Aging-US

Aging-US published a Special Collection on Eye Disease which included "Pineal gland volume is associated with prevalent and incident isolated rapid eye movement sleep behavior disorder" which reported that pineal gland volume may be associated with the risk of isolated rapid eye movement (REM) sleep behavior disorder (RBD). The authors enrolled 245 cognitively normal elderly individuals without major psychiatric or neurological disorders at the baseline evaluation and 2-year follow-up evaluation. The smaller the baseline pineal glands volume, the more severe the RBD symptoms at baseline. The individuals with isolated rBD showed smaller pineal gland volumes than those without isolated pRBD. Dr. Ki Woong Kim from The Seoul National University College of Natural Sciences, The Seoul National University Bundang Hospital as well as The Seoul National University College of Medicine said, "Rapid eye movement (REM) sleep behavior disorder (RBD) is a parasomnia characterized by the loss of normal skeletal muscle atonia during REM sleep and dream-enacting behaviors." RBD can occur in association with (secondary RBD), or without (isolated RBD) a neurodegenerative disorder such as Parkinson's disease or Lewy body disease. A series of clinical trials found that the symptoms of RBD were improved by N-acetyl-5-methoxytryptamine (melatonin). In RBD patients, dream-enacting behaviors were reduced and REM sleep muscle atonia were restored by the administration of melatonin. Melatonin is a multifunctioning indoleamine produced by the pineal gland, which regulates sleep and circadian rhythm through its production and synthesis. VPG may predict the risk of developing RBD; they investigated the association of VPG with current RBD symptoms cross-sectionally and with the future risk prospectively in cognitively normal individuals without neurological or psychiatric disorders. The Kim Research Team concluded in their Aging-US Research Output, "the smaller pineal gland was associated with the more current RBD symptoms and the higher future risk of RBD in cognitively normal elderly individuals, and VPP or VPG may be a candidate biomarker of RBD." Full Text - https://www.aging-us.com/article/102661/text Correspondence to: Ki Woong Kim email: kwkimmd@snu.ac.kr Keywords: pineal gland, RBD, MRI, aging, prospective 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

Aging-US published a Special Collection on Eye Disease which included "Age-related changes in eye lens biomechanics, morphology, refractive index and transparency" which reported that life-long eye lens function requires an appropriate gradient refractive index, biomechanical integrity and transparency. The authors conducted an extensive study of wild-type mouse lenses 1-30 months of age to define common age-related changes. Biomechanical testing and morphometrics revealed an increase in lens volume and stiffness with age. Their results suggest similarities between murine and primate lenses and provide a baseline for future lens aging studies. Dr. Velia M. Fowler and Dr. Catherine Cheng said, "The eye lens is required for fine focusing of light onto the retina to form a clear image, and the function of the lens is intimately tied to its shape, biomechanical properties, transparency and refractive index." The eye lens is required for fine focusing of light onto the retina to form a clear image. It has long been known that age-related changes in these lens properties lead to two major lens pathologies, cataracts and presbyopia. Presbyopia is caused by a reduction in the lens' ability to change shape during focusing (accommodation), and, by extension, the need for reading glasses. Mice offer an opportunity to investigate changes in lens morphometrics, stiffness, transparency and refractive properties with age in a relatively shortened period of time. Little is known about the morphological, mechanical, refractive and cellular changes that occur with advanced age in the lens. The authors demonstrate that age-related changes in mouse lenses mimic some aspects of aging in human lenses. The Fowler/Cheng Research Team concluded in their Aging-US Research Output, "the increases in lens size and nucleus size are correlated with increase stiffness with age. The addition of new fiber cells at the lens periphery becomes disordered with age, but this does not appear to impact lens biomechanical properties. Cataracts in aged lenses can be due to cell structural abnormalities, including incomplete suture closure, collapse of the lens epithelial cell layer into the suture gap and loss of epithelial-fiber cell attachments and compaction of the cortical lens fiber cells forming a circumferential light scattering ring. GRIN is present in the lens from 2 weeks of age and continues to increase until about 6 months of age, after which the maximum refractive index remains stable. The increase in the area of highest refractive index at the center of the lens is directly correlated with the increase in lens nucleus size, suggesting nuclear compaction drives the maximum GRIN. Whether there is a common molecular mechanism that drives changes in all the measured parameters remains unknown, but further biochemical and cell morphology studies will be needed to determine how subcellular aging affects the whole tissue. Thus, our study provides a baseline for future studies of lens aging by providing quantitative measurements of key parameters and identifying common age-related changes in the overall tissue and in individual cells" 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 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.

Boiled or iced with water or milk, blended in smoothies, condensed into shots or even baked into pastries—humans are infatuated with green tea. Today, green tea is one of the most widely consumed beverages in the world. Molecules found in this plant, named catechins, are known to have numerous evidence-based health benefits, including weight loss and age delaying properties. However, the mechanism by which these effects take place have yet to be fully elucidated. “The popularity of green tea makes it crucial to study its impact on health and aging.” Researchers from Friedrich Schiller University Jena, Huazhong Agricultural University, ETH Zurich, and the Medical University of Graz investigated green tea catechins and their effects in roundworms, known as Caenorhabditis elegans (C. elegans), and isolated rodent mitochondria. Their trending paper was published in October of 2021 by Aging (Aging-US), and entitled, “Green tea catechins EGCG and ECG enhance the fitness and lifespan of Caenorhabditis elegans by complex I inhibition.” “We have designed the current study to investigate the impact and to unveil the target of the most abundant green tea catechins, epigallocatechin gallate (EGCG) and epicatechin gallate (ECG).” Full blog - https://www.impactjournals.com/journals/blog/aging/trending-with-impact-green-tea-enhances-fitness-and-lifespan-in-worms/ Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.203597 DOI - https://doi.org/10.18632/aging.203597 Full text - https://www.aging-us.com/article/203597/text Correspondence to: Corina T. Madreiter-Sokolowski email: corina.madreiter@medunigraz.at and Michael Ristow email: michael-ristow@ethz.ch Keywords: aging, reactive oxygen species, mitochondria, polyphenols, C. elegans 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: Twitter - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ SoundCloud - https://soundcloud.com/aging-us​ YouTube - https://www.youtube.com/agingus​ LinkedIn - https://www.linkedin.com/company/aging​ 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 "Involvement of adiponectin in age-related increases in tear production in mice" which reported that the infiltration of lymphocytes into the lacrimal glands occurs with age, and age-related increases in tear production have also been observed in mice. The mechanisms underlying this increase remain unclear, but these authors show that it is not dependent on body weight gain or systemic conditions, such as insulin resistance, using aged mice and high-fat diet-fed mice. Senescence-associated T (SA-T) cells accumulated in the laceral glands of aged mice, particularly females, and they may represent potential targets for treating dry eyes in humans. Dr. Yosuke Shikama from The National Center for Geriatrics and Gerontology said, "Epidemiological studies have shown that the prevalence of dry eye increases every five years after the age of 50 years, with a higher prevalence being reported in women than in men." Age and female sex have been identified as the greatest risk factors for dry eye, and this is supported by clinical findings of decreased tear production in women through the 6th decade of life. Metabolic disorders, such as diabetes, affect tear production and are associated with dry eye. Adiponectin is a 30-kDa multimeric protein that is mainly secreted by white adipose tissue, and has insulin-sensitizing and anti-atherogenic properties. Adiponectin and adipoR2 mRNA expression levels significantly increased in the lacrimal glands of aged mice, but not in those of high-fat diet-fed mice. These results indicate that these molecules are involved in age-related increases in tear production in mice. The Shikama Research Team concluded in their Aging-US Research Output, "the present results demonstrated the accumulation of SA-T cells in aged mice, which occurred to a greater extent in female than in male mice. Furthermore, increased tear secretion in aged mice appeared to be mediated by PPARγ and adiponectin-mediated signaling. These results may explain the discrepancy in the volume of tears secreted with age between humans and mice." Full Text - https://www.aging-us.com/article/102322/text Correspondence to: Yosuke Shikama email: shikama@ncgg.go.jp Keywords: dry eye, adiponectin, peroxisome proliferator-activated receptor gamma, senescence-associated T cells, aging 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

Aging-US published a Special Collection on Eye Disease which included "PU-91 drug rescues human age-related macular degeneration RPE cells; implications for AMD therapeutics" which reported that the PU-91 drug upregulates PGC-1α which is a critical regulator of mitochondrial biogenesis. Since mitochondrial dysfunction is implicated in the pathogenesis of AMD, this study is based on the premise that repurposing of PU 91 might rescue AMD RPE cells from AMD mitochondria-induced damage. The authors report significant improvement in cell survival, mitochondrial health, and antioxidant potential following treatment with PU 91. Dr. M. Cristina Kenney from The University of California Irvine said, "The incidence of Age-related Macular Degeneration (AMD) is increasing at an alarming rate in elderly population in the United States." The incidence of Age-related Macular Degeneration (AMD) is increasing at an alarming rate in elderly population in the United States. Most AMD cases occur among Caucasian Americans, followed by Hispanic and other populations. Despite intensive study, a limited number of FDA-approved treatment options are available for treatment of AMD. National Eye Institute projection, the estimated number of AMD patients is expected to rise to 5.44 million by 2050. PU-91 is a pro-drug that when metabolized is PPARα ligand and which was developed for the treatment of dyslipidemia. The drug is estimated to have seen >5 million-years of patient exposure and remains an effective agent for certain dyslipidemias. These findings demonstrated that PU-91 preserved AMD mitochondrial function and integrity, and protected AMD RPE cybrids against oxidative stress-induced and mtDNA-induced apoptotic cell death. The Kenney Research Team concluded in their Aging-US Research Output, "PU-91 rescues AMD RPE cybrids, and potentially could be repurposed as an FDA-approved drug to prevent/treat AMD. Since it improves mitochondrial function and has already been FDA-approved, the candidate therapeutic PU-91 will be an excellent treatmentoption for AMD. Repositioning of PU-91 will be a smoother transition from lab bench to clinic since the pharmacological profiles of PU-91 have been examined already. Furthermore, because of its extensive safety record it could be potentially prosecuted through NDA more rapidly than a drug-like new chemical entity. Bringing a disease modifying therapeutic to market for the most prevalent form of blindness, AMD, has substantial potential benefit for our aging populations world-wide." Full Text - https://www.aging-us.com/article/102179/text Correspondence to: M. Cristina Kenney email: mkenney@uci.edu Keywords: age-related macular degeneration (AMD), RPE, PGC-1α, RPE, mitochondria, FDA-approved drugs 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

Whether they are sprinters or distance runners, sled dogs are known for their competitive nature and athletic prowess. With age, however, these athletes eventually run out of steam—just as humans inevitably do. Canines of all breeds are effected by aging, including a loss of resilience, accumulation of molecular damage and age-related diseases. These relatively short-lived, large mammals are one of the few to share environments with humans, and even have access to advanced medical care. Many believe the canine aging process resembles human aging the closest compared to any other animal. A team of scientists—from Cornell University, North Carolina State University, Tauber Bioinformatic Research Center, and Roswell Park Comprehensive Cancer Center—saw the opportunities and advantages of studying canine aging in a controlled environment. Co-founders Andrei Gudkov, PhD, Dr Sci, Katerina Andrianova, PhD, and Daria Fleyshman, PhD, established a non-profit organization called Vaika Inc. In 2018, Vaika allowed these researchers to begin collaborating in a longitudinal study on the mechanisms of aging among 103 retired sled dogs. The researchers authored a trending research perspective about the details of their long-term study. In September 2021, their paper was published on the cover of Aging (Aging-US)’s Volume 13, Issue 18, and entitled, “Development of infrastructure for a systemic multidisciplinary approach to study aging in retired sled dogs.” Full blog - https://www.impactjournals.com/journals/blog/aging/trending-with-impact-retired-sled-dogs-in-aging-research/ Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.203600 DOI - https://doi.org/10.18632/aging.203600 Full text - https://www.aging-us.com/article/203600/text Correspondence to: Andrei V. Gudkov email: andrei.gudkov@roswellpark.org and Ekaterina L. Andrianova email: kandrianova@vaika.org Keywords: canine, senescence, frailty, longevity, healthspan 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: Twitter - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ SoundCloud - https://soundcloud.com/aging-us​ YouTube - https://www.youtube.com/agingus​ LinkedIn - https://www.linkedin.com/company/aging​ 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 "Abnormalities of saccadic eye movements in dementia due to Alzheimer’s disease and mild cognitive impairment" which reported that there is increasing evidence that people in the early stages of Alzheimer’s disease have subtle impairments in cognitive inhibition that can be detected by using relatively simple eye-tracking paradigms, but these subtle impairments are often missed by traditional cognitive assessments. People with mild cognitive impairment are at an increased likelihood of dementia due to AD. Participants were 68 people with dementia due to AD, 42 had a diagnosis of aMCI, and 47 had a diagnosis of naMCI, and 92 age-matched cognitively healthy controls. Dr. Thomas D.W. Wilcockson from The Loughborough University as well as The Lancaster University said, "Alzheimer's disease (AD) is a severe neurodegenerative disease of the human brain, for which there is as yet no cure." When disease modifying therapy becomes available, it will be essential to administer this treatment in the very earliest stages of the disease, before pathological changes in the brain are widespread, rendering the treatment ineffective. Thus, identifying the presence of AD in the pre-dementia ‘prodromal’ or even ‘preclinical’ phase is essential. Current biomarkers that are able to detect AD in the earliest stages are either invasive or expensive. A critical issue then is whether eye-movement impairments are detectable in people who are in a preclinical stage of AD and therefore at a greater risk of developing clinical dementia. A strong correlation has been reported between antisaccade error rate with cortical thinning in a mild cognitive impairment group. However, this work did not distinguish between the different types of MCI, thus the low and high-risk of dementia participants were conflated in their study. People with a diagnosis of MCI are at an increased risk of developing dementia compared to cognitively healthy adults with 5-10% of MCI patients progressing to dementia annually. Traditionally, the clinical syndrome of MCI was considered to be a relatively distinct stage of dementia since the cognitive deficits were not severe enough to impact significantly on the individual’s ability to conduct their activities of daily living. The Wilcockson Research Team concluded in their Aging-US Research Output that inhibitory error rates in the antisaccade are sensitive to memory impairment, but may even precede it in a patient with dementia. The results obtained from this study demonstrate that eye movements during the AST could be used to automatically classify participants as being at a higher risk of AD. There are potentially a number of practical implications for this observation. Full Text - https://www.aging-us.com/article/102118/text Correspondence to: Thomas D.W. Wilcockson email: t.wilcockson@lboro.ac.uk Keywords: mild cognitive impairment, Alzheimer’s disease, inhibitory control, eye tracking, anti-saccade 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

Aging-US published a Special Collection on Eye Disease which included "HMGB1 and Caveolin-1 related to RPE cell senescence in age-related macular degeneration" and reported that AMD is a major unmet medical need as it is estimated that more than 20 million patients will be affected by 2050 in the US alone. STGD is the most common hereditary macular dystrophy, mostly affecting young patients aged between 6 and 15 years old with a prevalence of 1/8,000-1/10,000. It is formed by the reaction of 2 all-trans retinal molecules with phosphatidylethanolamine generating N-retinylidene-PE, as a detoxication mechanism of retinal isomers including all-trans and 11-cis-retinal. Indeed, it has been shown that as early as in 3-month-old Abca4-/- Rdh8-/- mice, the amplitudes of scotopic A and B waves and flicker ERG are reduced. Dr. Jin Yang and Dr. Xiaorong Li both from The Tianjin Medical University Eye Hospital said, "Age-related macular degeneration (AMD) is the leading cause of vision loss in older adults worldwide." AMD can be classified into early-stage or late-stage AMD. The latter is characterized by neovascularization, geographic atrophy, or both. Conversely, early-stage AMD is characterized by a limited amount of drusen, which is mainly caused by lipid and protein accumulation and thought to contribute to atrophic changes. As the disease progresses, neovascular changes or geographic atrophy involving the macular area can be present in patients for years. Therefore, the authors explored the relationship between dry AMD and RPE dysfunction and senescence using proteomic mass spectrometry to examine differential expression in induced pluripotent stem cell-derived RPE cell lines with and without A2E treatment. They have previously demonstrated that the iPSC-derived RPE is phenotypically and functionally similar to the native RPE. In addition, the young status of iPSC-RPE may provide an excellent means for observing changes in protein expression during the process of RPE cell aging. A2E photo-oxidation products can cause oxidative stress, membrane permeation, telomere dysfunction and accelerated RPE senescence. Although A2E is clearly present in the retina, there are rather different opinions regarding its distribution. Ablonczy et al. showed that levels of A2E decreased from the periphery to the centre region in aging tissue of macaques and humans but A2E was localized mainly in the centre region of young mouse retina. The Yang/Li Research Team concluded in their Aging-US Research Output, "upregulation of HMGB1 and Caveolin-1 caused RPE cell senescence and suppressed migration and invasion, and β-catenin and Zo-1 accumulation was enhanced by A2E in RPE cells. In particular, the results showed a change in expression of HMGB1 and Caveolin-1, which suggests that they are prime gatekeepers in RPE cell senescence. The above results indicate that stabilizing expression of HMGB1 and Caveolin-1 is a potential therapeutic target to prevent the progression of RPE cell senescence." Full Text - https://www.aging-us.com/article/102039/text Correspondence to: Jin Yang email: yangjinchina324@gmail.com and Xiaorong Li email: lixiaorong@tmu.edu.cn Keywords: A2E, HMGB1, Caveolin-1, RPE cell senescence, AMD 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

The root cause of Alzheimer’s disease (AD) is still unknown. For the past decades, the dominant paradigm many scientists have based their AD therapeutic solutions on has been the amyloid cascade hypothesis. The amyloid cascade hypothesis proposes that AD begins with the overproduction and accumulation of amyloid-β, followed by a number of other cascading symptoms. However, over 200 drug candidates based on this model have failed to prove clinical benefits in trial phases. “The unsettlingly consistent failure of clinical trials led to questioning of the amyloid cascade hypothesis, stimulating a search for alternative AD paradigms [10–13].” Researchers Alexei Kurakin and Dale E. Bredesen, from the University of California Los Angeles and the Buck Institute for Research on Aging, conducted detailed analyses of early-stage AD patient data and concluded their study by offering an alternative AD hypothesis. Their paper, published by Aging (Aging-US) in 2020, was entitled, “Alzheimer’s disease as a systems network disorder: chronic stress/dyshomeostasis, innate immunity, and genetics.” “In this report, we outline an alternative perspective on AD as a systems network disorder and discuss biochemical and genetic evidence suggesting the central role of chronic tissue injury/dyshomeostasis, innate immune reactivity, and inflammation in the etiopathobiology of Alzheimer’s disease.” Full blog - https://www.impactjournals.com/journals/blog/aging/trending-with-impact-alzheimers-disease-as-a-systems-network-disorder/ Press release - https://www.aging-us.com/news_room/alzheimers-disease-as-a-systems-network-disorder Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.103883 DOI - https://doi.org/10.18632/aging.103883 Full text - https://www.aging-us.com/article/103883/text Correspondence to: Alexei Kurakin email: akurakin@mednet.ucla.edu and Dale E. Bredesen email: dbredesen@mednet.ucla.edu Keywords: Alzheimer’s disease, neurodegeneration, complex chronic disorder, network biology, systems biology 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: Twitter - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ SoundCloud - https://soundcloud.com/aging-us​ YouTube - https://www.youtube.com/agingus​ LinkedIn - https://www.linkedin.com/company/aging​ 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 "Exploration of age-related mitochondrial dysfunction and the anti-aging effects of resveratrol in zebrafish retina" which reported that resveratrol was shown to not only increase mitochondrial quality and function, but also to suppress Akt/mTOR activity in zebrafish retinas. These results support the notion that mitochondrial dysfunction and increased Akt/mTOR activity are major players in age-related retinal neuropathy in zebrafish, and demonstrate a trend towards mitochondrial fragmentation in the aging retina. Importantly, resveratrol promoted mitochondrial function, up-regulating Ampk/Sirt1/Pgc1, and down-regulated Akt/mTOR pathway activity in zebrafish retinas, suggesting that it may be able to prevent age-related oculopathy. Dr. Xu Zhang from The Jiangxi Research Institute of Ophthalmology and Visual Science as well as The Jiangxi Provincial Collaborative Innovation Center for Cardiovascular said, "Aging is the biological process characterized by the accumulation of damage in structure and decline in function of cells and tissues over time, ultimately leading to organismal death." The causes of aging are complex but include abnormal mitochondria, epigenetic alterations, increased reactive oxygen species, increased DNA methylation, and decreased telomere length. Recently, both dysfunctional mitochondria that overproduce ROS and abnormal mitochondrial dynamics have been recognized as crucial contributors to the aging process as well as age-related neuronal diseases and age-related oculopathies such as glaucoma, age-related macular degeneration, and cataracts. Fusion can help relieve mtDNA damage by diluting mutant mtDNA with non-mutant mtDNA, whereas fission can allow for turnover of mutant mtDNA through mitophagy. On the other hand, mitochondrial fragmentation is associated with apoptosis and cell death rather than mitophagy and must be distinguished from fission. Resveratrol, a plant natural product found in high levels in peanuts and grape skin, has well-established antioxidant, anti-inflammatory, anti-mutagenic, neuroprotective, and anti-aging effects in many species. Current evidence suggests that the anti-aging effects of resveratrol are related to its ability to modulate mitochondria. Resveratrol has been found to increase mitochondrial fusion/fission as well as promote Pink1 expression and autophagic activity. The Zhang Research Team concluded in their Aging-US Research Output, "Maintaining mitochondrial health is crucial to prevent age-related neurodegenerative diseases, including oculopathy. We utilized the zebrafish retina as a model for age-related oculopathy and observed decreased mtDNA integrity, dysfunctional mitochondrial fission-fusion dynamics, decreased expression of antioxidant defense enzymes, and increased activity of the Akt/mTOR pathway in the aging retina. Consistent with its anti-aging effects in other species and model systems, resveratrol treatment helped alleviate most of the age-related changes observed in the zebrafish retina, suggesting its potential for the prevention of aging-induced oculopathy in other species including humans. This study indicates that further testing of resveratrol for oculopathy is warranted, and helps establish the zebrafish retina as a viable model of age-related oculopathy for further studies on the molecular mechanisms and for novel drug screening." Full Text - https://www.aging-us.com/article/101966/text Correspondence to: Xu Zhang email: xuzhang19@163.com Keywords: aging zebrafish, retina, mitochondrial dysfunction, mitophagy, mTOR, resveratrol