even a modest impairment of cognitive function is likely to be associated with significant disability in a rapidly evolving, technology-based society. Unfortunately, the currently available therapies designed to improve cognition (i.e., for AD and other forms of dementia) are limited by modest efficacy and adverse side effects, and their effects on cognitive function are not sustained over time. Accordingly, it is incumbent on the scientific community to develop safer and more effective therapies that improve and/or sustain cognitive function in the elderly allowing them to remain mentally active and productive for as long as possible. As diagnostic criteria for memory disorders evolve, the demand for pro-cognitive therapeutic agents is likely to surpass AD and dementia to include MCI and potentially even less severe forms of memory decline. The purpose of this review is to provide an overview of the contemporary therapeutic targets and preclinical pharmacologic approaches (with representative drug examples) designed to enhance memory function.
| S-EPMC3113643 | biostudies-other
Project description:The disposable soma theory of ageing predicts that when organisms invest in reproduction they do so by reducing their investment in body maintenance, inducing a trade-off between reproduction and survival. Experiments on invertebrates in the lab provide support for the theory by demonstrating the predicted responses to manipulation of reproductive effort or lifespan. However, experimental studies in birds and evidence from observational (nonmanipulative) studies in nature do not consistently reveal trade-offs. Most species studied previously in the wild are mammals and birds that reproduce over multiple discrete seasons. This contrasts with temperate invertebrates, which typically have annual generations and reproduce over a single season. We expand the taxonomic range of senescence study systems to include life histories typical of most temperate invertebrates. We monitored reproductive effort, ageing, and survival in a natural field cricket population over ten years to test the prediction that individuals investing more in early-reproduction senesce faster and die younger. We found no evidence of a trade-off between early-life reproductive effort and survival, and only weak evidence for a trade-off with phenotypic senescence. We discuss the possibility that organisms with multiple discrete breeding seasons may have greater opportunities to express trade-offs between reproduction and senescence.
| S-EPMC6590129 | biostudies-literature