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International Urogynecology Journal Dec 2022The objective was to test the hypotheses that a linear relationship exists between age and levator bowl volume (LBV); and that age, parity, and prolapse are...
INTRODUCTION AND HYPOTHESIS
The objective was to test the hypotheses that a linear relationship exists between age and levator bowl volume (LBV); and that age, parity, and prolapse are independently associated with LBV.
METHODS
We conducted a secondary analysis of data from nulliparous women, parous controls, and prolapse (Pelvic Organ Prolapse Quantification (POP-Q) Ba ≥ 1 cm) cases from each of three age groups: young (≤40), mid-age (50-60), and older (≥70). LBV was measured using MRI at rest and Valsalva as the 3D space contained above the levator ani muscles and below the sacrococcygeal junction-to-inferior pubic point reference plane. Linear regression models were used to examine the effects of age, parity, prolapse, and their interactions (age*parity and age*prolapse) on LBV.
RESULTS
Each group consisted of 9-12 women. LBV increased with age in a nonlinear fashion. For nulliparous women, the median value increased 4.7% per decade from the young to mid-age group and 84% per decade from the mid-age to older group; for parous controls, the corresponding increases were 38% and -0.5%; and for women with prolapse, they were 46% and 11%. Age and prolapse status (both p<0.001) were found to be significant independent predictors of LBV. Interactions between age*prolapse (p=0.003) and age*parity (p=0.045) were also independently associated with LBV.
CONCLUSIONS
Parity and prolapse influence how age affects LBV. In nulliparous women, age had little effect on LBV until after mid-age. For women with prolapse, LBV increased at a much earlier age, with the biggest difference occurring between young and mid-age women.
Topics: Humans; Female; Pregnancy; Parity; Pelvic Floor; Pelvic Organ Prolapse; Magnetic Resonance Imaging; Ultrasonography
PubMed: 35503121
DOI: 10.1007/s00192-022-05203-8 -
Aging and Disease Aug 2023With aging, the incidence of age-related diseases increases. Hence, age-related diseases are inevitable. However, the mechanisms by which aging leads to the onset and... (Review)
Review
With aging, the incidence of age-related diseases increases. Hence, age-related diseases are inevitable. However, the mechanisms by which aging leads to the onset and progression of age-related diseases remain unclear. It has been reported that inflammation is closely associated with age-related diseases and that the cGAS-STING signaling pathway, which can sense the aberrant presence of cytosolic DNA during aging and induce an inflammatory response, is an important mediator of inflammation in age-related diseases. With a better understanding of the structure and molecular biology of the cGAS-STING signaling axis, numerous selective inhibitors and agonists targeting the cGAS-STING pathway in human age-related diseases have been developed to modulate inflammatory responses. Here, we provide a narrative review of the activity of the cGAS-STING pathway in age-related diseases and discuss its general mechanisms in the onset and progression of age-related diseases. In addition, we outline treatments targeting the cGAS-STING pathway, which may constitute a potential therapeutic alternative for age-related diseases.
PubMed: 37163421
DOI: 10.14336/AD.2023.0117 -
Acta Scientific Neurology Jan 2022In contrast to chronological aging, biological aging or metabolic aging is a relative age of cells and tissues and the damage they've accumulated over years. Comparison...
In contrast to chronological aging, biological aging or metabolic aging is a relative age of cells and tissues and the damage they've accumulated over years. Comparison of one's basal metabolic rate (BMR) to the average BMR of one's chronological age group gives the Metabolic age. Higher metabolic age of younger population is a serious concern and a key factor that leads to metabolic disorders in all age groups. Slower metabolism is a symbol of older age. Higher metabolic age indicates poor metabolism and higher risk of getting diseases and health complications later in life. Therefore, aging faster metabolically can severely impact chronological age. People with obesity and diabetes suffered the most due to current ongoing Covid-19 pandemic. Data suggest that SARS-CoV-2 patients with concomitant metabolic diseases had higher risk of worse prognosis and mortality. Lowering metabolic age can thus reduce the risk of getting age related health conditions and mitigate morbidities caused by pandemic like Covid-19. Therefore, maintaining healthy metabolic age in all age groups is required in the current unprecedented times. The aim of the review is to raise the prime concerns and to improve the population health outcomes by reducing the metabolic age.
PubMed: 35573983
DOI: No ID Found -
Neurobiology of Aging Dec 2023Biological age and brain age estimated using biological and neuroimaging measures have recently emerged as surrogate aging biomarkers shown to be predictive of diverse...
Biological age and brain age estimated using biological and neuroimaging measures have recently emerged as surrogate aging biomarkers shown to be predictive of diverse health outcomes. As aging underlies the development of many chronic conditions, surrogate aging biomarkers capture health at the whole person level, having the potential to improve our understanding of multimorbidity. Our study investigates whether elevated biological age and brain age are associated with an increased risk of multimorbidity using a large dataset from the Midlife in the United States Refresher study. Ensemble learning is utilized to combine multiple machine learning models to estimate biological age using a comprehensive set of biological markers. Brain age is obtained using Gaussian processes regression and neuroimaging data. Our study is the first to examine the relationship between accelerated brain age and multimorbidity. Furthermore, it is the first attempt to explore how biological age and brain age are related to multimorbidity in mental health. Our findings hold the potential to advance the understanding of disease accumulation and their relationship with aging.
Topics: Humans; United States; Multimorbidity; Mental Health; Aging; Brain; Biomarkers; Chronic Disease
PubMed: 37804610
DOI: 10.1016/j.neurobiolaging.2023.09.003 -
American Journal of Kidney Diseases :... May 2023The incidence of kidney failure is known to increase with age. We have previously developed and validated the use of retinal age based on fundus images as a biomarker of...
RATIONALE & OBJECTIVE
The incidence of kidney failure is known to increase with age. We have previously developed and validated the use of retinal age based on fundus images as a biomarker of aging. However, the association of retinal age with kidney failure is not clear. We investigated the association of retinal age gap (the difference between retinal age and chronological age) with future risk of kidney failure.
STUDY DESIGN
Prospective cohort study.
SETTING & PARTICIPANTS
11,052 UK Biobank study participants without any reported disease for characterizing retinal age in a deep learning algorithm. 35,864 other participants with retinal images and no kidney failure were followed to assess the association between retinal age gap and the risk of kidney failure.
EXPOSURE
Retinal age gap, defined as the difference between model-based retinal age and chronological age.
OUTCOME
Incident kidney failure.
ANALYTICAL APPROACH
A deep learning prediction model used to characterize retinal age based on retinal images and chronological age, and Cox proportional hazards regression models to investigate the association of retinal age gap with incident kidney failure.
RESULTS
After a median follow-up period of 11 (IQR, 10.89-11.14) years, 115 (0.32%) participants were diagnosed with incident kidney failure. Each 1-year greater retinal age gap at baseline was independently associated with a 10% increase in the risk of incident kidney failure (HR, 1.10 [95% CI, 1.03-1.17]; P=0.003). Participants with retinal age gaps in the fourth (highest) quartile had a significantly higher risk of incident kidney failure compared with those in the first quartile (HR, 2.77 [95% CI, 1.29-5.93]; P=0.009).
LIMITATIONS
Limited generalizability related to the composition of participants in the UK Biobank study.
CONCLUSIONS
Retinal age gap was significantly associated with incident kidney failure and may be a promising noninvasive predictive biomarker for incident kidney failure.
Topics: Humans; Prospective Studies; Biological Specimen Banks; Risk Factors; Renal Insufficiency; Biomarkers; United Kingdom
PubMed: 36481699
DOI: 10.1053/j.ajkd.2022.09.018 -
International Journal of Ophthalmology 2022To explore the changes in lens thickness and density with age.
AIM
To explore the changes in lens thickness and density with age.
METHODS
A Chinese population-based retrospective study was performed. A total of 497 individuals (490 right eyes and 495 left eyes), ranging from 3 to 69 years old were included. Lens images obtained from IOL Master 700 were used to measure lens thickness and density. Piecewise regression model was chosen to illustrate the relationship of lens thickness and density with age.
RESULTS
The proportion of people aged 3-18, 19-40, over 40 was 38.6%, 50.9% and 10.5% respectively. The whole lens thickness decreased with age during the first 7 years of life, kept stable from 8 to 16 years old, and then increased at the rate of about 27 µm per year. The thickness of the lens cortex and nucleus tended to decrease first and then increase with age, which was dependent on age stages. The whole lens density also decreased with age until 7 years old. The increasing rate of lens density was different in different age groups. The whole lens density increased rapidly from 7 to 22 years old and slowed down after 22 years old. Similarly, the changing tendency of lens cortical and nuclear density differed in different age phases.
CONCLUSION
Both lens thickness and density are significantly associated with age, whereas they do not change linearly with age. Moreover, it is necessary to increase the population over 40 years old and conduct further research.
PubMed: 36262855
DOI: 10.18240/ijo.2022.10.05 -
The Journals of Gerontology. Series A,... Jan 2024DNA methylation-derived epigenetic clocks offer the opportunity to examine aspects of age acceleration (ie, the difference between an individual's biological age and...
DNA methylation-derived epigenetic clocks offer the opportunity to examine aspects of age acceleration (ie, the difference between an individual's biological age and chronological age), which vary among individuals and may better account for age-related changes in cognitive function than chronological age. Leveraging existing ambulatory cognitive assessments in daily life from a genetically diverse sample of 142 adults in midlife, we examined associations between 5 measures of epigenetic age acceleration and performance on tasks of processing speed and working memory. Covarying for chronological age, we used multilevel models to examine associations of epigenetic age acceleration (Horvath 1, Horvath 2, Hannum, PhenoAge, and GrimAge clocks) with both average level and variability of cognitive performance. Positive age acceleration (ie, epigenetic age greater than chronological age) was associated with poorer mean processing speed (Horvath 1 and 2) and working memory (GrimAge). Higher chronological age was also associated with poorer mean processing speed and working memory performance. Further, positive age acceleration was generally associated with greater intraindividual variability in working memory and processing speed tasks, whereas being chronologically older was associated with less intraindividual variability. Although further work is needed, our results indicate age acceleration effects have comparable or greater size as those for chronological age differences, suggesting that epigenetic age acceleration may account for additional risk and interindividual variation in cognitive performance above chronological age.
Topics: Humans; Aging; Epigenesis, Genetic; DNA Methylation; Cognition; Acceleration
PubMed: 37899644
DOI: 10.1093/gerona/glad242 -
CNS Neuroscience & Therapeutics Jul 2023Age and sex are important individual factors modifying the clinical symptoms of patients with Parkinson's disease (PD). Our goal is to evaluate the effects of age and...
AIMS
Age and sex are important individual factors modifying the clinical symptoms of patients with Parkinson's disease (PD). Our goal is to evaluate the effects of age and sex on brain networks and clinical manifestations of PD patients.
METHODS
Parkinson's disease participants (n = 198) receiving functional magnetic resonance imaging from Parkinson's Progression Markers Initiative database were investigated. Participants were classified into lower quartile group (age rank: 0%~25%), interquartile group (age rank: 26%~75%), and upper quartile group (age rank: 76%~100%) according to their age quartiles to examine how age shapes brain network topology. The differences of brain network topological properties between male and female participants were also investigated.
RESULTS
Parkinson's disease patients in the upper quartile age group exhibited disrupted network topology of white matter networks and impaired integrity of white matter fibers compared to lower quartile age group. In contrast, sex preferentially shaped the small-world topology of gray matter covariance network. Differential network metrics mediated the effects of age and sex on cognitive function of PD patients.
CONCLUSION
Age and sex have diverse effects on brain structural networks and cognitive function of PD patients, highlighting their roles in the clinical management of PD.
Topics: Humans; Male; Female; Parkinson Disease; Brain; Gray Matter; Magnetic Resonance Imaging; White Matter
PubMed: 36890620
DOI: 10.1111/cns.14149 -
Scientific Reports Jun 2022Glycemia is linked with one of the key mechanisms underlying the aging process and inter-individual differences in biological age. Previous research showed that glucose...
Glycemia is linked with one of the key mechanisms underlying the aging process and inter-individual differences in biological age. Previous research showed that glucose level is linked with perceived age in elder individuals. This study aimed to verify if glycemia is related to perceived facial age in healthy adult individuals as interventions in younger and healthy cohorts are crucial for preventing the onset of age-related diseases. The study sample consisted of 116 healthy men of mean age 35.53 ± 3.54 years (29.95-44.29) and 163 healthy women of mean age 28.38 ± 2.40 (24.25-34.17) years. Glycemia was evaluated by fasting glucose, insulin, HOMA-IR, and glycated hemoglobin level. BMI, facial sexual dimorphism, estradiol, testosterone, and hsCRP levels were controlled. Perceived age was evaluated based on standardized facial photos in an online survey. Additionally perceived facial aging was calculated as a difference between perceived age and chronological age. No relationship between the levels of biochemical indicators of glycemia and perceived facial age or aging was found both in men and women, also when controlled for possible confounders. This study shows that perceived facial age in adult individuals is rather linked with body adiposity of sexual dimorphism but not with glycemic markers.
Topics: Adult; Aged; Blood Glucose; Fasting; Female; Glucose; Glucose Tolerance Test; Humans; Insulin; Insulin Resistance; Male
PubMed: 35710822
DOI: 10.1038/s41598-022-14555-6 -
BioRxiv : the Preprint Server For... Oct 2023The differentiation of human pluripotent stem cells (hPSCs) provides access to most cell types and tissues. However, hPSC-derived lineages capture a fetal-stage of...
The differentiation of human pluripotent stem cells (hPSCs) provides access to most cell types and tissues. However, hPSC-derived lineages capture a fetal-stage of development and methods to accelerate progression to an aged identity are limited. Understanding the factors driving cellular age and rejuvenation is also essential for efforts aimed at extending human life and health span. A prerequisite for such studies is the development of methods to score cellular age and simple readouts to assess the relative impact of various age modifying strategies. Here we established a transcriptional score (RNAge) in young versus old primary fibroblasts, frontal cortex and substantia nigra tissue. We validated the score in independent RNA-seq datasets and demonstrated a strong cell and tissue specificity. In fibroblasts we observed a reset of RNAge during iPSC reprogramming while direct reprogramming of aged fibroblasts to induced neurons (iN) resulted in the maintenance of both a neuronal and a fibroblast aging signature. Increased RNAge in hPSC-derived neurons was confirmed for several age-inducing strategies such as SATB1 loss, progerin expression or chemical induction of senescence (SLO). Using RNAge as a probe set, we next performed an in-silico screen using the LINCS L1000 dataset. We identified and validated several novel age-inducing and rejuvenating compounds, and we observed that RNAage captures age-related changes associated with distinct cellular hallmarks of age. Our study presents a simple tool to score age manipulations and identifies compounds that greatly expand the toolset of age-modifying strategies in hPSC derived lineages.
PubMed: 37461485
DOI: 10.1101/2023.07.03.547539