Aging-US

Listen to the list of the 10 most-viewed papers on Aging-US.com of 2021. 10 - “Iron: an underrated factor in aging” DOI - https://doi.org/10.18632/aging.203612 9 - “Reversal of cognitive decline: A novel therapeutic program” https://doi.org/10.18632/aging.100690 8 - “Shorter telomere lengths in patients with severe COVID-19 disease” https://doi.org/10.18632/aging.202463 7 - “Hyperbaric oxygen therapy alleviates vascular dysfunction and amyloid burden in an Alzheimer’s disease mouse model and in elderly patients” https://doi.org/10.18632/aging.203485 6 - “Fighting the storm: could novel anti-TNFα and anti-IL-6 C. sativa cultivars tame cytokine storm in COVID-19?” https://doi.org/10.18632/aging.202500 5 - “Examining sleep deficiency and disturbance and their risk for incident dementia and all-cause mortality in older adults across 5 years in the United States” https://doi.org/10.18632/aging.202591 4 - “Rejuvant®, a potential life-extending compound formulation with alpha-ketoglutarate and vitamins, conferred an average 8 year reduction in biological aging, after an average of 7 months of use, in the TruAge DNA methylation test” https://doi.org/10.18632/aging.203736 3 - “Aging and rejuvenation - a modular epigenome model” https://doi.org/10.18632/aging.202712 2 - “Potential reversal of epigenetic age using a diet and lifestyle intervention: a pilot randomized clinical trial” https://doi.org/10.18632/aging.202913 1 - “Hyperbaric oxygen therapy increases telomere length and decreases immunosenescence in isolated blood cells: a prospective trial” https://doi.org/10.18632/aging.202188 Keywords - aging, science, research, longevity, lifespan, healthspan, openaccess, researchpapers, journalpublication 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: 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/ Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com​​ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

Is muscle wasting a fate humans can avoid, or will the problem of aging-related muscle loss only be resolved when the mystery of aging is solved? Researchers—from Vrije Universiteit Amsterdam, University of Amsterdam, Sorbonne Université, Amsterdam University Medical Center VUmc, Université Catholique de Louvain, KU Leuven, and Institut NeuroMyoGène—conducted a study aimed at elucidating whether muscle stem cells are inherently impaired by the aging process in their ability to sense and respond to mechanical cues. Their priority research paper was published on the cover of Aging (Aging-US) Volume 14, Issue 1, and entitled, “Reduced growth rate of aged muscle stem cells is associated with impaired mechanosensitivity.” MUSCLE STEM CELLS Muscle stem cells (MuSCs) are stem cells located within skeletal muscle tissues. MuSCs function to repair damaged myofibers and give rise to new skeletal muscle cells. These self-renewing stem cells are involved in muscle growth, repair and regeneration. As we age, MuSCs decline in number and lose their potential to regenerate damaged myofibers, leading to sarcopenia. The researchers in this study hypothesized that the responsiveness of aged MuSCs is impared by the aging process both physically and mechanically. “We postulated that aged MuSCs are intrinsically impaired in their responsiveness to omnipresent mechanical cues through alterations in MuSC morphology, mechanical properties, and number of integrins, culminating in impaired proliferative capacity.” Full blog - https://www.impactjournals.com/journals/blog/trending-with-impact/trending-with-impact-are-our-muscles-intrinsically-impaired-by-aging/ DOI - https://doi.org/10.18632/aging.203830 Correspondence to - Richard T. Jaspers - r.t.jaspers@vu.nl Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.203830 Keywords - aging, mechanosensitivity, muscle stem cell, proliferation, YAP signaling 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: 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/ Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com​​ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

A variety of eye disorders can occur as humans age, including age-related macular degeneration, cataracts, presbyopia, glaucoma, dry eyes, and temporal arteritis. These conditions can contribute to vision impairment and even vision loss. Unfortunately, the full gambit of common age-related eye lens changes which contribute to these disorders is not yet fully defined. However, while mice and primates are different species, their eye lenses share common characteristics. This means that studies in murine models regarding age-related eye lens changes may provide a baseline for aging studies on human eye lenses in the future. “Little is known about the morphological, mechanical, refractive and cellular changes that occur with advanced age in the lens. Mice offer an opportunity to investigate changes in lens morphometrics, stiffness, transparency and refractive properties with age in a relatively shortened period of time.” To further define common age-related changes in eye lenses, researchers—from The Scripps Research Institute, University of Delaware, Morehouse School of Medicine, Nottingham Trent University, Japan Synchrotron Radiation Research Institute, and Boston University School of Medicine—conducted an extensive study of eye lenses among mice between one and 30 months of age. Their paper was published by Aging (Aging-US) in 2019, and entitled, “Age-related changes in eye lens biomechanics, morphology, refractive index and transparency.” Full bog - https://www.impactjournals.com/journals/blog/trending-with-impact/common-age-related-changes-in-eye-lenses/ Special collection on eye disease - https://www.aging-us.com/special-collections-archive/eye-disease Press release - https://www.aging-us.com/news_room/age-related-changes-in-eye-lens-biomechanics Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.102584 DOI - https://doi.org/10.18632/aging.102584 Full text - https://www.aging-us.com/article/102584/text Correspondence to: Velia M. Fowler email: vfowler@udel.edu and Catherine Cheng email: ckcheng@iu.edu Keywords: fiber cell, strain, epithelial cell, cataract, stiffness 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 on: 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/ Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com​​ or connect with @ImpactJrnls Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

Chronobiology is the study of biological rhythms. The human circadian system is a biological process known to regulate the sleeping and waking cycle (circadian rhythm; CR). Components of the circadian system are known as ​​clock genes. Clock genes generate daily oscillations of gene expression and interact as an intricate network to influence biological processes in organisms, tissues and cells. This system is primarily regulated by Earth’s day and night cycles (light and darkness), though it can be affected by other factors, including nutrition, cellular devices, stress, illness, jet lag, and aging. “It is well established that aging interferes with the regulation of the circadian system, which, in return, contributes to the manifestation and progression of aging-related diseases (reviewed in [4, 5]).” Across an organism’s lifespan, changes in circadian rhythm take place. These changes can cause aging-related diseases to become more prevalent. Studies have also shown that age-independent alterations in the circadian system can result in premature aging. This interrelation between aging and CR means that aging may play a role in the circadian system and that the circadian system may play a role in aging. However, researchers have not yet fully illuminated the impact of aging-related circadian system changes on healthy organs and tissues. “Whether aging-related changes of the circadian system’s regulation follow a conserved pattern across different species and tissues, hence representing a common driving force of aging, is unclear.” In an effort to identify circadian rhythm regulatory patterns over the course of aging, researchers—from Friedrich Schiller University Jena, FLI Leibniz Institute for Age Research, Jena University Hospital, German Center for Integrative Biodiversity Research, and European Virus Bioinformatics Center—performed inter-species and inter-organ transcriptional analyses. The research paper was published in December of 2021 as the cover of Aging (Aging-US) Volume 12, Issue 24, and entitled, “Age-dependent expression changes of circadian system-related genes reveal a potentially conserved link to aging.” Full blog - https://www.impactjournals.com/journals/blog/aging/aging-and-circadian-rhythm-does-a-conserved-link-exist/ Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.203788 DOI - https://doi.org/10.18632/aging.203788 Full Text - https://www.aging-us.com/article/203788/text Correspondence to: Emanuel Barth email: emanuel.barth@uni-jena.de Keywords: aging, circadian clock system, circadian rhythm, inter-species comparison, longevity, RNA-Seq 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 on: 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/ Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com​​ or connect with @ImpactJrnls Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

Aging-US published "DNA methylation-based measures of biological age: meta-analysis predicting time to death" in 2016, which reported that estimates of biological age based on DNA methylation patterns, often referred to as "epigenetic age", "DNAm age", have been shown to be robust biomarkers of age in humans. These authors previously demonstrated that independent of chronological age, epigenetic age assessed in blood predicted all-cause mortality in four human cohorts. Here, they expanded their original observation to 13 different cohorts for a total sample size of 13,089 individuals, including three racial/ethnic groups. In addition, they examined whether incorporating information on blood cell composition into the epigenetic age metrics improves their predictive power for mortality. All considered measures of epigenetic age acceleration were predictive of mortality, independent of chronological age, even after adjusting for additional risk factors. The authors said, "DNA methylation-based biomarkers, often referred to as ‘epigenetic age’ or ‘epigenetic clock’, are robust estimators of chronological age of an individual." Full Press Release - https://www.aging-us.com/news_room/dna-methylation-based-measures-of-biological-age Full Text - https://www.aging-us.com/article/101020/text/ Correspondence to: Steve Horvath email: shorvath@mednet.ucla.edu Keywords: all-cause mortality, lifespan, epigenetics, epigenetic clock, DNA+methylation, mortality 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 on: 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/ Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com​​ or connect with @ImpactJrnls Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

Aging-US published "Epigenetic age of the pre-frontal cortex is associated with neuritic plaques, amyloid load, and Alzheimer’s disease related cognitive functioning" in 2015, which reported that there is an urgent need to develop molecular biomarkers of brain age in order to advance our understanding of age related neurodegeneration. Here the authors use n=700 dorsolateral prefrontal cortex samples from Caucasian subjects of the Religious Order Study and the Rush Memory and Aging Project to examine the association between epigenetic age and Alzheimer’s disease related cognitive decline, and AD related neuropathological markers. The neuropathological markers may mediate the association between epigenetic age and cognitive decline. Genetic complex trait analysis revealed that epigenetic age acceleration is heritable and has significant genetic correlations with diffuse plaques and possibly working memory. Overall, these results suggest that the epigenetic clock may lend itself as a molecular biomarker of brain age. Dr. Steve Horvath said, "Cognitive aging is on a continuum from normality, to mild cognitive impairment (MCI), to dementia." Complete Press Release - https://www.aging-us.com/news_room/epigenetic-age-of-the-pre-frontal-cortex Full Text - https://www.aging-us.com/article/100864/text/ Correspondence to: Steve Horvath email: shorvath@mednet.ucla.edu Keywords: epigenetics, neuritic plaques, amyloids, cognitive functioning, memory, Alzheimer's disease, epigenetic clock, DNA methylation About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, 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 on: 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/ Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com​​ or connect with @ImpactJrnls Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

In 2017, the 2nd Interventions in Aging Conference on "Understanding Mechanisms & Compressing Morbidity in Aging Humans" was held in Cancun, Mexico. The co-chairs of this conference, and speakers in this Aging (Aging-US) video, are Drs. Dame Linda Partridge DBE, FRS, FRSE, FMedSci, and Brian Kennedy Ph.D. Dr. Partridge is currently the Weldon Professor of Biometry in the Department of Genetics, Evolution and Environment at the University College London (UCL), Director of UCL's Institute of Healthy Ageing, and the Founding Director of the Max Planck Institute for the Biology of Ageing. Dr. Kennedy is a Distinguished Professor in the Department of Biochemistry and Physiology at the National University of Singapore (NUS)'s Yong Loo Lin School of Medicine. Dr. Kennedy is also Director of the National University Health System (NUHS) Centre for Healthy Ageing in Singapore, Professor at the Buck Institute for Research on Ageing, Adjunct Professor at the University of Southern California's Leonard Davis School of Gerontology, and Affiliate Faculty in Department of Biochemistry at the University of Washington. In this video, these two prominent researchers briefly discussed the state of aging research in 2017, and postulated what the future of aging interventions may look like. Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.101221 DOI - https://doi.org/10.18632/aging.101221 Full Text - https://www.aging-us.com/article/101221/text#fulltext Correspondence to: Brian K. Kennedy email: bkennedy@buckinstitute.org and Linda Partridge email: partridge@age.mpg.de Keywords: healthspan, organismal aging, epigenetics, longevity, cellular mechanisms, metabolism, aging, conference About Aging (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 on: 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/ Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com​​ or connect with @ImpactJrnls Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

The researchers recruited healthy older participants to two groups according to their history of tea drinking frequency and investigated both functional and structural networks to reveal the role of tea drinking on brain organization. The suppression of hemispheric asymmetry in the structural connectivity network was observed as a result of tea drinking. The authors did not observe any significant effects of tea drinking on the hemispheric asymmetry of the functional connectivity network. Dr. Junhua Li and Dr. Lei Feng said, "Tea has been a popular beverage since antiquity, with records referring to consumption dating back to the dynasty of Shen Nong (approximately 2700 BC) in China." Tea is consumed in diverse ways, with brewed tea and products with a tea ingredient extremely prevalent in Asia, especially in China and Japan. Although individual constituents of tea have been related to the roles of maintaining cognitive abilities and preventing cognitive decline, a study with behavioural and neurophysiological measures showed that there was a degraded effect or no effect when a constituent was administered alone and a significant effect was observed only when constituents were combined. The superior effect of the constituent combination was also demonstrated in a comparative experiment that suggested that tea itself should be administered instead of tea extracts; a review of tea effects on the prevention of Alzheimers disease, found that the neuroprotective role of herbal tea was apparent in eight out of nine studies. It is worth noting that the majority of studies thus far have evaluated tea effects from the perspective of neurocognitive and neuropsychological measures, with direct measurement of brain structure or function less-well represented in the extant literature. These studies focusing on brain regional alterations did not ascertain tea effects on interregional interactions at the level of the entire brain. The Li/Feng Research team concluded, "In summary, our study comprehensively investigated the effects of tea drinking on brain connectivity at both global and regional scales using multi-modal imaging data and provided the first compelling evidence that tea drinking positively contributes to brain structure making network organization more efficient." Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.102023 DOI - https://doi.org/10.18632/aging.102023 Full Text - https://www.aging-us.com/article/102023/text Correspondence to: Junhua Li email: junhua.li@essex.ac.uk and Lei Feng email: pcmfl@nus.edu.sg Keywords: tea drinking, brain efficiency, fMRI, DTI, default mode network, hemispheric asymmetry About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, 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 on: 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/ Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls Media Contact 18009220957x105 MEDIA@IMPACTJOURNALS.COM

Men and women universally experience a decrease in sex hormones with age. Given this knowledge, researchers previously conducted a study to assess the correlation between aging, estrogen levels and the release of glycans (carbohydrate-based polymers) among all proteins in the body. Glycans are also important components of immunoglobulin G (IgG). IgGs are serum antibodies which provide immune protection against bodily infections and mediate systemic inflammation. Each IgG molecule usually includes about 3% glycans. However, changes in the composition of glycans attached to IgGs can significantly influence antibody activity. A decrease in galactosylation has been correlated with the onset of disease and aging. “The decrease in IgG galactosylation was first reported over 35 years ago in patients with rheumatoid arthritis and osteoarthritis [4].” The researchers found that estrogen regulates glycosylation. However, the data they analyzed did not differentiate IgG glycosylation from the other proteins. The Glycan Age Index (a combination of three IgG glycans that appear to be both biomarkers and effectors of aging) can be used to calculate glycan age. Glycan age is associated with lifestyle and disease-risk biomarkers, and could potentially be used to monitor healthy or unhealthy aging. “Here arises probably the most exciting aspect of the relationship between aging and IgG glycosylation: the potential of IgG glycans to distinguish between healthy and unhealthy aging, and to monitor the effect of introduced life-style changes on biological age.” To identify changes in IgG glycans, researchers—from Genos Glycoscience Research Laboratory, University of Colorado Anschutz Medical Campus, Eastern Colorado VA Geriatric Research, University of Zagreb, Brigham and Women’s Hospital, and Boston Children’s Hospital—reanalyzed samples from the previous intervention study using state-of-the-art glycoprofiling technology. The focus of this study was to evaluate the effects of estrogen suppression, followed by estradiol supplementation, on biological age measured by the glycan age. Their paper was published in Aging (Aging-US) Volume 12, Issue 19, in 2020, and entitled, “Effects of estradiol on biological age measured using the glycan age index”. Full blog - https://www.impactjournals.com/journals/blog/aging/can-hormone-therapy-improve-aging/ Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.104060 DOI - https://doi.org/10.18632/aging.104060 Full text - https://www.aging-us.com/article/104060/text Correspondence to: Gordan Lauc email: glauc@pharma.hr Keywords: biological age, glycan age, estrogen, aging biomarkers, glycosylation 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 on: 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/ Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com​​ or connect with @ImpactJrnls Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

Aging-US published a Special Collection on Eye Disease which included "Activation of C-reactive protein proinflammatory phenotype in the blood retinal barrier in vitro: implications for age-related macular degeneration" which reported that the retinal pigment epithelium (RPE) is considered one of the main targets of age-related macular degeneration (AMD), the leading cause of irreversible vision loss among the ageing population worldwide. Increased levels of circulating pentameric C-reactive protein (pCRP) are associated with higher risk of AMD. Monomeric form of pCRP has been detected in drusen, the hallmark deposits associated with AMD, and we have found that mCRP induces oBRB disruption Dr. Blanca Molins from The IDIBAPS, Hospital Clínic de Barcelona said, "Age-related macular degeneration (AMD) is the primary cause of irreversible vision loss among the ageing population worldwide." AMD presents RPE cell abnormalities, disruption of the outer blood-retinal-barrier (oBRB), and degeneration of photoreceptors. Altered immune responses are thought to contribute to the dry AMD phenotype. Loss of parainflammation control contributes to AMD by invoking a chronic, heightened immune response that causes tissue destruction. mCRP has been identified in ocular drusen and other subepithelial deposits, as well as in the choroid, and contributes to oBRB disruption in vitro. The "non-risk" Factor H (FH) variant can effectively bind to mCRP to dampen its proinflammatory activity. MCRP levels are elevated in individuals with the high-risk CFH genotype [29, 30] - this is because there is no CRP transcription in retinal tissue. The Molins Research Team concluded in their https://www.aging-us.com/article/103655/">Aging-US Research Output, "our findings further support mCRP direct contribution to progression of AMD, at least at the RPE level. The topological experiments elicit that mCRP is proinflammatory when present on the apical side of the RPE. However, mCRP is likely to only reach the apical side of the RPE in compromised RPE health and where barrier functions are compromised. Thus, a plausible scenario would infer that, in the presence of an already aged/damaged RPE, mCRP reaches the apical side of the RPE to amplify the proinflammatory microenvironment and enhance barrier disruption. With respect to previous findings, this pathologic mechanism will be more prevalent in patients carrying the FH risk polymorphism for AMD, where mCRP proinflammatory effects remain unrestrained." Full Text - https://www.aging-us.com/article/103655/text Correspondence to: Blanca Molins email: bmolins@clinic.cat Keywords: age-related macular degeneration, retinal pigment epithelium, inflammation, C-reactive protein About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways. To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls Media Contact 18009220957x105 MEDIA@IMPACTJOURNALS.COM