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This presentation describes the study conceptualization and design. The underlying physiology is conceptualized as a dynamical system, and resilience, as a property thereof. Resilience signatures will be grounded in dynamical data from multiple stress-response assessments; many other markers are being collected.
We propose a data analytic strategy to build signatures, and evaluate their success predicting both short-and long-term responses to stressors, with both data- and theory-driven elements. If successful, our study will generate new means to identify individuals with impaired resiliency to stressors, deepen knowledge of age-related biological changes that impair stress-response, and open the way for novel interventions to bolster resiliency. To study resiliencies among older adults, we designed and are implementing pilot projects in three clinical stressors: total knee replacement surgery TKR ; initiation of hemodialysis; and bone marrow transplantation BMT in hematologic malignancies.
Each study aims to characterize signatures of resiliency in older adults by gathering extensive measurements before, during and after a stressor. For each stressor, we present rationale for stressor selection, considerations for conceptualizing resilience, study design and progress, and challenges encountered in the research. Re-attainment of baseline physical function or improvement over baseline function as in TKR is a shared resiliency response whereas resolution of pain, post-dialysis recovery time, and immune recovery exemplify responses specific to the respective stressors.
Challenges include uncertainty in hemodialysis initiation timing and BMT eligibility. Each stressor is increasingly prevalent in older adults and elicits heterogeneous responses. The development of resiliency signatures may allow targeted interventions before stressor onset. Resilience of an organism is essentially a dynamic property. Hence, in order to characterize the resilience of an organism, it is essential to perturb it and study its response.
These include response of cardiac autonomic nervous system using Holtermonitoring, oral glucose tolerance test, hour diurnal cortisol response, fatigability to treadmill test, and ACTH stimulation test. We have collected pilot data in 58 subjects undergoing 3 clinical stressors. The data will be analyzed using a dynamical systems modeling framework that we have developed.
Our preliminary results show that the stimulus-response data from multiple dynamic systems can be parsimoniously characterized using two principal components, which reflect overall and adaptive homeostatic regulation. We will evaluate how these two measures of resiliency predict the recovery of physical, cognitive, and clinical trajectories. We will present the preliminary findings from these dynamic responses in three different clinical stressors: bone-marrow transplantation in hematologic malignancies, hemodialysis initiation in end-stage renal disease, and total knee replacement.
Professor Kritchevsky will introduce the symposium. Professor Clark will introduce the premise that strength is a simple measure of physical performance that provides a marker of skeletal muscle status in general, and sarcopenia in particular. He will then present recent data and analyses arguing that central neural mechanisms are a, if not the, critical determinant of the age-related loss of muscle strength as well as mobility.
Here, he will provide an overview of the concept of dynapenia age-related loss of muscle strength highlighting key findings suggesting that dynapenia and the age-related loss of muscle mass, which was originally defined as sarcopenia, are not as mechanistically linked as originally believed. In this context, he will discuss the evolution of the definition of sarcopenia over the past decade, and present new data illustrating that older adults with clinically-meaningful leg extensor muscle weakness exhibit impairments in their central neural activation capacity of muscle and corticospinal hypoexcitability.
He will also present neuroimaging data examining the neural correlates of weakness and mobility. Communication 3: Get a grip: individual variations in grip strength are a marker of brain health , Richard G. Professor Carson will argue that the application of grip force is a complex coordinated behavior that is mediated by integrated activity across distributed brain networks, with individual variations in the capacity to generate grip force being closely associated with a broad spectrum of markers that reflect brain health.
Collectively, this symposium will highlight the convergent functional and structural mediation of cognitive and motor processes by the brain. Accordingly, the origins of the close and pervasive relationships between age- related declines in maximum grip strength and expressions of cognitive dysfunction will be readily appreciated.
The overriding conclusion arising from the analyses that will be presented is that maximum strength testing provides a discriminating measure of neurological function. The ramifications are clear. To the extent that changes in maximum strength can be registered over relatively short periods, they have the potential to serve as early markers of incipient changes in brain health. In presaging the accumulation of deficits that will ultimately impact negatively not only on cognitive status but also give rise to manifestations of frailty, loss of functional independence, and reduced quality of life, the monitoring of strength may assist in prognosis and facilitate early intervention.
With respect to various conditions of aging, including those to which the designations sarcopenia or frailty have been applied, the implications of this symposium will extend beyond our understanding of etiology. They also bear prominently upon the design and deployment of therapeutic interventions geared to combat these conditions. Although the basis for such conclusions is typically evidence e. Although the respective efficacy of these treatments is a matter for empirical enquiry, it is clear that the assumed nature of the underlying pathophysiology does not in most cases extend to the brain.
Why is this of practical concern? The achievement of a useful endpoint in phase II trials of such treatments may be defined in terms of some measure of muscle mass or muscle quality i.
Stated directly, a case will be made that the steps that are being taken presently to address a perceived deficiency in muscle mass or muscle quality are quite distinct from those actually mandated by what are evidently deficits in neuromuscular control. There exists unmet needs in ageing populations that require to be addressed using integrated health and social care systems in the primary care setting.
Problems commonly encountered include poor oral health, problems with hearing and vision, physical and cognitive frailty, poor psychological wellbeing, dependency in instrumental activities of daily living, problems with medication and polypharmacy, problems with finance and care, all of which promote increase use of hospital services.
This presentation describes a step care model involving community centres in all 18 districts of Hong Kong, using automated means to carry out geriatric screening as well as blood pressure measurements, followed by protocols for dealing with identified problems. Data are transferred to cloud for analysis and generation of individual reports. Subsequent action may include one on one consultation with a nurse or social worker, or group activities.
Only if necessary will the older person be directed to a medical clinic for further management. Exercise programs for sarcopenia improve strength, physical function and activities of daily living that lasted 12 weeks beyond the cessation of exercise program, while addition of a nutrition supplement containing HMB has incremental effect on muscle mass but not function, only during the period of supplementation.
A multi-component frailty prevention program also reverses frailty and improves physical and cognitive functions as well as self-rated health among those who were pre-frail. Opportunities exist in the primary care setting to address unmet needs of older people by detection of geriatric syndromes followed by community-based intervention programs. A medico social model could represent the first step in a step care approach that can be linked to healthcare facilities with multidisciplinary health care professionals.
All are validated in multiple continents. We will give an overview of its validation and on the results of its use in over 14, older persons in multiple clinical sites in Missouri. With rapid increase in ageing population, especially in Asian countries and limited number of geriatricians, there is an immediate need to enhance ability of primary care physicians, coordinators and nurses to screen and manage geriatric syndromes.
There is increasing emphasis on primary care in the 21st century to provide comprehensive, preventive and person-centered care plan, and are well positioned to succeed in population health. Frailty, Sarcopenia, cognitive impairment, falls, nutrition and loneliness are well known precursors of functional decline and disability. In addition to screening, the RGA also includes additional questions should a person screen positive eg for fatigue, to exclude depression, sleep apnoea and additional investigations to exclude hypothyroidism, B12 deficiency and management plans eg recommendations on exercise and vitamin D.
RGA application eRGA is practical, fast and efficient app which can be used by coordinator and nurse in primary care. For those with fatigue, depression was measured using PHQ Using Sarc-F, 1 in 5 had underlying sarcopenia. The RGA app identified relevant geriatric syndromes and with appropriate implementation pathway could lead to improved outcomes.
Inflammatory markers are well known to be associated with frailty and other comorbidities including cognitive impairment. The most significant association was found with TNFR1 and composite global cognitive score with a 7. Of these, only TNFR1 was associated with all five cognitive domains examined.
Communication 2: Circulating cell-free DNA is associated with faster rates of cognitive decline and worsening physical measures over time , L. In tissue homeostasis, damaged and dysfunctional cells die, releasing DNA fragments into circulation.
The quantity of ccf-nDNA serves as a marker of total cell death, while the size and relative abundance of ccf-mtDNA fragments can be utilized to distinguish mechanism of cell death. Ccf-DNA levels were correlated with physical and cognitive performance scores including walking speed, grip strength, frailty score as well as composite cognitive testing scores.
Associations with trajectories of physical and cognitive decline as well as other molecular measures including serum cytokines were also determined. Longitudinal analysis showed baseline increases in ccf-nDNA resulted in decreased global cognition score of 0. Mitochondrial dysfunction and cellular senescence constitute primary theories of aging and are commonage-related changes seen in patients with physical and cognitive decline.
Our data highlights the utility of ccf-DNA fragments inidentifying and risk stratifying older patients at high risk for frailty and AD. Chronic inflammation commonly accompanies frailty and increases risk of cognitive decline and the progression of AD. Our data suggests that in older adults with normal cognition, higher serum levels of AT1RaAb were strongly associated with higher inflammation and frailty; the risk of all-cause mortality was 4 times higher than in those with lower AT1RaAb levels.
This excess risk of death did not diminish after multiple adjustments. Dissecting and understanding circulating and tissue specific RAS changes in frailty and AD is therefore critical for accurately targeting the impaired parts of the system. The aims of this study were to: 1 describe the utilisation of comprehensive assessments within 6 months of the national Aged Care Assessment Program ACAP assessment for home care packages HCPs ; and 2 investigate the impact of the comprehensive assessment item numbers on the risk of mortality and entry into permanent residential aged care PRAC.
Of the 75, individuals, The utilisation of comprehensive assessments was associated with a lower risk of mortality. Mortality was matched to official death records with a minimum 10 years follow-up. Both instruments demonstrated significant predictive validity for mortality up to 10 years in an analysis adjusted for sex, age, education, and income FRAIL scale.
HR: 2. All patients were systematically assigned to either a nurse nurse 1 or a healthcare assistant HCA 1 for their first PFFS-M assessment and a second assessment was done by a second staff member from the same professional category nurse 2 and HCA 2 on the same day.
The research assistant completed the Adelaide Frailty Index. All patients returned after one week for a reassessment by the same health care professionals who had assessed them at recruitment stage and they were also required to complete the PFFS-M for a second time. Chronic inflammation is associated with frailty and functional decline in older adults but the molecular mechanisms of this linkage are not well understood.
The interleukin 10tm1Cgn IL10tm mouse develops chronic inflammation, a frailty-like phenotype with age, and has increased mortality making it an ideal model to study the biological mechanisms of frailty and functional decline.
In order to pinpoint specific biological pathways that change with age as well as connect chronic inflammation to functional decline and physical frailty, we utilized a targeted metabolomic platform to agnostically identify differences inmetabolite levels in chronically inflamed IL10tm mice. Our initial profiling identified several metabolite alterations in the plasma of the IL10tm mouse compared to controls, with the most prominent and consistent alterations being in metabolites of the tryptophan degradation pathway TDP , including decreased tryptophan and concomitantly increased kynurenine in middle-agedILtm mice, and an intensification of these changes in old aged ILtm mice relative to controls.
Analysis of metabolites revealed significant alterations in the TDP with aging and frailty. Profiling of downstream metabolites of the TDP revealed the accumulation of 3-hydroxykynurenine, a cytotoxic and neurotoxic intermediate metabolite, with frailty. The increased levels of cytotoxic and neurotoxic molecules in the TDP may in part explain the link between inflammation and cognitive and physical decline in frailty.
Chronic inflammation is known to be associated with frailty and sarcopenia, but the underlying mechanisms are not well understood. In order to pinpoint specific biological pathways that connect chronic inflammation to functional decline and physical frailty, we recently utilized a targeted metabolomic platform to identify categories or signatures of differences in metabolite levels and saw increased tryptophan degradation and production of kynurenines in the ILtm mouse model of chronic inflammation.
Interestingly, some of kynurenine metabolites are neurotoxic and known to play a role in the pathogenesis of various neurodegenerative diseases, such as Alzheimer and Parkinson diseases. Therefore, we hypothesized that chronic inflammationis related to age-associated muscle weakness via neurotoxic kynurenines. We then harvested EDL muscles and performed immunofluorescent staining of neuromuscular junction NMJ for morphological study.
Using laser confocal microscope, we compared presynaptic to postsynaptic areas in a semi-quantitative way, and found that reduced presynaptic to postsynaptic coverage is significantly reduced in ILtm mice, suggesting increased partial denervation in their muscles.
Finally, we tested the neurotoxicity of 3-hydroxykynurenine 3-HK or quinolinic acid QA on a model of peripheral spinal motor neuron, MN1 cells.
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This presentation describes the study conceptualization and design. The underlying physiology is conceptualized as a dynamical system, and resilience, as a property thereof. Resilience signatures will be grounded in dynamical data from multiple stress-response assessments; many other markers are being collected. We propose a data analytic strategy to build signatures, and evaluate their success predicting both short-and long-term responses to stressors, with both data- and theory-driven elements. If successful, our study will generate new means to identify individuals with impaired resiliency to stressors, deepen knowledge of age-related biological changes that impair stress-response, and open the way for novel interventions to bolster resiliency. To study resiliencies among older adults, we designed and are implementing pilot projects in three clinical stressors: total knee replacement surgery TKR ; initiation of hemodialysis; and bone marrow transplantation BMT in hematologic malignancies.
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