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Our understanding of age-related physiology and metabolism has grown through the study of systems biology, including transcriptomics, single-cell analysis, proteomics and metabolomics. Studies in lab organisms in controlled environments, while powerful and complex, fall short of capturing the breadth of genetic and environmental variation in nature. Thus, there is now a major effort in geroscience to identify aging biomarkers and to develop aging interventions that might be applied across the diversity of humans and other free-living species. To meet this challenge, the Dog Aging Project (DAP) is designed to identify cross-sectional and longitudinal patterns of aging in complex systems, and how these are shaped by the diversity of genetic and environmental variation among companion dogs. Here we surveyed the plasma metabolome from the first year of sampling of the Precision Cohort of the DAP. By incorporating extensive metadata and whole genome sequencing information, we were able to overcome the limitations inherent in breed-based estimates of genetic and physiological effects, and to probe the physiological and dietary basis of the age-related metabolome. We identified a significant effect of age on approximately 40% of measured metabolites. Among other insights, we discovered a potentially novel biomarker of age in the post-translationally modified amino acids (ptmAAs). The ptmAAs, which can only be generated by protein hydrolysis, covaried both with age and with other biomarkers of amino acid metabolism, and in a way that was robust to diet. Clinical measures of kidney function mediated about half of the higher ptmAA levels in older dogs. This work identifies ptmAAs as robust indicators of age in dogs, and points to kidney function as a physiological mediator of age-associated variation in the plasma metabolome.

Frailty represents diminished reserve across multiple physiologic systems, accompanied by increased vulnerability to stressors and increased morbidity and mortality. With population aging, strategies to prevent and manage frailty are priorities in clinical medicine and public health. Current evidence-based approaches to frailty management are multimodal in nature. Yoga, an increasingly popular and highly adaptable mind-body practice, is multi-component, incorporating physical postures, breathing practices, meditation, and other elements, and may be a strategy for frailty management. Here, we summarize the evidence linking yoga practice to mitigation of age-related degradation across multiple physiologic systems, including cardiovascular, pulmonary, musculoskeletal, and nervous systems. We discuss putative mechanisms of action including modulation of the hypothalamic–pituitary–adrenal axis. Finally, we consider implications for clinical practice and future research.

Frailty represents diminished reserve across multiple physiologic systems, accompanied by increased vulnerability to stressors and increased morbidity and mortality. With population aging, strategies to prevent and manage frailty are priorities in clinical medicine and public health. Current evidence-based approaches to frailty management are multimodal in nature. Yoga, an increasingly popular and highly adaptable mind-body practice, is multi-component, incorporating physical postures, breathing practices, meditation, and other elements, and may be a strategy for frailty management. Here, we summarize the evidence linking yoga practice to mitigation of age-related degradation across multiple physiologic systems, including cardiovascular, pulmonary, musculoskeletal, and nervous systems. We discuss putative mechanisms of action including modulation of the hypothalamic-pituitary-adrenal axis. Finally, we consider implications for clinical practice and future research., (Copyright © 2023 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Abstract High caliber master athletes provide a valuable model for studying inherent physiological aging and performance capacity, without the confounding factor of physical inactivity. Despite the remarkable achievements of female master athletes, their participation rates remain significantly lower than those of their male counterparts, particularly at more advanced ages. This review examines the biological sex gap in sports participation among master athletes and the subsequent disparity in empirical research, thereafter exploring possible contributing factors. It highlights the importance of studying female master athletes to better understand the aging process and offers recommendations to address current evidence gaps. The need for more comprehensive mechanistic data on highly trained older women, novel cataloguing and analysis of real‐world datasets, case studies/series, and longitudinal research are also emphasized. Although analyzing the records of female master athletes as a surrogate to determine age‐related physiological and performance changes is a common approach, the process may be hindered by the considerably lower participation rates of women. Therefore, an important step toward bridging these gaps is the longitudinal, integrative study of female athletes engaged in lifelong exercise. Such analyses would improve our understanding of senescence in women and may inform interventions targeting the promotion of physical function in older adults.

Background: Despite evidence that psychological stress is an important risk factor for age-related cognitive loss, little research has directly evaluated psychological and physiological mediators of the relationship between stressful experiences and cognitive function. A key objective of the ESCAPE (Effects of Stress on Cognitive Aging, Physiology, and Emotion) project is to evaluate whether engaging in stress-related unconstructive repetitive thought (URT) is a pathway through which stressful experiences negatively affect cognitive health over the short- and long-term. Over the short-term, we hypothesize that engaging in URT will deplete attentional resources and result in worse cognitive performance in daily life. Over the long-term, we expect that the effects of chronic stress, from repeated exposure to stressors and regular engagement in URT, will be apparent in dysregulated hypothalamic-pituitary-adrenal (HPA) axis function and inflammation. Over time, stress-related physiological dysregulation will result in accelerated cognitive decline. Methods/Design: This study utilizes a prospective longitudinal measurement-burst design. A systematic probability sample of participants aged 25 to 65 is recruited from residents of the Bronx, NY. Consenting participants complete a baseline assessment and follow-up waves at 9, 18, and 27 months post-baseline. At each wave, participants complete a 14 day measurement burst of brief surveys and cognitive assessments delivered via study smartphones during daily life. Participants provide saliva samples four times each day for five days during the measurement burst and fasting blood samples at the end of each burst from which cortisol and dehydroepiandrosterone sulfate (DHEAS), circulating inflammatory markers, and stimulated inflammatory responses to lipopolysaccharide in whole blood are determined. Discussion: This study takes a multi-pronged approach to assessing stress (i.e., early adversity, chronic strains, major events, daily hassles), psychological mediators (e.g., URT), biological mechanisms (i.e., HPA function, inflammation) and outcomes across different time-scales (i.e., momentary cognitive performance, cognitive decline across years). The systematic probability sample is locally representative and can be compared with national norms on key markers of health and well-being. The findings will improve our understanding of how environmental, psychological, and physiological stress-related influences accumulate to affect cognitive health and identify potential targets (e.g., URT, inflammation) for prevention and intervention promoting cognitive health. [ABSTRACT FROM AUTHOR]

High caliber master athletes provide a valuable model for studying inherent physiological aging and performance capacity, without the confounding factor of physical inactivity. Despite the remarkable achievements of female master athletes, their participation rates remain significantly lower than those of their male counterparts, particularly at more advanced ages. This review examines the biological sex gap in sports participation among master athletes and the subsequent disparity in empirical research, thereafter exploring possible contributing factors. It highlights the importance of studying female master athletes to better understand the aging process and offers recommendations to address current evidence gaps. The need for more comprehensive mechanistic data on highly trained older women, novel cataloguing and analysis of real‐world datasets, case studies/series, and longitudinal research are also emphasized. Although analyzing the records of female master athletes as a surrogate to determine age‐related physiological and performance changes is a common approach, the process may be hindered by the considerably lower participation rates of women. Therefore, an important step toward bridging these gaps is the longitudinal, integrative study of female athletes engaged in lifelong exercise. Such analyses would improve our understanding of senescence in women and may inform interventions targeting the promotion of physical function in older adults. [ABSTRACT FROM AUTHOR]

There are physiologic changes associated with aging. There are also medical conditions that occur more commonly with advancing age. These changes and conditions increase an older adult's vulnerability to and injuries from abuse or neglect. An older adult may have more difficulty recovering from an abuse incident. The investigation of abuse or neglect may be more difficult because of aging changes., (Copyright © 2014 Elsevier Inc. All rights reserved.)

In developed countries, premature death and morbidity caused by cardiovascular diseases of the aged are an important issue. This is also an increasing problem in the developing world. This symposium discussed the structural and functional changes, which underlie the way in which the susceptibility of the cardiovascular system to disease increases with age, and how such changes are influenced by external factors.

This article provides an overview of the normal, physiologic changes in vision that are a part of the aging process. Associated symptoms noted by and worrisome to many patients also are discussed. Clear explanations of the rationale and cause of these concerning complaints reduces anxiety and enables people to function more safely in environments in which visual loss is likely to have a deleterious effect. Likewise, accurate understanding of normal versus pathological vision symptoms assists health care providers, such as nurse practitioners, to better triage, assess, and treat ophthalmic-related problems.

The study of heart aging physiology at Kazan Pedagogical University was for many years headed by Professor Farit Gabdulkhakovich Sitdikov, Doctor of Biology, Meritorious Scientist of the Russian Federation and the Republic of Tatarstan. The focus of his research interests was membranous and cellular mechanisms of heart regulation in ontogeny and adaptation of children and adolescents to studying and physical activities. T.L. Zefirov, the successor of F.G. Sitdikov, continued and promoted these investigations within the walls of the Institute of Fundamental Medicine and Biology of Kazan Federal University. The experiments are performed here with the use of unique physiological equipment that helps to spot the age-related features of heart functioning at the organ, tissue, and cellular levels, as well as to find out how various medications affect the heart. The most important results have been published in the leading Russian and foreign journals.

A chart review from 151 dysphonic patients over the age of 60 was done to define aging related voice disorders. Overwhelmingly, patients suffered from dysphonia due to disease processes associated with aging rather than to physiologic aging alone. These include: 1. central neurological disorders affecting laryngeal function (e.g., stroke, Parkinson's disease, essential tremor, Alzheimer's disease); 2. benign vocal fold lesions (e.g., Reinke's edema, benign and dysplastic epithelial lesions); 3. inflammatory disorders (e.g., laryngitis sicca, medication effect); 4. laryngeal neoplasia; and 5. laryngeal paralysis. Typical laryngeal findings of vocal fold bowing and breathiness consistent with presbylarynges were present in only six patients. Presbylarynges is not a common disorder and should be a diagnosis of exclusion made only after careful medical and speech evaluation.

Ghrelin, a hormone produced mainly by gastric mucosal cells stimulates growth hormone (GH) release. Ghrelin is also expressed in the endothelial cells of blood vessels suggesting its physiological role and a function in these cells. We recently demonstrated that ghrelin induces angiogenesis--new capillary blood vessel formation- in neonatal human microvascular endothelial cells (HMVECs). Angiogenesis is impaired in aging individuals both in vitro and in vivo, but the precise mechanism(s) of this phenomenon is unknown. We examined whether HMVECs derived from aging individuals (66 years and 90 years old), 66-HMVECs and 90-HMVECs have reduced ghrelin levels vs. neonatal (Neo) HMVECs and whether treatment with exogenous ghrelin can restore impaired in vitro angiogenesis on matrigel in aged HMVECs. Ghrelin levels were reduced in the aged HMVECs by 3.2-fold (p

Studies of how aging affects brain plasticity have largely focused on old animals. However, deterioration of memory begins well in advance of old age in animals, including humans; the present review is concerned with the possibility that changes in synaptic plasticity, as found in the long-term potentiation (LTP) effect, are responsible for this. Recent results indicate that impairments to LTP are in fact present by early middle age in rats but only in certain dendritic domains. The search for the origins of these early aging effects necessarily involves ongoing analyses of how LTP is induced, expressed, and stabilized. Such work points to the conclusion that cellular mechanisms responsible for LTP are redundant and modulated both positively and negatively by factors released during induction of potentiation. Tests for causes of the localized failure of LTP during early aging suggest that the problem lies in excessive activity of a negative modulator. The view of LTP as having redundant and modulated substrates also suggests a number of approaches for reversing age-related losses. Particular attention will be given to the idea that induction of brain-derived neurotrophic factor, an extremely potent positive modulator, can be used to provide long periods of normal plasticity with very brief pharmacological interventions. The review concludes with a consideration of how the selective, regional deficits in LTP found in early middle age might be related to the global phenomenon of brain aging.

Memory loss in humans begins early in adult life and progresses thereafter. It is not known whether these losses reflect the failure of cellular processes that encode memory or disturbances in events that retrieve it. Here, we report that impairments in hippocampal long-term potentiation (LTP), a form of synaptic plasticity associated with memory, are present by middle age in rats but only in select portions of pyramidal cell dendritic trees. Specifically, LTP induced with theta-burst stimulation in basal dendrites of hippocampal field CA1 decayed rapidly in slices prepared from 7- to 10-month-old rats but not in slices from young adults. There were no evident age-related differences in LTP in the apical dendrites. Both the adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine and a positive AMPA receptor modulator (ampakine) offset age-related LTP deficits. Adenosine produced greater depression of synaptic responses in middle-aged versus young adult slices and in basal versus apical dendrites. These results were not associated with variations in A1 receptor densities and may instead reflect regional and age-related differences in adenosine clearance. Pertinent to this, brief applications of A1 receptor antagonists immediately after theta stimulation fully restored LTP in middle-aged rats. We hypothesize that the build-up of extracellular adenosine during theta activity persists into the postinduction period in the basal dendrites of middle-aged slices and thereby activates the A1 receptor-dependent LTP reversal effect. Regardless of the underlying mechanism, the present results provide a candidate explanation for memory losses during normal aging and indicate that, with regard to plasticity, different segments of pyramidal neurons age at different rates.

Somatosensory thalamus and cortex in rodents contain topological representations of the facial whisker pad. The thalamic representation of a single whisker ("barreloid") is presumed to project exclusively to the cortical representation ("barrel") of the same whisker; however, it was not known when this correspondence is established during early development, nor how precise the thalamocortical projection is at birth, before formation of barrels and barreloids. To answer these questions, we retrogradely labeled thalamocortical projection neurons in fixed brain slices from 0-8 d old (P0-P8) mice, by placing paired deposits of two fluorescent dyes in adjacent barrels or (before barrel formation) in adjacent loci in upper cortical layers. At all ages studied, a negligible fraction of the retrogradely labeled cells was double labeled, implying that branches of single thalamocortical axons never extended within layer IV over an area wider than a single barrel. In P0 preparations, 70% of paired dye deposits placed 75-200 microns apart resulted in statistically significant segregation of labeled cell clusters in the thalamus. Quantitative analysis indicated that on P0 about 70% of thalamocortical axons were within 1.3 presumptive barrel diameters from their topologically precise target. In P4-P8 preparations, the great majority of thalamic cells retrogradely labeled from a single barrel were found in a single barreloid, implying a 1:1 projection of barreloids to barrels. The postnatal increase in topological precision was reproduced by a computer simulation, which assumed that many aberrant axons corrected their initial targeting error by extending terminal arborizations asymmetrically, towards the center of their appropriate barrel.

The increasing biologic uniqueness of older persons requires an individualized approach to their medical care. The physician must be aware of his or her own attitudes and beliefs regarding aging and death and how these views influence the physician-patient relationship. The physician must understand how older persons behave when they are ill and know how to interpret a changing constellation of multiple disease possibilities and interrelationships. The physician requires knowledge skills and the willingness to carefully evaluate each individual situation and to formulate a specifically tailored care plan. Because of the magnitude and complexity of medical, psychological, and social problems in older persons, the physician must cooperate with other members of the health care team. The accumulation and constant refinement of these skills defines the maturity and scientific grounding of the physician.