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Lipidomic Insight into Membrane Remodeling in Aging and Neurodegenerative Diseases
Published in Abhai Kumar, Debasis Bagchi, Antioxidants and Functional Foods for Neurodegenerative Disorders, 2021
Aging is the primary risk factor for most neurodegenerative diseases, including dementia and the two most prevalent AD and PD. One in ten individuals aged ≥65 years has AD, and its prevalence continues to increase with rising age. Very limited, if any, effective treatments are currently available for aging-related neurodegenerative diseases, which develop irreparably and are associated with a high societal, economic, and personal burden. Aging, always associated with physical deterioration, is the main risk factor for most neurodegenerative diseases, including dementia, AD, and PD, and leads to an increased risk of chronic diseases and death. Among the different age-related chronic diseases, neurodegeneration and the accompanying cognitive decline is particularly deteriorating healthspan and quality of life [11]. Potential biomarkers of aging bring into line crucial molecular mechanisms responsible for aging, with nine so-called critical hallmarks of the aging process identified recently [12].
Anti-Aging and Regenerative Medicine
Published in Aruna Bakhru, Nutrition and Integrative Medicine, 2018
There is a heterogeneity observed in the lifespan of every individual human just as is in the aging rate (measurement of decline in functional capacity and stress resistance). Some biomarkers are potent enough to determine an individual's biological age as compared to chronological age. Basically, a biomarker of aging refers to a biological parameter of an organism which predicts the biological age which can be similar or different from chronological age. These markers change with advancing age. Therefore, they are targeted as a preventive or therapeutic strategy for various developing diseases (Baker and Sprott 1988, Hamilton 1970, Simm et al. 2008).
Manipulating Aging to Treat Age-Related Disease
Published in Shamim I. Ahmad, Aging: Exploring a Complex Phenomenon, 2017
Metformin is an antidiabetic drug that has been shown to have pleiotropic downstream effects that extend the murine life span.23 Metformin is known to modulate glucose and energy homeostasis through regulation of 5′ adenosine monophosphate-activated protein kinase (AMPK) activity.24 However, others have shown that metformin can also affect many other pathways that can contribute to its antiaging and longevity-enhancing effects.25,26 Recently, metformin has become the subject of a first-of-its-kind clinical trial (funded by the American Federation of Aging Research) to see if metformin can delay the progression of age-related diseases.27 Importantly, the TAME (Targeting Aging with Metformin) study will set a benchmark in trial design and data analysis for any future potential antiaging drugs. Obviously, measuring life spans and constructing Kaplan–Meier survival curves is not possible in human cohorts within a practical time frame. However, as co-morbidities appear with increasing frequency in aging human populations, the TAME study aims to measure any effect on the aging process by measuring the time between appearance of new comorbidities in adults aged over 65 years. This approach could still require upwards of 10 years to measure significant effects. It remains to be seen if aging can be quantified through the development of more efficient biomarker-based approaches (see References 9, 28 for reviews covering the use of biomarkers for aging research).
Can we make drug discovery targeting fundamental mechanisms of aging a reality?
Published in Expert Opinion on Drug Discovery, 2022
David G. Le Couteur, Rozalyn M. Anderson, Rafael de Cabo
How and which of the findings emerging from rodent studies will ultimately be translated to humans remains to be seen. Nevertheless, well-controlled studies on large cohorts of mice using various strains and both sexes are crucial to gaining solid footing for translation. The Study of Longitudinal Aging in Mice (SLAM) at the NIA/NIH is well suited to make significant contributions to our understanding of normative mouse aging [16]. Validated predictors, biomarkers and/or surrogate markers of aging are essential for drug discovery and will be crucial for clinical trials [17]. Clinical trials in humans that have lifespan as an outcome are not feasible, although other clinical outcomes closely related to aging such as the onset of frailty, cognitive impairment, or any age-related disease, and institutionalization might be feasible depending upon the age of the clinical trial participants. There has been extensive research to identify blood biomarkers of aging that reflect aging biology and measurably change in opposite directions with aging or with interventions acting on aging. Proposed blood biomarkers include those linked mechanistically with aging or identified as specific risk factors for diseases associated with aging [17]. Some of these markers perform well in defining chronological age but there remains a gap in our ability to quantify biological age, a measure of health and disease risk status.
Serum sodium level variability as a prognosticator in older adults
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 2018
Maryam A. Barma, Roy L. Soiza, Peter T. Donnan, Mark M. McGilchrist, Helen Frost, Miles D. Witham
Whilst frailty is undoubtedly a useful concept in caring for older people, it is not a well-defined entity. In fact, the two most established models of frailty – the frailty index (a model of deficit accumulation) [2], and the phenotype model (using specific functional criteria to define a syndrome) [3] – rarely identify the same individuals as frail [5]. Our novel approach, using routinely collected biochemical data, aims to identify objective biomarkers of ageing. The advantages of this would be two-fold, with both clinical and academic implications. Firstly, we may be able to add additional prognostic value to traditional risk-prediction models, aid decision-making, and allow for earlier detection of declining function, before frailty has become established [4, 6]. Secondly, it may give insight into the biological processes that underpin ageing. Both are of relevance given the shift in goals towards maintaining health and maximising quality of life in older individuals [4, 7].
What is the future of telomere length testing in telomere biology disorders?
Published in Expert Review of Hematology, 2023
Telomere biology disorders (TBDs) are a spectrum of genetic disorders caused by pathogenic or likely pathogenic (P/LP) rare germline variants in genes encoding essential components of telomere maintenance. Telomeres consist of long nucleotide repeats (TTAGGG)n and a protein complex at chromosome ends essential for maintaining chromosome integrity [1]. Telomere nucleotide repeats shorten with each cell division due to the inability of DNA polymerase to fully replicate DNA ends. The reverse transcriptase, telomerase, can lengthen telomeres but is primarily expressed only in germ and stem cells. Telomere length is often considered a biomarker of aging because when telomeres reach critically short lengths cellular senescence or apoptosis is triggered.