Aging-US

Listen to a blog summary of an editorial published in Volume 14, Issue 14 of Aging (Aging-US), entitled, "Restoring rhythm to prevent age-related fractures.”

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The circadian rhythm is a daily cycle (24 hours) of biological activity that is driven by an internal biological clock. A regular circadian rhythm is important for maintaining numerous facets of human life. Aging-related changes to this delicate rhythm have demonstrated negative consequences in many aspects of health, including bone health.

“Among the many risk factors for osteoporosis, a new kid on the block is disruption of the biological clock.”

On July 19, 2022, an editorial paper was published in Aging‘s Volume 14, Issue 14, entitled, “Restoring rhythm to prevent age-related fractures.” In this editorial, Annelies E. Smit, Maaike Schilperoort and Elizabeth M. Winter from Leiden University Medical Center discuss the treatment of osteoporosis by way of restoring the circadian rhythm. The researchers review the use of both medical and lifestyle interventions that aim to restore the circadian rhythm to minimize the risk of aging-related osteoporotic fractures.

Full blog - https://aging-us.org/2022/08/osteoporosis-linked-to-age-related-changes-in-circadian-rhythm/

DOI - https://doi.org/10.18632/aging.204192 (PDF Download)

Corresponding author - Elizabeth M. Winter - [email protected]

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Keywords - aging, circadian rhythm, fractures, osteoporosis, glucocorticoids, chronotherapy

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

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A new research paper was published in Aging (Aging-US) Volume 14, Issue 14, entitled, “Common electrocardiogram measures are not associated with telomere length.”

Aging is accompanied by telomere shortening. Increased telomere shortening is considered a marker of premature aging. Cardiac aging results in the development of cardiac pathologies.

Electrocardiogram (ECG) measures reflect cardiac excitation, conduction, and repolarization. ECG measures also prolong with aging and are associated with cardiac pathologies including atrial fibrillation. As premature prolongation of ECG measures is observed, researchers (Aenne S. von Falkenhausen, Rebecca Freudling, Melanie Waldenberger, Christian Gieger, Annette Peters, Martina Müller-Nurasyid, Stefan Kääb, and Moritz F. Sinner), from Ludwig-Maximilians-University Munich, Partner Site Munich Heart Alliance, German Research Center for Environmental Health, and Johannes Gutenberg University, hypothesized that such prolongation may be associated with telomere length.

“We studied the large, community-based KORA F4 Study. Of 3,080 participants enrolled between 2006 and 2007 with detailed information on demographic, anthropometric, clinical, and ECG characteristics, 2,575 presented with available data on leukocyte telomere length.”

Telomere length was determined by real-time quantitative PCR and expressed relative to a single copy gene. The researchers fitted multivariable adjusted linear regression models to associate the ECG measures RR-interval, PR-interval, QRS-duration, and heart rate corrected QTc with telomere length.

In this cohort, the mean age was 54.9±12.9 years and 46.6% were men. Increased age was associated with shorter telomere length (p<0.01), and men had shorter telomere length than women (p<0.05). In unadjusted models, heart rate (p=0.023), PR-interval (p<0.01), and QTc-interval (p<0.01) were significantly associated with shorter telomere length. However, no significant associations remained after accounting for age, sex, and covariates.

The researchers found that ECG measures are age-dependent, but not associated with shortened telomere length as a marker of biological aging. Further research is warranted to clarify if shortened telomeres are associated with clinical cardiac pathologies including atrial fibrillation.

“In conclusion, ECG measures are clearly age-dependent. However, in a large, well-characterized, and sufficiently powered cohort we were not able to substantiate the hypothesis that telomere length as a marker of biological age is a relevant contributor to this age-dependent prolongation of ECG measures.”

DOI: https://doi.org/10.18632/aging.204149

Corresponding Author: Moritz F. Sinner – Email: [email protected]

Keywords: electrocardiogram, telomere length, cardiac aging

About Aging-US:

Launched in 2009, Aging (Aging-US) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

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In the second installment of the Longevity & Aging Series, Dr. Steve Horvath, a world-renowned researcher, geneticist, biostatistician, Professor of Human Genetics and Biostatistics at the University of California, and Principal Investigator at Altos Labs, revisits 29 papers he co-authored that were published by Aging (Aging-US) and featured as a special collection of his research.

Special Collection - https://www.aging-us.com/special-collections-archive/steve-horvath

Author contact - Steve Horvath - [email protected]

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

Please visit our website at https://www.Aging-US.com​​ or connect with us:

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Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com​​

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A new research paper was published in Aging (abbreviated as "Aging (Albany NY)" by Medline/PubMed and as "Aging-US" by Web of Science) on the cover of Volume 14, Issue 14, entitled, “Aging the brain: multi-region methylation principal component based clock in the context of Alzheimer’s disease.”

Alzheimer’s disease (AD) risk increases exponentially with age and is associated with multiple molecular hallmarks of aging, one of which is epigenetic alterations. Epigenetic age predictors based on 5’ cytosine methylation (DNAm), or epigenetic clocks, have previously suggested that epigenetic age acceleration may occur in AD brain tissue.

“Epigenetic clocks are promising tools for the quantification of biological aging, yet we hypothesize that investigation of brain aging in AD will be assisted by the development of brain-specific epigenetic clocks.”

In this new study, researchers Kyra L. Thrush, David A. Bennett, Christopher Gaiteri, Steve Horvath, Christopher H. van Dyck, Albert T. Higgins-Chen, and Morgan E. Levine, from Yale University, Rush University Medical Center, University of California Los Angeles, VA Connecticut Healthcare System, and Altos Labs, hypothesized that a brain age methylation-based predictor could be developed with meaningful disease associations and broad multi-brain-region utility.

“To test this, we used DNAm capture to generate a PC-based epigenetic predictor of brain aging which we show to: (1) strongly reflect AD neuropathology and cognitive decline, and (2) track age across multiple brain regions.”

The team generated a novel age predictor, termed PCBrainAge, that was trained solely in cortical samples. This predictor utilizes a combination of principal components analysis and regularized regression, which reduces technical noise and greatly improves test-retest reliability.

“To characterize the scope of PCBrainAge’s utility, we generated DNAm data from multiple brain regions in a sample from the Religious Orders Study and Rush Memory and Aging Project.”

PCBrainAge captures meaningful heterogeneity of aging: Its acceleration demonstrates stronger associations with clinical AD dementia, pathologic AD, and APOE ε4 carrier status compared to extant epigenetic age predictors. It further does so across multiple cortical and subcortical regions.

“Overall, PCBrainAge’s increased reliability and specificity makes it a particularly promising tool for investigating heterogeneity in brain aging, as well as epigenetic alterations underlying AD risk and resilience.”

DOI: https://doi.org/10.18632/aging.204196

Corresponding Author: Albert T. Higgins-Chen - Email: [email protected]

Keywords: epigenetic clocks, unsupervised machine learning, brain, Alzheimer's disease, age acceleration

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About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

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Dr. Cristina Aguayo-Mazzucato from Beta Cell Aging Lab, Joslin Diabetes Center, Harvard Medical School, discusses an editorial she co-authored that was published by Aging (Aging-US) in Volume 14, Issue 11, entitled, “Biological age in diabetes and precision medicine.”

DOI - https://doi.org/10.18632/aging.204123 (PDF download)

Corresponding author - Cristina Aguayo-Mazzucato - [email protected]

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Keywords - biological age, diabetes mellitus, chronological age, DNA methylation, clinical biomarkers

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

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A new research paper was published in Aging (Aging-US / Albany NY)’s Volume 14, Issue 13, entitled, “Age-related neuroendocrine, cognitive, and behavioral co-morbidities are promoted by HIV-1 Tat expression in male mice.”

In the United States, approximately 1.2 million people are living with human immunodeficiency virus type-1 (HIV-1), with men accounting for the majority of cases (~75%). About half of HIV-infected individuals are 50 years of age and older. People living with HIV contend with an accelerated onset of age-related diseases and disorders; however, the pathophysiology underlying accelerated aging is poorly understood.

While the mechanisms(s) are unknown, the HIV-1 trans-activator of transcription (Tat) protein disrupts neuroendocrine function in mice partly by dysregulating mitochondria and neurosteroidogenesis.

Researchers Alaa N. Qrareya, Fakhri Mahdi, Marc J. Kaufman, Nicole M. Ashpole, and Jason J. Paris, from the University of Mississippi and Harvard Medical School’s McLean Hospital, investigated the combined effects of aging and HIV-1 Tat expression on the development of neuroHIV-like sequelae in young adult (6–8 months) and middle-aged (11–13 months) male mice to determine whether Tat precipitates age-related dysfunction.

“We hypothesized that conditional Tat expression in middle-aged male transgenic mice [Tat(+)] would promote age-related comorbidities compared to age-matched controls [Tat(−)]. We expected Tat to alter steroid hormone milieu consistent with behavioral deficits.”

Middle-aged Tat(+) mice had lower circulating testosterone and progesterone than age-matched controls and greater circulating corticosterone and central allopregnanolone than other groups. Young Tat(+) mice had greater circulating progesterone and estradiol-to-testosterone ratios. Older age or Tat exposure increased anxiety-like behavior (open field; elevated plus-maze), increased cognitive errors (radial arm water maze), and reduced grip strength. Young Tat(+), or middle-aged Tat(−), males had higher mechanical nociceptive thresholds than age-matched counterparts. Steroid levels correlated with behaviors. Thus, Tat may contribute to HIV-accelerated aging.

“In conclusion, our data suggest that older age and Tat expression exert independent and interactive effects to worsen neuroendocrine, affective, cognitive, and neuromuscular comorbidities. Novel steroid replacement therapies may be useful adjunctive therapeutics to cART in the aging HIV+ population.”

DOI: https://doi.org/10.18632/aging.204166

Corresponding Author: Jason J. Paris - Email: [email protected]

Keywords: aging, hypothalamic-pituitary-adrenal axis, hypothalamic-pituitary-gonadal axis, secondary hypogonadism, trans-activating transcriptor

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About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

Please visit our website at https://www.Aging-US.com​​ and connect with us:

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Listen to a press release about the cover paper of Volume 14, Issue 13, entitled, "Epigenetic clocks and their association with trajectories in perceived discrimination and depressive symptoms among US middle-aged and older adults.”

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A new research paper was published in Aging (Aging-US / Albany NY) on the cover of Volume 14, Issue 13, entitled, “Epigenetic clocks and their association with trajectories in perceived discrimination and depressive symptoms among US middle-aged and older adults.”

“Perceived discrimination may be associated with accelerated aging later in life, with depressive symptoms acting as potential mediator.”

In this recently published study, researchers May A. Beydoun, Hind A. Beydoun, Nicole Noren Hooten, Ana I. Maldonado, Jordan Weiss, Michele K. Evans, and Alan B. Zonderman from the National Institute on Aging’s Intramural Research Program, Fort Belvoir Community Hospital, University of Maryland, and University of California Berkeley examined a nationally representative sample of 2,806 older U.S. adults. The team evaluated associations of perceived discrimination measures with 13 DNA methylation (DNAm)-based measures of epigenetic aging. They used group-based trajectory and four-way mediation analyses.

“Here we examined retrospective data from the HRS [Health and Retirement Study 2010–2016] cohort study of U.S. adults aged 50–100 years and investigated measures of perceived discrimination and depressive symptoms in relation to 13 different DNAm-based epigenetic clocks (EPICLOCK) age-estimators.”

Read the full press release - https://www.aging-us.com/news_room/epigenetic-clocks-and-their-association-with-perceived-discrimination-and-depressive-symptoms

DOI - https://doi.org/10.18632/aging.204150

Corresponding Author: May A. Beydoun – Email: [email protected]

Keywords: DNA methylation, epigenetic clocks, biological age, perceived discrimination, depressive symptoms

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About Aging-US:

Launched in 2009, Aging (Aging-US / Albany NY) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

Please visit our website at www.Aging-US.com​​ and connect with us:

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Aging Journal Office

6666 E. Quaker Str., Suite 1B

Orchard Park, NY 14127

Phone: 1-800-922-0957, option 1

Aging is indexed by Web of Science: Science Citation Index Expanded (abbreviated as Aging‑US). As of June 29, 2022, Web of Science (Clarivate Analytics) released their 2021 JCR Impact Factor List. Aging is pleased to report that our 2021 impact factor is 5.955. This number has increased from last year’s 5.682.

Aging is listed in the Web of Science: Science Citation Index Expanded in two categories: Cell Biology and Geriatrics & Gerontology. According to the Journal Citation Indicator (JCI), Aging is ranked in the Q1 quartile in both categories.

Since 2009, Aging has published research papers in all fields of aging research including, but not limited to, aging from yeast to mammals, cellular senescence, age-related diseases such as cancer and Alzheimer’s diseases and their prevention and treatment, anti-aging strategies and drug development, and especially the role of signal transduction pathways such as mTOR in aging and potential approaches to modulate these signaling pathways to extend lifespan.

This journal aims to promote treatment of age-related diseases by slowing down aging, validation of anti-aging drugs by treating age-related diseases, and prevention of cancer by inhibiting aging. Cancer and COVID-19 are age-related diseases.

To learn more about Aging, publication standards, and past or current issues, visit www.aging-us.com.

About Aging-US:

Launched in 2009, Aging (Aging-US) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

Follow Aging on social media:

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For media inquiries, please contact [email protected].

Aging (Aging-US) Journal Office

6666 E. Quaker Str., Suite 1B

Orchard Park, NY 14127

Phone: 1-800-922-0957, option 1

A new research paper was published in Aging (Aging-US) on the cover of Volume 14, Issue 12, entitled, “Time makes histone H3 modifications drift in mouse liver.”

Aging is known to involve epigenetic histone modifications, which are associated with transcriptional changes, occurring throughout the entire lifespan of an individual.

“So far, no study discloses any drift of histone marks in mammals which is time-dependent or influenced by pro-longevity caloric restriction treatment.”

To detect the epigenetic drift of time passing, researchers—from Istituto di Ricovero e Cura a Carattere Scientifico, University of Urbino ‘Carlo Bo’, University of Milan, and University of Padua—determined the genome-wide distributions of mono- and tri-methylated lysine 4 and acetylated and tri-methylated lysine 27 of histone H3 in the livers of healthy 3, 6 and 12 months old C57BL/6 mice.

“In this study, we used chromatin immunoprecipitation sequencing technology to acquire 108 high-resolution profiles of H3K4me3, H3K4me1, H3K27me3 and H3K27ac from the livers of mice aged between 3 months and 12 months and fed 30% caloric restriction diet (CR) or standard diet (SD).”

The comparison of different age profiles of histone H3 marks revealed global redistribution of histone H3 modifications with time, in particular in intergenic regions and near transcription start sites, as well as altered correlation between the profiles of different histone modifications. Moreover, feeding mice with caloric restriction diet, a treatment known to retard aging, reduced the extent of changes occurring during the first year of life in these genomic regions.

“In conclusion, while our data do not establish that the observed changes in H3 modification are causally involved in aging, they indicate age, buffered by caloric restriction, releases the histone H3 marking process of transcriptional suppression in gene desert regions of mouse liver genome most of which remain to be functionally understood.”

DOI: https://doi.org/10.18632/aging.204107

Corresponding Author: Marco Giorgio - [email protected]

Keywords: epigenetics, aging, histones, ChIP-seq, diet

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About Aging-US:

Launched in 2009, Aging (Aging-US) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

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Dr. Liang-Kung Chen from the National Yang-Ming Chiao-Tung University, Taipei, Taiwan details a research paper he co-authored that was published by Aging (Aging-US) in Volume 14, Issue 3, entitled, “Predicting neuropsychiatric symptoms of persons with dementia in a day care center using a facial expression recognition system.”

DOI - https://doi.org/10.18632/aging.203869

Corresponding author - Liang-Kung Chen - [email protected]

Video - https://www.youtube.com/watch?v=wO7PulizlR0

Video transcript - https://aging-us.net/2022/06/28/behind-the-study-facial-expression-recognition-predicts-neuropsychiatric-symptoms-of-dementia/

Abstract

Background: Behavioral and psychological symptoms of dementia (BPSD) affect 90% of persons with dementia (PwD), resulting in various adverse outcomes and aggravating care burdens among their caretakers. This study aimed to explore the potential of artificial intelligence-based facial expression recognition systems (FERS) in predicting BPSDs among PwD.

Methods: A hybrid of human labeling and a preconstructed deep learning model was used to differentiate basic facial expressions of individuals to predict the results of Neuropsychiatric Inventory (NPI) assessments by stepwise linear regression (LR), random forest (RF) with importance ranking, and ensemble method (EM) of equal importance, while the accuracy was determined by mean absolute error (MAE) and root-mean-square error (RMSE) methods.

Results: Twenty-three PwD from an adult day care center were enrolled with ≥ 11,500 FERS data series and 38 comparative NPI scores. The overall accuracy was 86% on facial expression recognition. Negative facial expressions and variance in emotional switches were important features of BPSDs. A strong positive correlation was identified in each model (EM: r = 0.834, LR: r = 0.821, RF: r = 0.798 by the patientwise method; EM: r = 0.891, LR: r = 0.870, RF: r = 0.886 by the MinimPy method), and EM exhibited the lowest MAE and RMSE.

Conclusions: FERS successfully predicted the BPSD of PwD by negative emotions and the variance in emotional switches. This finding enables early detection and management of BPSDs, thus improving the quality of dementia care.

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Keywords - aging, artificial intelligence, behavioral and psychological symptoms of dementia, dementia, facial expression recognition system, machine learning

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

Please visit our website at http://www.Aging-US.com​​ or connect with us:

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Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com​​

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