A traditional, twice-monthly, peer-reviewed, open-access journal covering all areas of research on aging and age-related diseases, including cancer and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome.

In June 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.

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Aging (Aging-US)

Aging (Aging-US) published this trending research paper in Volume 14, Issue 17, entitled, “Aging, prevalence and risk factors of MRI-visible enlarged perivascular spaces” by researchers from Boston University School of Medicine, Boston, MA, NHLBI’s Framingham Heart Study, Framingham, MA, Department of Biostatistics, Boston University School of Public Health, Boston, MA, Department of Radiology, Veterans Affairs Boston Health System, Boston, MA, Department of Neurology, Boston University School of Medicine, Boston, MA, The Glenn Biggs Institute for Alzheimer's and Neurodegenerative Diseases, University of Texas Health Sciences Center, San Antonio, TX, Department of Neurology, University of California at Davis, Davis, CA.

DOI - https://doi.org/10.18632/aging.204181

Corresponding author - Jose R. Romero - joromero@bu.edu 

Abstract

Background and purpose: Cerebral small vessel disease (CSVD) increases with age and is associated with stroke and cognitive decline. Enlarged Perivascular Spaces (ePVS) is an emerging marker of CSVD, but its prevalence over the life span remain unclear. We characterized the age and sex-specific prevalence of ePVS and relation to age-specific risk factors, in a large community-based sample.

Methods: We included 3,710 Framingham Heart Study participants with available brain MRI (average age 61.4±14.6, 46% men). ePVS burden was rated in the centrum semiovale (CSO) and basal ganglia (BG) regions. Individual vascular risk factors were related to ePVS burden in the CSO, BG, and mixed CSO-BG regions using multivariable adjusted ordinal logistic regression analysis.

Results: Severe ePVS prevalence increased with age in men and women, and paralleled increase in vascular risk factors, and prevention treatment use. Older age, hypertension (and resulting higher treatment use), higher systolic and diastolic blood pressure, and smoking were associated with higher burden of ePVS in the CSO, BG and mixed regions.

Conclusions: Our observations reinforce the hypothesis that ePVS may be a marker of aging-driven brain vascular pathologies, and its association with vascular risk factors support their role as CSVD imaging biomarker.

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Keywords - cerebral small vessel disease, neurological markers, aging, disease marker, perivascular spaces

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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Paper Spotlight: Aging, Prevalence and Risk Factors of MRI-Visible Enlarged Perivascular Spaces

Dr. May Beydoun from the Laboratory of Epidemiology and Population Sciences, NIA/NIH/IRP, in Baltimore, MD, discusses a research paper she co-authored that was published by Aging (Aging-US) as the cover for 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.”

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

Corresponding author - May A. Beydoun - baydounm@mail.nih.gov

Abstract

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

Methods: A nationally representative sample of older adults was used [Health and Retirement Study 2010–2016, Age: 50–100 y in 2016, N = 2,806, 55.6% female, 82.3% Non-Hispanic White (NHW)] to evaluate associations of perceived discrimination measures [Experience of discrimination or EOD; and Reasons for Perceived discrimination or RPD) and depressive symptoms (DEP)] with 13 DNAm-based measures of epigenetic aging. Group-based trajectory and four-way mediation analyses were used.

Results: Overall, and mostly among female and NHW participants, greater RPD in 2010–2012 had a significant adverse total effect on epigenetic aging [2016: DNAm GrimAge, DunedinPoAm38 (MPOA), Levine (PhenoAge) and Horvath 2], with 20–50% of this effect being explained by a pure indirect effect through DEP in 2014–2016. Among females, sustained elevated DEP (2010–2016) was associated with greater LIN DNAm age (β ± SE: +1.506 ± 0.559, p = 0.009, reduced model), patterns observed for elevated DEP (high vs. low) for GrimAge and MPOA DNAm markers. Overall and in White adults, the relationship of the Levine clock with perceived discrimination in general (both EOD and RPD) was mediated through elevated DEP.

Conclusions: Sustained elevations in DEP and RPD were associated with select biological aging measures, consistently among women and White adults, with DEP acting as mediator in several RPD-EPICLOCK associations.

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

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

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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Behind the Study: Epigenetic Clocks Association with Perceived Discrimination, Depressive Symptoms

Aging-US published this research paper as the cover for Volume 14, Issue 17, entitled, "Extracellular microRNA and cognitive function in a prospective cohort of older men: The Veterans Affairs Normative Aging Study” by researchers from the Department of Environmental Health Sciences, Columbia University Mailman School of Public Health, New York, NY; Department of Obstetrics, Gynecology, and Reproductive Sciences, University of California San Diego, La Jolla, CA; VA Normative Aging Study, VA Boston Healthcare System, Boston, MA; Department of Medicine, Boston University School of Medicine, Boston, MA; Massachusetts Veterans Epidemiology and Research Information Center, VA Boston Healthcare System, Boston, MA; Department of Epidemiology, Boston University School of Public Health, Boston, MA; Department of Psychiatry, Boston University School of Medicine, Boston, MA; Department of Environmental Health, Harvard TH Chan School of Public Health, Boston, MA; Department of Biostatistics, Harvard TH Chan School of Public Health, Boston, MA.

DOI - https://doi.org/10.18632/aging.204268

Corresponding authors - Nicole Comfort - nicole.comfort@columbia.edu

Abstract
Background: Aging-related cognitive decline is an early symptom of Alzheimer’s disease and other dementias, and on its own can have substantial consequences on an individual’s ability to perform important everyday functions. Despite increasing interest in the potential roles of extracellular microRNAs (miRNAs) in central nervous system (CNS) pathologies, there has been little research on extracellular miRNAs in early stages of cognitive decline. We leverage the longitudinal Normative Aging Study (NAS) cohort to investigate associations between plasma miRNAs and cognitive function among cognitively normal men.

Methods: This study includes data from up to 530 NAS participants (median age: 71.0 years) collected from 1996 to 2013, with a total of 1,331 person-visits (equal to 2,471 years of follow up). Global cognitive function was assessed using the Mini-Mental State Examination (MMSE). Plasma miRNAs were profiled using small RNA sequencing. Associations of expression of 381 miRNAs with current cognitive function and rate of change in cognitive function were assessed using linear regression (N = 457) and linear mixed models (N = 530), respectively.

Results: In adjusted models, levels of 2 plasma miRNAs were associated with higher MMSE scores (p < 0.05). Expression of 33 plasma miRNAs was associated with rate of change in MMSE scores over time (p < 0.05). Enriched KEGG pathways for miRNAs associated with concurrent MMSE and MMSE trajectory included Hippo signaling and extracellular matrix-receptor interactions. Gene targets of miRNAs associated with MMSE trajectory were additionally associated with prion diseases and fatty acid biosynthesis.

Conclusions: Circulating miRNAs were associated with both cross-sectional cognitive function and rate of change in cognitive function among cognitively normal men. Further research is needed to elucidate the potential functions of these miRNAs in the CNS and investigate relationships with other neurological outcomes.

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Press release - https://aging-us.com/news_room/Extracellular-microRNA-and-cognitive-function-in-a-prospective-cohort-of-older-men

Keywords - aging, plasma, extracellular RNA, RNA-seq, microRNA, cognitive decline, cognitive impairment

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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Extracellular microRNA and Cognitive Function in Older Men

In the fourth episode of the Longevity & Aging Series, Dr. Carly Bobak from Dartmouth College, Dr. Cristian Coarfa from Baylor College of Medicine, and Dr. Andrew DiNardo from Baylor College of Medicine, discuss a research paper they co-authored that was published in Volume 14, Issue 5 of Aging (Aging-US), entitled, “Increased DNA methylation, cellular senescence and premature epigenetic aging in guinea pigs and humans with tuberculosis.”

DOI - https://doi.org/10.18632/aging.203936

Corresponding Authors - Carly A. Bobak - carlybobak@dartmouth.edu, Cristian Coarfa - coarfa@bcm.edu, and Andrew R. DiNardo - andrew.dinardo@bcm.edu

Abstract

Background: Tuberculosis (TB) is the archetypical chronic infection, with patients having months of symptoms before diagnosis. In the two years after successful therapy, survivors of TB have a three-fold increased risk of death.

Methods: Guinea pigs were infected with Mycobacterium tuberculosis (Mtb) for 45 days, followed by RRBS DNA methylation analysis. In humans, network analysis of differentially expressed genes across three TB cohorts were visualized at the pathway-level. Serum levels of inflammation were measured by ELISA. Horvath (DNA methylation) and RNA-seq biological clocks were used to investigate shifts in chronological age among humans with TB.

Results: Guinea pigs with TB demonstrated DNA hypermethylation and showed system-level similarity to humans with TB (p-value = 0.002). The transcriptome in TB in multiple cohorts was enriched for DNA methylation and cellular senescence. Senescence associated proteins CXCL9, CXCL10, and TNF were elevated in TB patients compared to healthy controls. Humans with TB demonstrate 12.7 years (95% CI: 7.5, 21.9) and 14.38 years (95% CI: 10.23–18.53) of cellular aging as measured by epigenetic and gene expression based cellular clocks, respectively.

Conclusions: In both guinea pigs and humans, TB perturbs epigenetic processes, promoting premature cellular aging and inflammation, a plausible means to explain the long-term detrimental health outcomes after TB.

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Keywords - aging, tuberculosis, multi-cohort analysis, network analysis, DNA methylation, senescence, Cavia porcellus, DNA hypermethylation, epigenetic aging
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:

SoundCloud - https://soundcloud.com/Aging-Us
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Longevity & Aging Series (EP 4): Drs. Carly Bobak, Cristian Coarfa, Andrew DiNardo

Aging-US published this trending review in Volume 14, Issue 16, entitled, "New hallmarks of ageing: a 2022 Copenhagen ageing meeting summary" by researchers from the Department of Clinical Molecular Biology, University of Oslo and Akershus University Hospital, Lørenskog 1478, Norway; Jagiellonian Centre for Experimental Therapeutics (JCET), Jagiellonian University, Krakow 30-348, Poland; Center for Healthy Ageing, Department of Cellular and Molecular Medicine, University of Copenhagen, Copenhagen 2400, Denmark; Institute of Sports Medicine Copenhagen, Department of Orthopedic Surgery, Copenhagen University Hospital – Bispebjerg and Frederiksberg, Copenhagen 2400, Denmark; Molecular Medicine and Gene Therapy, Lund Stem Cell Center, Lund University, Lund, Sweden; Stem Cell Laboratory, UCL Cancer Institute, University College London, London, UK; Department of Clinical Physiology and Nuclear Medicine, Copenhagen University Hospital Rigshospitalet, Glostrup 2600, Denmark; The David and Inez Myers Laboratory of Cancer Genetics, Department of Human Molecular Genetics and Biochemistry, Tel Aviv University School of Medicine P.O.B 39040, Tel Aviv, Israel; Department of Environmental and Occupational Health, University of Pittsburgh School of Public Health, Pittsburgh, PA; Department of Functional Genomics and Cancer, IGBMC, CNRS/INSERM/University of Strasbourg, Equipe labellisée Ligue contre le Cancer, Strasbourg, France; College of Medicine, Center for Genomics and Precision Medicine, National Taiwan University, Taipei City, Taiwan; UK National Innovation Centre for Ageing, The Catalyst, 3 Science Square, Newcastle University, Newcastle upon Tyne, NE4 5TG, UK; Buck Institute for Research on Ageing, Novato, CA; Section on DNA Repair, National Institute on Ageing, Baltimore, MD; Department of Biochemistry, University of Oxford, Oxford OX1 3QU, UK; Department of Molecular Biology and Genetics, Aarhus University, Aarhus 8000, Denmark; The Norwegian Centre on Healthy Ageing (NO-Age), Oslo, Norway; UPMC Hillman Cancer Center, Pittsburgh, PA. 
#openaccess #meeting #aging #science #peerreview

DOI - https://doi.org/10.18632/aging.204248

Corresponding authors - Tinna Stevnsner - tvs@mbg.au.dk, Lene Juel Rasmussen - lenera@sund.ku.dk, Evandro F. Fang - e.f.fang@medisin.uio.no

Abstract

Genomic instability, telomere attrition, epigenetic alterations, mitochondrial dysfunction, loss of proteostasis, deregulated nutrient-sensing, cellular senescence, stem cell exhaustion, and altered intercellular communication were the original nine hallmarks of ageing proposed by López-Otín and colleagues in 2013. The proposal of these hallmarks of ageing has been instrumental in guiding and pushing forward research on the biology of ageing. In the nearly past 10 years, our in-depth exploration on ageing research has enabled us to formulate new hallmarks of ageing which are compromised autophagy, microbiome disturbance, altered mechanical properties, splicing dysregulation, and inflammation, among other emerging ones. Amalgamation of the ‘old’ and ‘new’ hallmarks of ageing may provide a more comprehensive explanation of ageing and age-related diseases, shedding light on interventional and therapeutic studies to achieve healthy, happy, and productive lives in the elderly.

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Keywords - aging, hallmarks of ageing, neurodegeneration, healthspan, longevity, autophagy

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:

SoundCloud - https://soundcloud.com/Aging-Us
Facebook - https://www.facebook.com/AgingUS/
Twitter - https://twitter.com/AgingJrnl
Instagram - https://www.instagram.com/agingjrnl/
YouTube - https://www.youtube.com/agingus​
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Paper Spotlight: New Hallmarks of Ageing 2022 Meeting Summary

Aging-US published this trending research paper in Volume 14, Issue 16, entitled, "Systemic lipolysis promotes physiological fitness in Drosophila melanogaster" by researchers the Department of Biochemistry, Molecular Biology and Biophysics, University of Minnesota, Minneapolis, MN; Department of Genetics, Cell Biology, and Development, University of Minnesota, Minneapolis, MN; Department of Environmental and Occupational Health Sciences, University of Washington, Seattle, WA; University of Minnesota Informatics Institute, Minneapolis, MN; Minnesota Supercomputing Institute, University of Minnesota, Minneapolis, MN; Department of Biology, University of Washington, Seattle, WA; Department of Lab Medicine and Pathology, University of Washington School of Medicine, Seattle, WA; Department of Medicine, Division of Diabetes, Endocrinology and Metabolism, University of Minnesota, Minneapolis, MN.

DOI - https://doi.org/10.18632/aging.204251

Corresponding author - Douglas G. Mashek - dmashek@umn.edu

Abstract

Since interventions such as caloric restriction or fasting robustly promote lipid catabolism and improve aging-related phenotypical markers, we investigated the direct effect of increased lipid catabolism via overexpression of bmm (brummer, FBgn0036449), the major triglyceride hydrolase in Drosophila, on lifespan and physiological fitness. Comprehensive characterization was carried out using RNA-seq, lipidomics and metabolomics analysis. Global overexpression of bmm strongly promoted numerous markers of physiological fitness, including increased female fecundity, fertility maintenance, preserved locomotion activity, increased mitochondrial biogenesis and oxidative metabolism. Increased bmm robustly upregulated the heat shock protein 70 (Hsp70) family of proteins, which equipped the flies with higher resistance to heat, cold, and ER stress via improved proteostasis. Despite improved physiological fitness, bmm overexpression did not extend lifespan. Taken together, these data show that bmm overexpression has broad beneficial effects on physiological fitness, but these effects did not impact lifespan.

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Press release - https://www.aging-us.com/news_room/Systemic-lipolysis-promotes-physiological-fitness-in-Drosophila-melanogaster

Keywords - aging, brummer, lipolysis, physiological fitness, stress resistance, proteostasis

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:

SoundCloud - https://soundcloud.com/Aging-Us
Facebook - https://www.facebook.com/AgingUS/
Twitter - https://twitter.com/AgingJrnl
Instagram - https://www.instagram.com/agingjrnl/
YouTube - https://www.youtube.com/agingus​
LinkedIn - https://www.linkedin.com/company/aging/
Pinterest - https://www.pinterest.com/AgingUS/

Media Contact
18009220957
MEDIA@IMPACTJOURNALS.COM

Aging (Aging-US)

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