| | 1. Relationship between the severity of pre-frailty and the degree of adaptation of Ninjin’yoeito (NYT) on pre-frailtyÏò, 12 àïð[-/+]Àâòîð(?) | With the global trend towards longer life expectancies, there’s an increasing emphasis on not just living longer, but also maintaining health and wellbeing into older age. This study explores the efficacy of Ninjin’yoeito (NYT) in the early stages of frailty, a critical period for preventive interventions. Taking account of the knowledge gap regarding the association between early frailty and NYT, we use data from workplace health checkups to examine the relationship between pre-frailty severity and NYT adaption. The objective of our research is to enhance the comprehension of early treatments using NYT to prevent the progression of frailty. A total of 314 employees of the Kyoto Industrial Health Association who received workplace health checkups between November 2021 and March 2023 and consented to this study were included in the analysis. Information on gender, age, body mass index (BMI), NYT-specific symptoms assessment, the Japanese version of the General Health Questionnaire-12 (GHQ-12), and the Kihon Checklist (KCL) were obtained. The correlation analysis revealed that there was a strong positive correlation between the number of applicable NYT indications and the GHQ-12 score (r= 0.5992, p < 0.0001). Similarly, a moderate positive correlation was observed between the number of applicable NYT indications and the KCL score (r= 0.5030, p < 0.0001). In the multivariate analysis, both GHQ-12 (?= 0.49, SE= 0.06, t= 7.66, 95% CI: 0.36 to 0.62, p= 0.000) and KCL (?= 0.54, SE= 0.12, t= 4.29, 95% CI: 0.29 to 0.79, p= 0.000) showed significant positive associations with the variance in the number of applicable NYT indications, indicating that higher scores on these measures were related to a greater number of indications. NYT has the potential to be utilized not only as a therapeutic intervention for frailty, but also as a preventive measure. | ↑ |
2. Unraveling the association between major depressive disorder and senescent biomarkers in immune cells of older adults: a single-cell phenotypic analysis×ò, 11 àïð[-/+]Àâòîð(?) | Background: Little is known about the prevalence of cellular senescence among immune cells (i.e., immune cells expressing senescence markers, iSCs) nor is there a gold-standard to efficiently measure iSCs. Major depressive disorder (MDD) in older adults has been associated with many hallmarks of senescence in whole blood, leukocytes, and plasma, supporting a strong connection between iSCs and MDD. Here, we investigated the prevalence and phenotype of iSCs in older adults with MDD. Using a single-cell phenotypic approach, circulating immune cells were examined for iSC biomarkers and their relationship to depression and inflammation.Results: PBMCs from older adults with MDD (aged 69.75 ± 5.23 years) and healthy controls (aged 71.25 ± 8.8 years) were examined for immune subset distribution and senescence biomarkers (i.e., lack of proliferation, senescence-associated heterochromatin foci (SAHF), and DNA damage). Dual-expression of SAHF and DNA damage was categorized by low, intermediate, and high expression. A significant increase in the number of high expressing total PBMCs (p= 0.01), monocytes (p= 0.008), a trending increase in the number of high expressing CD4 T cells (p= 0.06) was observed overall in those with MDD. There was also a significantly lower proportion of intermediate expressing cells in monocytes and CD4 T cells in MDD (p= 0.01 and p= 0.05, respectively). Correlation analysis revealed associations between iSCs and mRNA expression of factors related to SASP and immune cell function.Conclusion: MDD is associated with increased senescent cell biomarkers in immune cell populations delineated by distinct levels of SAHF and DNA damage. Inflammatory markers might serve as potent indicators of iSC burden in MDD. | ↑ |
3. Associations between monitor-independent movement summary (MIMS) and fall risk appraisal combining fear of falling and physiological fall risk in community-dwelling older adultsÂò, 09 àïð[-/+]Àâòîð(?) | Introduction: Fall Risk Appraisal (FRA), a process that integrates perceived and objective fall risk measures, serves as a crucial component for understanding the incongruence between fear of falling (FOF) and physiological fall risk in older adults. Despite its importance, scant research has been undertaken to investigate how habitual physical activity (PA) levels, quantified in Monitor-Independent Movement Summary (MIMS), vary across FRA categories. MIMS is a device-independent acceleration summary metric that helps standardize data analysis across studies by accounting for discrepancies in raw data among research-grade and consumer devices.Objective: This cross-sectional study explores the associations between MIMS (volume and intensity) and FRA in a sample of older adults in the United States.Methods: We assessed FOF (Short Falls Efficacy Scale-International), physiological fall risk (balance: BTrackS Balance, leg strength: 30-s sit-to-stand test) and 7-day free-living PA (ActiGraph GT9X) in 178 community-dwelling older adults. PA volume was summarized as average daily MIMS (MIMS/day). PA intensity was calculated as peak 30-min MIMS (average of highest 30 non-consecutive MIMS minutes/day), representing a PA index of higher-intensity epochs. FRA categorized participants into following four groups: Rational (low FOF-low physiological fall risk), Irrational (high FOF-low physiological fall risk), Incongruent (low FOF-high physiological fall risk) and Congruent (high FOF-high physiological fall risk).Results: Compared to rational group, average MIMS/day and peak 30-min MIMS were, respectively, 15.8% (p= .025) and 14.0% (p= .004) lower in irrational group, and 16.6% (p= .013) and 17.5% (p < .001) lower in congruent group. No significant differences were detected between incongruent and rational groups. Multiple regression analyses showed that, after adjusting for age, gender, and BMI (reference: rational), only irrational FRA was significantly associated with lower PA volume (?= –1,452.8 MIMS/day, p= .034); whereas irrational and congruent FRAs were significantly associated with lower “peak PA intensity” (irrational: ?= –5.40 MIMS/day, p= .007; congruent: ?= –5.43 MIMS/day, p= .004).Conclusion: These findings highlight that FOF is a significant barrier for older adults to participate in high-intensity PA, regardless of their balance and strength. Therefore, PA programs for older adults should develop tailored intervention strategies (cognitive reframing, balance and strength exercises, or both) based on an individual’s FOF and physiological fall risk. | ↑ |
4. Ageing as a two-phase process: theoretical frameworkÏí, 08 àïð[-/+]Àâòîð(?) | Human ageing, along with the ageing of conventional model organisms, is depicted as a continuous and progressive decline of biological capabilities accompanied by an exponentially increasing mortality risk. However, not all organisms experience ageing identically and our understanding of the phenomenon is coloured by human-centric views. Ageing is multifaceted and influences a diverse range of species in varying ways. Some undergo swift declines post-reproduction, while others exhibit insubstantial changes throughout their existence. This vast array renders defining universally applicable “ageing attributes” a daunting task. It is nonetheless essential to recognize that not all ageing features are organism-specific. These common attributes have paved the way for identifying “hallmarks of ageing,” processes that are intertwined with age, amplified during accelerated ageing, and manipulations of which can potentially modulate or even reverse the ageing process. Yet, a glaring observation is that individuals within a single population age at varying rates. To address this, demographers have coined the term ‘frailty’. Concurrently, scientific advancements have ushered in the era of molecular clocks. These innovations enable a distinction between an individual’s chronological age (time since birth) and biological age (physiological status and mortality risk). In 2011, the “Smurf” phenotype was unveiled in Drosophila, delineating an age-linked escalation in intestinal permeability that presages imminent mortality. It not only acts as a predictor of natural death but identifies individuals exhibiting traits normally described as age-related. Subsequent studies have revealed the phenotype in organisms like nematodes, zebrafish, and mice, invariably acting as a death predictor. Collectively, these findings have steered our conception of ageing towards a framework where ageing is not linear and continuous but marked by two distinct, necessary phases, discernible in vivo, courtesy of the Smurf phenotype. This framework includes a mathematical enunciation of longevity trends based on three experimentally measurable parameters. It facilitates a fresh perspective on the evolution of ageing as a function. In this article, we aim to delineate and explore the foundational principles of this innovative framework, emphasising its potential to reshape our understanding of ageing, challenge its conventional definitions, and recalibrate our comprehension of its evolutionary trajectory. | ↑ |
5. Exploring juventology: unlocking the secrets of youthspan and longevity programs×ò, 04 àïð[-/+]Àâòîð(?) | In recent decades, the study of biological aging has evolved from simplistic theories like the free radical theory to more complex and nuanced perspectives. In particular, the identification of evolutionary conserved genes and signaling pathways that can modulate both lifespan but also healthspan has resulted in the expanding understanding of the link between nutrients, signal transduction proteins, and aging along with substantial support for the existence of multiple “longevity programs,” which are activated based on the availability of nutrients. Periodic fasting and other dietary restrictions can promote entry into a longevity program characterized by cellular protection and optimized function, and the activation of regenerative processes that lead to rejuvenation. This review discusses the idea of juventology, a novel field proposing the existence of longevity programs that can maintain organisms in a highly functional state for extended periods of time. Drawing upon research on Saccharomyces cerevisiae and other model organisms, the review explores the distinctiveness of juventology from traditional aging-centered views. The focus on the “age of youth” challenges conventional thinking and opens new avenues for understanding and extending the period of peak functionality in organisms. Thus, a “juventology”-based strategy can complement the traditional gerontology approach by focusing not on aging but on the longevity program affecting the life history period in which mortality is very low and organisms remain youthful, healthy, and fully functional. | ↑ |
6. Decoding the secrets of longevity: unraveling nutraceutical and miRNA-Mediated aging pathways and therapeutic strategies×ò, 28 ìàð[-/+]Àâòîð(?) | MicroRNAs (miRNAs) are short RNA molecules that are not involved in coding for proteins. They have a significant function in regulating gene expression after the process of transcription. Their participation in several biological processes has rendered them appealing subjects for investigating age-related disorders. Increasing data indicates that miRNAs can be influenced by dietary variables, such as macronutrients, micronutrients, trace minerals, and nutraceuticals. This review examines the influence of dietary factors and nutraceuticals on the regulation of miRNA in relation to the process of aging. We examine the present comprehension of miRNA disruption in age-related illnesses and emphasize the possibility of dietary manipulation as a means of prevention or treatment. Consolidating animal and human research is essential to validate the significance of dietary miRNA control in living organisms, despite the abundance of information already provided by several studies. This review elucidates the complex interaction among miRNAs, nutrition, and aging, offering valuable insights into promising areas for further research and potential therapies for age-related disorders. | ↑ |
7. Decoding lifespan secrets: the role of the gonad in Caenorhabditis elegans agingÂò, 26 ìàð[-/+]Àâòîð(?) | The gonad has become a central organ for understanding aging in C. elegans, as removing the proliferating stem cells in the germline results in significant lifespan extension. Similarly, when starvation in late larval stages leads to the quiescence of germline stem cells the adult nematode enters reproductive diapause, associated with an extended lifespan. This review summarizes recent advancements in identifying the mechanisms behind gonad-mediated lifespan extension, including comparisons with other nematodes and the role of lipid signaling and transcriptional changes. Given that the gonad also mediates lifespan regulation in other invertebrates and vertebrates, elucidating the underlying mechanisms may help to gain new insights into the mechanisms and evolution of aging. | ↑ |
8. Senescence: A DNA damage response and its role in aging and Neurodegenerative Diseases×ò, 21 ìàð[-/+]Àâòîð(?) | Senescence is a complicated, multi-factorial, irreversible cell cycle halt that has a tumor-suppressing effect in addition to being a significant factor in aging and neurological diseases. Damaged DNA, neuroinflammation, oxidative stress and disrupted proteostasis are a few of the factors that cause senescence. Senescence is triggered by DNA damage which initiates DNA damage response. The DNA damage response, which includes the formation of DNA damage foci containing activated H2AX, which is a key factor in cellular senescence, is provoked by a double strand DNA break. Oxidative stress impairs cognition, inhibits neurogenesis, and has an accelerated aging effect. Senescent cells generate pro-inflammatory mediators known as senescence-associated secretory phenotype (SASP). These pro-inflammatory cytokines and chemokines have an impact on neuroinflammation, neuronal death, and cell proliferation. While it is tempting to think of neurodegenerative diseases as manifestations of accelerated aging and senescence, this review will present information on brain ageing and neurodegeneration as a result of senescence and DNA damage response. | ↑ |
9. Menopause and facial skin microbiomes: a pilot study revealing novel insights into their relationship×ò, 21 ìàð[-/+]Àâòîð(?) | Introduction: The human skin microbial composition is affected by age. Previous studies reported skin microbiome diversity shifts between elderly and significantly younger subjects. Some studies implied that menopausal status, which is inherently linked to age, could be associated with changes in skin microbial compositions. Nevertheless, the influence of menopausal status on skin microbiome profiles while minimizing the impact of aging-associated changes in skin parameters still needs further clarification.Methods: We performed an observational study on healthy Caucasian female volunteers, which were grouped according to their pre- or postmenopausal status. Bacterial community structures on facial skin were analyzed using 16S rRNA gene sequencing. Cutometer® measurements were performed to evaluate aging-associated changes in facial skin biophysical properties.Results: The relative abundance of the lipophilic Cutibacterium genus was decreased, and bacterial diversity was increased in skin samples of postmenopausal volunteers. The mean age difference between examined groups in this study was 12.4 years only. Accordingly, Cutometer® measurements revealed no differences in aging-associated skin biophysical parameters between pre- and postmenopausal groups. Consequently, no correlation was detected between Shannon diversity and measured age-dependent biomechanical properties of facial skin.Discussion: These findings are in line with previous studies, which investigated the wide-ranging impact of chronological aging on skin microbial communities. However, this work reports for the first time a direct association between menopausal status and facial microbiomes on skin of similarly aged study participants, and hence uncouples aging-associated skin biophysical parameters, such as viscoelastic properties, from the equation. These findings open avenues for the development of microbiome-targeting strategies for treatment of menopause-associated skin disorders. | ↑ |
10. Mother’s Curse effects on lifespan and agingÏò, 08 ìàð[-/+]Àâòîð(?) | The Mother’s Curse hypothesis posits that mothers curse their sons with harmful mitochondria, because maternal mitochondrial inheritance makes selection blind to mitochondrial mutations that harm only males. As a result, mitochondrial function may be evolutionarily optimized for females. This is an attractive explanation for ubiquitous sex differences in lifespan and aging, given the prevalence of maternal mitochondrial inheritance and the established relationship between mitochondria and aging. This review outlines patterns expected under the hypothesis, and traits most likely to be affected, chiefly those that are sexually dimorphic and energy intensive. A survey of the literature shows that evidence for Mother’s Curse is limited to a few taxonomic groups, with the strongest support coming from experimental crosses in Drosophila. Much of the evidence comes from studies of fertility, which is expected to be particularly vulnerable to male-harming mitochondrial mutations, but studies of lifespan and aging also show evidence of Mother’s Curse effects. Despite some very compelling studies supporting the hypothesis, the evidence is quite patchy overall, with contradictory results even found for the same traits in the same taxa. Reasons for this scarcity of evidence are discussed, including nuclear compensation, factors opposing male-specific mutation load, effects of interspecific hybridization, context dependency and demographic effects. Mother’s Curse effects may indeed contribute to sex differences, but the complexity of other contributing factors make Mother’s Curse a poor general predictor of sex-specific lifespan and aging. | ↑ |
11. Endurance exercise preserves physical function in adult and older male C57BL/6 mice: high intensity interval training (HIIT) versus voluntary wheel running (VWR)×ò, 07 ìàð[-/+]Àâòîð(?) | Exercise has been shown to improve physical function, mitigate aspects of chronic disease and to potentially alter the trajectory of age-related onset of frailty and sarcopenia. Reliable and valid preclinical models are necessary to elucidate the underlying mechanisms at the intersection of age, exercise, and functional decline. The purpose of this study was to compare, head to head, the effects of two common pre-clinical models of endurance exercise: high intensity interval training (HIIT) and voluntary wheel running (VWR). The hypothesis was that a prescribed and regimented exercise program, HIIT, would prove to be a superior training method to unregulated voluntary exercise, VWR. To investigate this hypothesis, we evaluated adult (n= 24, designated 10 m, aged 6 months at the beginning of the study, 10 months at its completion) and older adult (n= 18, designated 26 m, aging from 22 months to 26 months over the course of the study) C57BL/6 male mice. These mice were randomly assigned (with selection criteria) to a 13-week program of voluntary wheel running (VWR), high intensity interval training (HIIT), or sedentary control (SED). The functional aptitude of each mouse was determined pre- and post-training using our composite CFAB (comprehensive functional assessment battery) scoring system consisting of voluntary wheel running (volitional exercise and activity rate), treadmill (endurance), rotarod (overall motor function), grip meter (forelimb strength), and inverted cling (whole body strength/endurance). To measure sarcopenia, we tracked body mass, body composition (with EchoMRI), plantar flexor torque (in 10 m), and measured muscle wet mass post-training. Overall, adult CFAB scores decreased while body mass and percent body fat increased as they matured; however, exercise significantly mitigated the changes (p < 0.05) compared to SED. Older adults demonstrated preservation of function (CFAB) and reduced body fat (p < 0.05) compared to SED. To conclude, both types of exercise maintained physical function equally in older mice. | ↑ |
13. Assessing muscular power in older adults: evaluating the predictive capacity of the 30-second chair rise testÑð, 06 ìàð[-/+]Àâòîð(?) | Background: Timed chair rise tests are frequently used as a substitute for assessing leg muscle strength or power. To determine if timed chair rise tests are an indicator of lower extremity muscle power, we examined the relationship between the repetitions completed in a 30-s chair rise test and the power generated during the test.Methods: Seventy-five individuals participated in this study (n= 30 < 65 years and 45 >= 65 years). Participants underwent a 30-s chair rise test while instrumented with a power analyzer. Handgrip strength was also evaluated.Results: The relationship between chair rise repetitions and average chair rise power was R2= 0.32 (p < 0.001). Chair rise repetitions when regressed on a total (i.e., summed) chair rise power, it yielded R2= 0.70 with data from all participants combined (p < 0.001). A mediation analysis indicated that anthropometrics partially mediates the relationship between chair rise repetitions and total chair rise power accounting for 2.8%–6.9% of the variance.Conclusion: Our findings indicate that in older adults, the overall performance of chair rises offers limited information about the average power per rise but is more indicative of the cumulative power exerted. Thus, the total number of chair rises in a 30-s test is likely a more comprehensive metric of overall muscular power, reflecting endurance aspects as well. Additionally, we found that personal physical attributes, such as height and weight, partially influence the link between chair rise count and total power, highlighting the importance of factoring in individual body metrics in assessments of muscular performance. | ↑ |
16. Alterations in metabolic pathways: a bridge between aging and weaker innate immune responseÂò, 05 ìàð[-/+]Àâòîð(?) | Aging is a time-dependent progressive physiological process, which results in impaired immune system function. Age-related changes in immune function increase the susceptibility to many diseases such as infections, autoimmune diseases, and cancer. Different metabolic pathways including glycolysis, tricarboxylic acid cycle, amino acid metabolism, pentose phosphate pathway, fatty acid oxidation and fatty acid synthesis regulate the development, differentiation, and response of adaptive and innate immune cells. During aging all these pathways change in the immune cells. In addition to the changes in metabolic pathways, the function and structure of mitochondria also have changed in the immune cells. Thereby, we will review changes in the metabolism of different innate immune cells during the aging process. | ↑ |
17. Disrupting the SKN-1 homeostat: mechanistic insights and phenotypic outcomesÏí, 04 ìàð[-/+]Àâòîð(?) | The mechanisms that govern maintenance of cellular homeostasis are crucial to the lifespan and healthspan of all living systems. As an organism ages, there is a gradual decline in cellular homeostasis that leads to senescence and death. As an organism lives into advanced age, the cells within will attempt to abate age-related decline by enhancing the activity of cellular stress pathways. The regulation of cellular stress responses by transcription factors SKN-1/Nrf2 is a well characterized pathway in which cellular stress, particularly xenobiotic stress, is abated by SKN-1/Nrf2-mediated transcriptional activation of the Phase II detoxification pathway. However, SKN-1/Nrf2 also regulates a multitude of other processes including development, pathogenic stress responses, proteostasis, and lipid metabolism. While this process is typically tightly regulated, constitutive activation of SKN-1/Nrf2 is detrimental to organismal health, this raises interesting questions surrounding the tradeoff between SKN-1/Nrf2 cryoprotection and cellular health and the ability of cells to deactivate stress response pathways post stress. Recent work has determined that transcriptional programs of SKN-1 can be redirected or suppressed to abate negative health outcomes of constitutive activation. Here we will detail the mechanisms by which SKN-1 is controlled, which are important for our understanding of SKN-1/Nrf2 cytoprotection across the lifespan. | ↑ |
18. Identification of dihydromyricetin as a natural DNA methylation inhibitor with rejuvenating activity in human skinÏí, 04 ìàð[-/+]Àâòîð(?) | Changes in DNA methylation patterning have been reported to be a key hallmark of aged human skin. The altered DNA methylation patterns are correlated with deregulated gene expression and impaired tissue functionality, leading to the well-known skin aging phenotype. Searching for small molecules, which correct the aged methylation pattern therefore represents a novel and attractive strategy for the identification of anti-aging compounds. DNMT1 maintains epigenetic information by copying methylation patterns from the parental (methylated) strand to the newly synthesized strand after DNA replication. We hypothesized that a modest inhibition of this process promotes the restoration of the ground-state epigenetic pattern, thereby inducing rejuvenating effects. In this study, we screened a library of 1800 natural substances and 640 FDA-approved drugs and identified the well-known antioxidant and anti-inflammatory molecule dihydromyricetin (DHM) as an inhibitor of the DNA methyltransferase DNMT1. DHM is the active ingredient of several plants with medicinal use and showed robust inhibition of DNMT1 in biochemical assays. We also analyzed the effect of DHM in cultivated keratinocytes by array-based methylation profiling and observed a moderate, but significant global hypomethylation effect upon treatment. To further characterize DHM-induced methylation changes, we used published DNA methylation clocks and newly established age predictors to demonstrate that the DHM-induced methylation change is associated with a reduction in the biological age of the cells. Further studies also revealed re-activation of age-dependently hypermethylated and silenced genes in vivo and a reduction in age-dependent epidermal thinning in a 3-dimensional skin model. Our findings thus establish DHM as an epigenetic inhibitor with rejuvenating effects for aged human skin. | ↑ |
19. Evidence that the loss of colonic anti-microbial peptides may promote dysbiotic Gram-negative inflammaging-associated bacteria in aging miceÏí, 04 ìàð[-/+]Àâòîð(?) | Introduction: Aging studies in humans and mice have played a key role in understanding the intestinal microbiome and an increased abundance of “inflammaging” Gram-negative (Gn) bacteria. The mechanisms underlying this inflammatory profile in the aging microbiome are unknown. We tested the hypothesis that an aging-related decrease in colonic crypt epithelial cell anti-microbial peptide (AMP) gene expression could promote colonic microbiome inflammatory Gn dysbiosis and inflammaging.Methods: As a model of aging, C57BL/6J mice fecal (colonic) microbiota (16S) and isolated colonic crypt epithelial cell gene expression (RNA-seq) were assessed at 2 months (mth) (human: 18 years old; yo), 15 mth (human: 50 yo), and 25 mth (human: 84 yo). Informatics examined aging-related microbial compositions, differential colonic crypt epithelial cell gene expressions, and correlations between colonic bacteria and colonic crypt epithelial cell gene expressions.Results: Fecal microbiota exhibited significantly increased relative abundances of pro-inflammatory Gn bacteria with aging. Colonic crypt epithelial cell gene expression analysis showed significant age-related downregulation of key AMP genes that repress the growth of Gn bacteria. The aging-related decrease in AMP gene expressions is significantly correlated with an increased abundance in Gn bacteria (dysbiosis), loss of colonic barrier gene expression, and senescence- and inflammation-related gene expression.Conclusion: This study supports the proposed model that aging-related loss of colonic crypt epithelial cell AMP gene expression promotes increased relative abundances of Gn inflammaging-associated bacteria and gene expression markers of colonic inflammaging. These data may support new targets for aging-related therapies based on intestinal genes and microbiomes. | ↑ |
20. How are APOE4, changes in body weight, and longevity related? Insights from a causal mediation analysisÏò, 01 ìàð[-/+]Àâòîð(?) | The ?4 allele of the APOE gene (APOE4) is known for its negative association with human longevity; however, the mechanism is unclear. APOE4 is also linked to changes in body weight, and the latter changes were associated with survival in some studies. Here, we explore the role of aging changes in weight in the connection between APOE4 and longevity using the causal mediation analysis (CMA) approach to uncover the mechanisms of genetic associations. Using the Health and Retirement Study (HRS) data, we tested a hypothesis of whether the association of APOE4 with reduced survival to age 85+ is mediated by key characteristics of age trajectories of weight, such as the age at reaching peak values and the slope of the decline in weight afterward. Mediation effects were evaluated by the total effect (TE), natural indirect effect, and percentage mediated. The controlled direct effect and natural direct effect are also reported. The CMA results suggest that APOE4 carriers have 19%–22% (TE p= 0.020–0.039) lower chances of surviving to age 85 and beyond, in part, because they reach peak values of weight at younger ages, and their weight declines faster afterward compared to non-carriers. This finding is in line with the idea that the detrimental effect of APOE4 on longevity is, in part, related to the accelerated physical aging of ?4 carriers. | ↑ |
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