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    1480 results match your criteria Aging Cell [Journal]

    1 OF 30

    The companion dog as a model for human aging and mortality.
    Aging Cell 2018 Feb 19. Epub 2018 Feb 19.
    Department of Pathology, University of Washington, Seattle, WA, USA.
    Around the world, human populations have experienced large increases in average lifespan over the last 150 years, and while individuals are living longer, they are spending more years of life with multiple chronic morbidities. Researchers have used numerous laboratory animal models to understand the biological and environmental factors that influence aging, morbidity, and longevity. However, the most commonly studied animal species, laboratory mice and rats, do not experience environmental conditions similar to those to which humans are exposed, nor do we often diagnose them with many of the naturally occurring pathologies seen in humans. Read More

    Aging impacts CD103CD8T cell presence and induction by dendritic cells in the genital tract.
    Aging Cell 2018 Feb 18. Epub 2018 Feb 18.
    Department of Microbiology and Immunology, Geisel School of Medicine at Dartmouth, Lebanon, NH, USA.
    As women age, susceptibility to systemic and genital infections increases. Tissue-resident memory T cells (TRMs) are CD103CD8long-lived lymphocytes that provide critical mucosal immune protection. Mucosal dendritic cells (DCs) are known to induce CD103 expression on CD8T cells. Read More

    Amyloid-beta 1-40 is associated with alterations in NG2+ pericyte population ex vivo and in vitro.
    Aging Cell 2018 Feb 17. Epub 2018 Feb 17.
    Clinical Memory Research Unit, Department of Clinical Sciences Malmö, Lund University, Malmö, Sweden.
    The population of brain pericytes, a cell type important for vessel stability and blood brain barrier function, has recently been shown altered in patients with Alzheimer's disease (AD). The underlying reason for this alteration is not fully understood, but progressive accumulation of the AD characteristic peptide amyloid-beta (Aβ) has been suggested as a potential culprit. In the current study, we show reduced number of hippocampal NG2+ pericytes and an association between NG2+ pericyte numbers and Aβ1-40 levels in AD patients. Read More

    The SCN9A channel and plasma membrane depolarization promote cellular senescence through Rb pathway.
    Aging Cell 2018 Feb 15. Epub 2018 Feb 15.
    Inserm U1052, CNRS UMR 5286, Université de Lyon & Centre Léon Bérard, Centre de Recherche en Cancérologie de Lyon, Lyon, France.
    Oncogenic signals lead to premature senescence in normal human cells causing a proliferation arrest and the elimination of these defective cells by immune cells. Oncogene-induced senescence (OIS) prevents aberrant cell division and tumor initiation. In order to identify new regulators of OIS, we performed a loss-of-function genetic screen and identified that the loss of SCN9A allowed cells to escape from OIS. Read More

    Overexpression of PGC-1α in aging muscle enhances a subset of young-like molecular patterns.
    Aging Cell 2018 Feb 10. Epub 2018 Feb 10.
    Department of Neurology, University of Miami Miller School of Medicine, Miami, FL, USA.
    PGC-1α is a transcriptional co-activator known as the master regulator of mitochondrial biogenesis. Its control of metabolism has been suggested to exert critical influence in the aging process. We have aged mice overexpressing PGC-1α in skeletal muscle to determine whether the transcriptional changes reflected a pattern of expression observed in younger muscle. Read More

    Effects of 2 years of caloric restriction on oxidative status assessed by urinary F2-isoprostanes: The CALERIE 2 randomized clinical trial.
    Aging Cell 2018 Feb 9. Epub 2018 Feb 9.
    School of Public Health, Georgia State University, Atlanta, GA, USA.
    Calorie restriction (CR) without malnutrition slows aging in animal models. Oxidative stress reduction was proposed to mediate CR effects. CR effect on urinary F2-isoprostanes, validated oxidative stress markers, was assessed in CALERIE, a two-year randomized controlled trial. Read More

    Transcriptomics of aged Drosophila motor neurons reveals a matrix metalloproteinase that impairs motor function.
    Aging Cell 2018 Feb 7. Epub 2018 Feb 7.
    Department of Cellular and Integrative Physiology, UTHSCSA, San Antonio, TX, USA.
    The neuromuscular junction (NMJ) is responsible for transforming nervous system signals into motor behavior and locomotion. In the fruit fly Drosophila melanogaster, an age-dependent decline in motor function occurs, analogous to the decline experienced in mice, humans, and other mammals. The molecular and cellular underpinnings of this decline are still poorly understood. Read More

    Smurf2 regulates stability and the autophagic-lysosomal turnover of lamin A and its disease-associated form progerin.
    Aging Cell 2018 Feb 5. Epub 2018 Feb 5.
    Laboratory of Molecular and Cellular Cancer Biology, Azrieli Faculty of Medicine, Bar-Ilan University, Safed, Israel.
    A-lamins, encoded by the LMNA gene, are major structural components of the nuclear lamina coordinating essential cellular processes. Mutations in the LMNA gene and/or alterations in its expression levels have been linked to a distinct subset of human disorders, collectively known as laminopathies, and to cancer. Mechanisms regulating A-lamins are mostly obscure. Read More

    Treatment with the mitochondrial-targeted antioxidant peptide SS-31 rescues neurovascular coupling responses and cerebrovascular endothelial function and improves cognition in aged mice.
    Aging Cell 2018 Feb 6. Epub 2018 Feb 6.
    Reynolds Oklahoma Center on Aging, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
    Moment-to-moment adjustment of cerebral blood flow (CBF) via neurovascular coupling has an essential role in maintenance of healthy cognitive function. In advanced age, increased oxidative stress and cerebromicrovascular endothelial dysfunction impair neurovascular coupling, likely contributing to age-related decline of higher cortical functions. There is increasing evidence showing that mitochondrial oxidative stress plays a critical role in a range of age-related cellular impairments, but its role in neurovascular uncoupling remains unexplored. Read More

    High-throughput serum proteomics for the identification of protein biomarkers of mortality in older men.
    Aging Cell 2018 Feb 5. Epub 2018 Feb 5.
    Oregon Health & Science University, Portland, OR, USA.
    The biological perturbations associated with incident mortality are not well elucidated, and there are limited biomarkers for the prediction of mortality. We used a novel high-throughput proteomics approach to identify serum peptides and proteins associated with 5-year mortality in community-dwelling men age ≥65 years who participated in a longitudinal observational study of musculoskeletal aging (Osteoporotic Fractures in Men: MrOS). In a discovery phase, serum specimens collected at baseline in 2473 men were analyzed using liquid chromatography-ion mobility-mass spectrometry, and incident mortality in the subsequent 5 years was ascertained by tri-annual questionnaire. Read More

    α-Motor neurons are spared from aging while their synaptic inputs degenerate in monkeys and mice.
    Aging Cell 2018 Feb 4. Epub 2018 Feb 4.
    Virginia Tech Carilion Research Institute, Virginia Tech, Roanoke, VA, USA.
    Motor function deteriorates with advancing age, increasing the risk of adverse health outcomes. While it is well established that skeletal muscles and neuromuscular junctions (NMJs) degenerate with increasing age, the effect of aging on α-motor neurons and their innervating synaptic inputs remains largely unknown. In this study, we examined the soma of α-motor neurons and innervating synaptic inputs in the spinal cord of aged rhesus monkeys and mice, two species with vastly different lifespans. Read More

    Aging affects the in vivo regenerative potential of human mesoangioblasts.
    Aging Cell 2018 Feb 4. Epub 2018 Feb 4.
    Translational Cardiomyology Laboratory, Stem Cell Institute of Leuven, Unit of Stem Cell Research, Cluster of Stem Cell and Developmental Biology, Department of Development and Regeneration, University of Leuven, Leuven, Belgium.
    Sarcopenia is the age-related loss of muscle mass, strength, and function. Although the role of human satellite cells (SCs) as adult skeletal muscle stem cells has been deeply investigated, little is known about the impact of aging on muscle interstitial stem cells. Here, we isolated the non-SC CD56fraction from human muscle biopsies of young and elderly subjects. Read More

    Emerging roles of extracellular vesicles in cellular senescence and aging.
    Aging Cell 2018 Feb 1. Epub 2018 Feb 1.
    Department of Biology, University of Rochester, Rochester, NY, USA.
    Cellular senescence is a cellular program that prevents the proliferation of cells at risk of neoplastic transformation. On the other hand, age-related accumulation of senescent cells promotes aging at least partially due to the senescence-associated secretory phenotype, whereby cells secrete high levels of inflammatory cytokines, chemokines, and matrix metalloproteinases. Emerging evidence, however, indicates that extracellular vesicles (EVs) are important mediators of the effects of senescent cells on their microenvironment. Read More

    Metformin regulates metabolic and nonmetabolic pathways in skeletal muscle and subcutaneous adipose tissues of older adults.
    Aging Cell 2018 Jan 31. Epub 2018 Jan 31.
    Division of Endocrinology, Department of Medicine, Albert Einstein College of Medicine, Bronx, NY, USA.
    Administration of metformin increases healthspan and lifespan in model systems, and evidence from clinical trials and observational studies suggests that metformin delays a variety of age-related morbidities. Although metformin has been shown to modulate multiple biological pathways at the cellular level, these pleiotropic effects of metformin on the biology of human aging have not been studied. We studied ~70-year-old participants (n = 14) in a randomized, double-blind, placebo-controlled, crossover trial in which they were treated with 6 weeks each of metformin and placebo. Read More

    Long-lasting pathological consequences of overexpression-induced α-synuclein spreading in the rat brain.
    Aging Cell 2018 Jan 30. Epub 2018 Jan 30.
    German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.
    Increased expression of α-synuclein can initiate its long-distance brain transfer, representing a potential mechanism for pathology spreading in age-related synucleinopathies, such as Parkinson's disease. In this study, the effects of overexpression-induced α-synuclein transfer were assessed over a 1-year period after injection of viral vectors carrying human α-synuclein DNA into the rat vagus nerve. This treatment causes targeted overexpression within neurons in the dorsal medulla oblongata and subsequent diffusion of the exogenous protein toward more rostral brain regions. Read More

    Ablation of PPARγ in subcutaneous fat exacerbates age-associated obesity and metabolic decline.
    Aging Cell 2018 Jan 31. Epub 2018 Jan 31.
    Genetics of Development and Disease Branch, NIDDK, National Institutes of Health, Bethesda, MD, USA.
    It is well established that aging is associated with metabolic dysfunction such as increased adiposity and impaired energy dissipation; however, the transcriptional mechanisms regulating energy balance during late life stages have not yet been fully elucidated. Here, we show that ablation of the nuclear receptor PPARγ specifically in inguinal fat tissue in aging mice is associated with increased fat tissue expansion and insulin resistance. These metabolic effects are accompanied by decreased thermogenesis, reduced levels of brown fat genes, and browning of subcutaneous adipose tissue. Read More

    ATF3 represses PINK1 gene transcription in lung epithelial cells to control mitochondrial homeostasis.
    Aging Cell 2018 Jan 24. Epub 2018 Jan 24.
    Vascular Medicine Institute, Department of Medicine, University of Pittsburgh, Pittsburgh, PA, USA.
    PINK1 (PTEN-induced putative kinase 1) is a key regulator of mitochondrial homeostasis that is relatively depleted in aging lungs and in lung epithelial cells from patients with idiopathic pulmonary fibrosis (IPF), a disease linked with aging. Impaired PINK1 expression and accumulation of damaged mitochondria in lung epithelial cells from fibrotic lungs were associated with the presence of ER stress. Here, we show that ATF3 (activating transcription factor 3), a member of the integrated stress response (ISR), negatively regulates transcription of the PINK1 gene. Read More

    Skeletal muscle ex vivo mitochondrial respiration parallels decline in vivo oxidative capacity, cardiorespiratory fitness, and muscle strength: The Baltimore Longitudinal Study of Aging.
    Aging Cell 2018 Jan 21. Epub 2018 Jan 21.
    Longitudinal Studies Section, Translational Gerontology Branch, National Institute on Aging, Baltimore, MD, USA.
    Mitochondrial function in human skeletal muscle declines with age. Most evidence for this decline comes from studies that assessed mitochondrial function indirectly, and the impact of such deterioration with respect to physical function has not been clearly delineated. We hypothesized that mitochondrial respiration in permeabilized human muscle fibers declines with age and correlates with phosphocreatine postexercise recovery rate (kPCr), muscle performance, and aerobic fitness. Read More

    T-cell Immunoglobulin and ITIM Domain Contributes to CD8T-cell Immunosenescence.
    Aging Cell 2018 Jan 19. Epub 2018 Jan 19.
    Beijing Key Laboratory of Emerging Infectious Diseases, Institute of Infectious Diseases, Beijing Ditan Hospital, Capital Medical University, Beijing, China.
    Aging is associated with immune dysfunction, especially T-cell defects, which result in increased susceptibility to various diseases. Previous studies showed that T cells from aged mice express multiple inhibitory receptors, providing evidence of the relationship between T-cell exhaustion and T-cell senescence. In this study, we showed that T-cell immunoglobulin and immunoreceptor tyrosine-based inhibitory motif (ITIM) domain (TIGIT), a novel co-inhibitory receptor, was upregulated in CD8T cells of elderly adults. Read More

    Senescence chips for ultrahigh-throughput isolation and removal of senescent cells.
    Aging Cell 2018 Jan 16. Epub 2018 Jan 16.
    Newomics Inc., Emeryville, CA, USA.
    Cellular senescence plays an important role in organismal aging and age-related diseases. However, it is challenging to isolate low numbers of senescent cells from small volumes of biofluids for downstream analysis. Furthermore, there is no technology that could selectively remove senescent cells in a high-throughput manner. Read More

    Endothelium-specific CYP2J2 overexpression attenuates age-related insulin resistance.
    Aging Cell 2018 Jan 10. Epub 2018 Jan 10.
    Department of Geriatric Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
    Ample evidences demonstrate that cytochrome P450 epoxygenase-derived epoxyeicosatrienoic acids (EETs) exert diverse biological activities, which include potent vasodilatory, anti-inflammatory, and cardiovascular protective effects. In this study, we investigated the effects of endothelium-specific CYP2J2 overexpression on age-related insulin resistance and metabolic dysfunction. Endothelium-specific targeting of the human CYP epoxygenase, CYP2J2, transgenic mice (Tie2-CYP2J2-Tr mice) was utilized. Read More

    The mitochondrial ATP synthase is a shared drug target for aging and dementia.
    Aging Cell 2018 Jan 7. Epub 2018 Jan 7.
    Cellular Neurobiology, The Salk Institute for Biological Studies, La Jolla, CA, USA.
    Aging is a major driving force underlying dementia, such as that caused by Alzheimer's disease (AD). While the idea of targeting aging as a therapeutic strategy is not new, it remains unclear how closely aging and age-associated diseases are coupled at the molecular level. Here, we discover a novel molecular link between aging and dementia through the identification of the molecular target for the AD drug candidate J147. Read More

    UNC-120/SRF independently controls muscle aging and lifespan in Caenorhabditis elegans.
    Aging Cell 2018 Jan 3. Epub 2018 Jan 3.
    University of Lyon, University of Lyon1 Claude Bernard Lyon1, NeuroMyoGene Institute, CNRS UMR5310, INSERM U1217, Lyon, France.
    Aging is commonly defined as the loss of global homeostasis, which results from progressive alteration of all organs function. This model is currently challenged by recent data showing that interventions that extend lifespan do not always increase the overall fitness of the organism. These data suggest the existence of tissue-specific factors that regulate the pace of aging in a cell-autonomous manner. Read More

    Circulating levels of monocyte chemoattractant protein-1 as a potential measure of biological age in mice and frailty in humans.
    Aging Cell 2017 Dec 31. Epub 2017 Dec 31.
    Department of Molecular Medicine, Center on Aging, The Scripps Research Institute, Jupiter, FL, USA.
    A serum biomarker of biological versus chronological age would have significant impact on clinical care. It could be used to identify individuals at risk of early-onset frailty or the multimorbidities associated with old age. It may also serve as a surrogate endpoint in clinical trials targeting mechanisms of aging. Read More

    Senescence promotes in vivo reprogramming through p16and IL-6.
    Aging Cell 2017 Dec 27. Epub 2017 Dec 27.
    Tumor Suppression Group, Spanish National Cancer Research Centre (CNIO), Madrid, Spain.
    Cellular senescence is a damage response aimed to orchestrate tissue repair. We have recently reported that cellular senescence, through the paracrine release of interleukin-6 (IL6) and other soluble factors, strongly favors cellular reprogramming by Oct4, Sox2, Klf4, and c-Myc (OSKM) in nonsenescent cells. Indeed, activation of OSKM in mouse tissues triggers senescence in some cells and reprogramming in other cells, both processes occurring concomitantly and in close proximity. Read More

    Plasticity of lifelong calorie-restricted C57BL/6J mice in adapting to a medium-fat diet intervention at old age.
    Aging Cell 2017 Dec 21. Epub 2017 Dec 21.
    Division of Human Nutrition, Nutrition, Metabolism & Genomics Group, Wageningen University, Wageningen, The Netherlands.
    Calorie restriction (CR) is a dietary regimen that supports healthy aging. In this study, we investigated the systemic and liver-specific responses caused by a diet switch to a medium-fat (MF) diet in 24-month-old lifelong, CR-exposed mice. This study aimed to increase the knowledge base on dietary alterations of gerontological relevance. Read More

    Movement decline across lifespan of Caenorhabditis elegans mutants in the insulin/insulin-like signaling pathway.
    Aging Cell 2018 Feb 7;17(1). Epub 2017 Dec 7.
    Institute for Behavioral Genetics, University of Colorado Boulder, Boulder, CO, USA.
    Research in aging biology has identified several pathways that are molecularly conserved across species that extend lifespan when mutated. The insulin/insulin-like signaling (IIS) pathway is one of the most widely studied of these. It has been assumed that extending lifespan also extends healthspan (the period of life with minimal functional loss). Read More

    Young plasma reverses age-dependent alterations in hepatic function through the restoration of autophagy.
    Aging Cell 2018 Feb 5;17(1). Epub 2017 Dec 5.
    Department of Pathophysiology, Anhui Medical University, Hefei, China.
    Recent studies showing the therapeutic effect of young blood on aging-associated deterioration of organs point to young blood as the solution for clinical problems related to old age. Given that defective autophagy has been implicated in aging and aging-associated organ injuries, this study was designed to determine the effect of young blood on aging-induced alterations in hepatic function and underlying mechanisms, with a focus on autophagy. Aged rats (22 months) were treated with pooled plasma (1 ml, intravenously) collected from young (3 months) or aged rats three times per week for 4 weeks, and 3-methyladenine or wortmannin was used to inhibit young blood-induced autophagy. Read More

    Autophagy controls mesenchymal stem cell properties and senescence during bone aging.
    Aging Cell 2018 Feb 6;17(1). Epub 2017 Dec 6.
    State Key Laboratory of Military Stomatology & National Clinical Research Center for Oral Diseases & Shaanxi International Joint Research Center for Oral Diseases, Center for Tissue Engineering, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi, China.
    Bone marrow-derived mesenchymal stem cells (BMMSCs) exhibit degenerative changes, including imbalanced differentiation and reduced proliferation during aging, that contribute to age-related bone loss. We demonstrate here that autophagy is significantly reduced in aged BMMSCs compared with young BMMSCs. The autophagy inhibitor 3-methyladenine (3-MA) could turn young BMMSCs into a relatively aged state by reducing their osteogenic differentiation and proliferation capacity and enhancing their adipogenic differentiation capacity. Read More

    FOXO protects against age-progressive axonal degeneration.
    Aging Cell 2018 Feb 26;17(1). Epub 2017 Nov 26.
    Department of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, NY, USA.
    Neurodegeneration resulting in cognitive and motor impairment is an inevitable consequence of aging. Little is known about the genetic regulation of this process despite its overriding importance in normal aging. Here, we identify the Forkhead Box O (FOXO) transcription factor 1, 3, and 4 isoforms as a guardian of neuronal integrity by inhibiting age-progressive axonal degeneration in mammals. Read More

    17α-estradiol acts through hypothalamic pro-opiomelanocortin expressing neurons to reduce feeding behavior.
    Aging Cell 2018 Feb 23;17(1). Epub 2017 Nov 23.
    Department of Nutritional Sciences, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
    Weight loss is an effective intervention for diminishing disease burden in obese older adults. Pharmacological interventions that reduce food intake and thereby promote weight loss may offer effective strategies to reduce age-related disease. We previously reported that 17α-estradiol (17α-E2) administration elicits beneficial effects on metabolism and inflammation in old male mice. Read More

    Comparative proteomic profiling reveals a role for Cisd2 in skeletal muscle aging.
    Aging Cell 2018 Feb 23;17(1). Epub 2017 Nov 23.
    Department of Life Sciences and Institute of Genome Sciences, National Yang-Ming University, Taipei, Taiwan.
    Skeletal muscle has emerged as one of the most important tissues involved in regulating systemic metabolism. The gastrocnemius is a powerful skeletal muscle composed of predominantly glycolytic fast-twitch fibers that are preferentially lost among old age. This decrease in gastrocnemius muscle mass is remarkable during aging; however, the underlying molecular mechanism is not fully understood. Read More

    DLP1-dependent mitochondrial fragmentation and redistribution mediate prion-associated mitochondrial dysfunction and neuronal death.
    Aging Cell 2018 Feb 22;17(1). Epub 2017 Nov 22.
    National Animal Transmissible Spongiform Encephalopathy Laboratory, State Key Laboratories for Agrobiotechnology, Key Laboratory of Animal Epidemiology and Zoonosis, College of Veterinary Medicine, Ministry of Agriculture, China Agricultural University, Beijing, 100193, China.
    Mitochondrial malfunction is a universal and critical step in the pathogenesis of many neurodegenerative diseases including prion diseases. Dynamin-like protein 1 (DLP1) is one of the key regulators of mitochondrial fission. In this study, we investigated the role of DLP1 in mitochondrial fragmentation and dysfunction in neurons using in vitro and in vivo prion disease models. Read More

    Cellular aging dynamics after acute malaria infection: A 12-month longitudinal study.
    Aging Cell 2018 Feb 16;17(1). Epub 2017 Nov 16.
    Unit of Infectious Diseases, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Accelerated cellular aging and reduced lifespan have recently been shown in birds chronically infected with malaria parasites. Whether malaria infection also affects cellular aging in humans has not been reported. Here, we assessed the effect of a single acute Plasmodium falciparum malaria infection on cellular aging dynamics in travelers prospectively followed over one year in Sweden. Read More

    SIRT3 deregulation is linked to mitochondrial dysfunction in Alzheimer's disease.
    Aging Cell 2018 Feb 11;17(1). Epub 2017 Nov 11.
    VA Boston Healthcare System, Boston, MA, 02130, USA.
    Alzheimer's disease (AD) is the leading cause of dementia in the elderly. Despite decades of study, effective treatments for AD are lacking. Mitochondrial dysfunction has been closely linked to the pathogenesis of AD, but the relationship between mitochondrial pathology and neuronal damage is poorly understood. Read More

    Running-wheel activity delays mitochondrial respiratory flux decline in aging mouse muscle via a post-transcriptional mechanism.
    Aging Cell 2018 Feb 9;17(1). Epub 2017 Nov 9.
    Section Systems Medicine of Metabolism and Signaling, Laboratory of Pediatrics, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
    Loss of mitochondrial respiratory flux is a hallmark of skeletal muscle aging, contributing to a progressive decline of muscle strength. Endurance exercise alleviates the decrease in respiratory flux, both in humans and in rodents. Here, we dissect the underlying mechanism of mitochondrial flux decline by integrated analysis of the molecular network. Read More

    Ketone body 3-hydroxybutyrate mimics calorie restriction via the Nrf2 activator, fumarate, in the retina.
    Aging Cell 2018 Feb 9;17(1). Epub 2017 Nov 9.
    Department of Ophthalmology, Keio University School of Medicine, Tokyo, Japan.
    Calorie restriction (CR) being the most robust dietary intervention provides various health benefits. D-3-hydroxybutyrate (3HB), a major physiological ketone, has been proposed as an important endogenous molecule for CR. To investigate the role of 3HB in CR, we investigated potential shared mechanisms underlying increased retinal 3HB induced by CR and exogenously applied 3HB without CR to protect against ischemic retinal degeneration. Read More

    Brain 5-lipoxygenase over-expression worsens memory, synaptic integrity, and tau pathology in the P301S mice.
    Aging Cell 2018 Feb 4;17(1). Epub 2017 Nov 4.
    Department of Pharmacology, Center for Translational Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, 19140, USA.
    Progressive accumulation of highly phosphorylated tau protein isoforms is the main feature of a group of neurodegenerative diseases collectively called tauopathies. Data from human and animal models of these diseases have shown that neuroinflammation often accompanies their pathogenesis. The 5-lipoxygenase (5LO) is an enzyme widely expressed in the brain and a source of potent pro-inflammatory mediators, while its pharmacological inhibition modulates the phenotype of a tau transgenic mouse model, the htau mice. Read More

    Amyloid Beta monomers regulate cyclic adenosine monophosphate response element binding protein functions by activating type-1 insulin-like growth factor receptors in neuronal cells.
    Aging Cell 2018 Feb 1;17(1). Epub 2017 Nov 1.
    Institute of Biostructures and Bioimaging, National Council of Research (IBB-CNR), Via Paolo Gaifami 18, 95126, Catania, Italy.
    Alzheimer's disease (AD) is a progressive neurodegenerative disorder associated with synaptic dysfunction, pathological accumulation of β-amyloid (Aβ), and neuronal loss. The self-association of Aβ monomers into soluble oligomers seems to be crucial for the development of neurotoxicity (J. Neurochem. Read More

    Sirt2-BubR1 acetylation pathway mediates the effects of advanced maternal age on oocyte quality.
    Aging Cell 2018 Feb 25;17(1). Epub 2017 Oct 25.
    State Key Laboratory of Reproductive Medicine, Nanjing Medical University, Nanjing, China.
    The level of Sirt2 protein is reduced in oocytes from aged mice, while exogenous expression of Sirt2 could ameliorate the maternal age-associated meiotic defects. To date, the underlying mechanism remains unclear. Here, we confirmed that specific depletion of Sirt2 disrupts maturational progression and spindle/chromosome organization in mouse oocytes, with compromised kinetochore-microtubule attachments. Read More

    PGC-1α affects aging-related changes in muscle and motor function by modulating specific exercise-mediated changes in old mice.
    Aging Cell 2018 Feb 25;17(1). Epub 2017 Oct 25.
    Biozentrum, University of Basel, Basel, Switzerland.
    The age-related impairment in muscle function results in a drastic decline in motor coordination and mobility in elderly individuals. Regular physical activity is the only efficient intervention to prevent and treat this age-associated degeneration. However, the mechanisms that underlie the therapeutic effect of exercise in this context remain unclear. Read More

    Enhanced inflammation and attenuated tumor suppressor pathways are associated with oncogene-induced lung tumors in aged mice.
    Aging Cell 2018 Feb 18;17(1). Epub 2017 Oct 18.
    Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX, 77030, USA.
    Aging is often accompanied by a dramatic increase in cancer susceptibility. To gain insights into how aging affects tumor susceptibility, we generated a conditional mouse model in which oncogenic Kraswas activated specifically in lungs of young (3-5 months) and old (19-24 months) mice. Activation of Krasin old mice resulted in shorter survival and development of higher-grade lung tumors. Read More

    Influence of cell distribution and diabetes status on the association between mitochondrial DNA copy number and aging phenotypes in the InCHIANTI study.
    Aging Cell 2018 Feb 19;17(1). Epub 2017 Oct 19.
    Longitudinal Studies Section, Translational Gerontology Branch, National Institute on Aging, Baltimore, MD, USA.
    Mitochondrial DNA copy number (mtDNA-CN) estimated in whole blood is a novel marker of mitochondrial mass and function that can be used in large population-based studies. Analyses that attempt to relate mtDNA-CN to specific aging phenotypes may be confounded by differences in the distribution of blood cell types across samples. Also, low or high mtDNA-CN may have a different meaning given the presence of diseases associated with mitochondrial damage. Read More

    Anti-inflammaging effects of human alpha-1 antitrypsin.
    Aging Cell 2018 Feb 17;17(1). Epub 2017 Oct 17.
    Department of Molecular Genetics & Microbiology, University of Florida, Gainesville, FL, USA.
    Inflammaging plays an important role in most age-related diseases. However, the mechanism of inflammaging is largely unknown, and therapeutic control of inflammaging is challenging. Human alpha-1 antitrypsin (hAAT) has immune-regulatory, anti-inflammatory, and cytoprotective properties as demonstrated in several disease models including type 1 diabetes, arthritis, lupus, osteoporosis, and stroke. Read More

    Age-associated microRNA expression in human peripheral blood is associated with all-cause mortality and age-related traits.
    Aging Cell 2018 Feb 17;17(1). Epub 2017 Oct 17.
    The Framingham Heart Study, Framingham, MA, USA.
    Recent studies provide evidence of correlations of DNA methylation and expression of protein-coding genes with human aging. The relations of microRNA expression with age and age-related clinical outcomes have not been characterized thoroughly. We explored associations of age with whole-blood microRNA expression in 5221 adults and identified 127 microRNAs that were differentially expressed by age at P < 3. Read More

    Human CD8EMRA T cells display a senescence-associated secretory phenotype regulated by p38 MAPK.
    Aging Cell 2018 Feb 12;17(1). Epub 2017 Oct 12.
    Translational Medicine and Therapeutics, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London, EC1M 6BQ, UK.
    Cellular senescence is accompanied by a senescence-associated secretory phenotype (SASP). We show here that primary human senescent CD8T cells also display a SASP comprising chemokines, cytokines and extracellular matrix remodelling proteases that are unique to this subset and contribute to age-associated inflammation. We found the CD8CD45RACD27EMRA subset to be the most heterogeneous, with a population aligning with the naïve T cells and another with a closer association to the effector memory subset. Read More

    Ghrelin deletion protects against age-associated hepatic steatosis by downregulating the C/EBPα-p300/DGAT1 pathway.
    Aging Cell 2018 Feb 12;17(1). Epub 2017 Oct 12.
    Department of Medicine, Baylor College of Medicine, Division of Endocrinology, Diabetes and Metabolism, MCL, Center for Translational Research in Inflammatory Diseases, Michael E. DeBakey Veterans Affairs Medical Center, Houston, TX, 77030, USA.
    Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease worldwide. NAFLD usually begins as low-grade hepatic steatosis which further progresses in an age-dependent manner to nonalcoholic steatohepatitis (NASH), fibrosis, cirrhosis, and hepatocellular carcinoma in some patients. Ghrelin is a hormone known to promote adiposity in rodents and humans, but its potential role in hepatic steatosis is unknown. Read More

    In vivo properties of the disaggregase function of J-proteins and Hsc70 in Caenorhabditis elegans stress and aging.
    Aging Cell 2017 Dec 10;16(6):1414-1424. Epub 2017 Oct 10.
    Center for Molecular Biology (ZMBH), Heidelberg University, 69120, Heidelberg, Germany.
    Protein aggregation is enhanced upon exposure to various stress conditions and aging, which suggests that the quality control machinery regulating protein homeostasis could exhibit varied capacities in different stages of organismal lifespan. Recently, an efficient metazoan disaggregase activity was identified in vitro, which requires the Hsp70 chaperone and Hsp110 nucleotide exchange factor, together with single or cooperating J-protein co-chaperones of classes A and B. Here, we describe how the orthologous Hsp70s and J-protein of Caenorhabditis elegans work together to resolve protein aggregates both in vivo and in vitro to benefit organismal health. Read More

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