TY  - JOUR
AB  - Aging constitutes the largest risk factor for melanoma progression. While a contribution of factors secreted from senescent skin fibroblasts to the progression of melanoma has been proposed, the nature of such factors and subsequent underlying mechanisms remains elusive. Here we show that the chemokine GCP-2 is excessively released by senescent fibroblasts in vitro and the skin of old melanoma patients. GCP-2 regulates, via phosphorylation of the transcription factor CREB at serine 133, defense-, cell cycle control-, and glycolysis-enhancing genes in melanoma cell lines. GCP-2 promotes oncogenic properties in vitro and in vivo in murine melanoma models. Inhibition of CREB phosphorylation in melanoma cells represses glycolytic target genes and induces a switch from glycolysis to oxidative phosphorylation that translates into a significant decline in tumor size in vivo in murine melanoma models. This study identifies a senescent fibroblast to chemokine to CREB to metabolic axis that drives melanoma progression. Targeting this axis may hold promise for novel therapeutic approaches in difficult-to-treat melanoma in older adults.
AU  - Basu, A.*
AU  - Farsam, V.*
AU  - Singh, K.*
AU  - Crisan, D.*
AU  - Treiber, N.*
AU  - Schneider, L.A.*
AU  - Huber, M.*
AU  - Engelmeyer, J.I.*
AU  - Schumacher, B.*
AU  - Maity, P.*
AU  - Brandt, D.
AU  - Jastroch, M.
AU  - Mauch, C.*
AU  - Geiger, H.*
AU  - Kletsas, D.*
AU  - Scharffetter-Kochanek, K.*
C1  - 76081
C2  - 58392
TI  - Senescent fibroblasts drive melanoma progression through GCP-2 induced CREB phosphorylation enhancing glycolysis.
JO  - Aging Cell
PY  - 2025
SN  - 1474-9718
ER  - 

TY  - JOUR
AB  - Across the lifespan, diet and physical activity profiles substantially influence immunometabolic health. DNA methylation, as a tissue-specific marker sensitive to behavioral change, may mediate these effects through modulation of transcription factor binding and subsequent gene expression. Despite this, few human studies have profiled DNA methylation and gene expression simultaneously in multiple tissues or examined how molecular levels react and interact in response to lifestyle changes. The Growing Old Together (GOTO) study is a 13-week lifestyle intervention in older adults, which imparted health benefits to participants. Here, we characterize the DNA methylation response to this intervention at over 750 thousand CpGs in muscle, adipose, and blood. Differentially methylated sites are enriched for active chromatin states, located close to relevant transcription factor binding sites, and associated with changing expression of insulin sensitivity genes and health parameters. In addition, measures of biological age are consistently reduced, with decreases in grimAge associated with observed health improvements. Taken together, our results identify responsive molecular markers and demonstrate their potential to measure progression and finetune treatment of age-related risks and diseases.
AU  - Sinke, L.*
AU  - Beekman, M.*
AU  - Raz, Y.*
AU  - Gehrmann, T.*
AU  - Moustakas, I.*
AU  - Boulinguiez, A.*
AU  - Lakenberg, N.*
AU  - Suchiman, E.*
AU  - Bogaards, F.A.*
AU  - Bizzarri, D.*
AU  - van den Akker, E.B.*
AU  - Waldenberger, M.
AU  - Butler-Browne, G.*
AU  - Trollet, C.*
AU  - de Groot, C.P.G.M.*
AU  - Heijmans, B.T.*
AU  - Slagboom, P.E.*
C1  - 72594
C2  - 56663
CY  - 111 River St, Hoboken 07030-5774, Nj Usa
TI  - Tissue-specific methylomic responses to a lifestyle intervention in older adults associate with metabolic and physiological health improvements.
JO  - Aging Cell
PB  - Wiley
PY  - 2024
SN  - 1474-9718
ER  - 

TY  - JOUR
AB  - Mechanistic insight into ageing may empower prolonging the lifespan of humans; however, a complete understanding of this process is still lacking despite a plethora of ageing theories. In order to address this, we investigated the association of lifespan with eight phenotypic traits, that is, litter size, body mass, female and male sexual maturity, somatic mutation, heart, respiratory, and metabolic rate. In support of the somatic mutation theory, we analysed 15 mammalian species and their whole-genome sequencing deriving somatic mutation rate, which displayed the strongest negative correlation with lifespan. All remaining phenotypic traits showed almost equivalent strong associations across this mammalian cohort, however, resting heart rate explained additional variance in lifespan. Integrating somatic mutation and resting heart rate boosted the prediction of lifespan, thus highlighting that resting heart rate may either directly influence lifespan, or represents an epiphenomenon for additional lower-level mechanisms, for example, metabolic rate, that are associated with lifespan.
AU  - Garger, D.
AU  - Meinel, M.
AU  - Dietl, T.
AU  - Hillig, C.
AU  - Garzorz-Stark, N.*
AU  - Eyerich, K.*
AU  - Hrabě de Angelis, M.
AU  - Eyerich, S.
AU  - Menden, M.P.
C1  - 67969
C2  - 54447
CY  - 111 River St, Hoboken 07030-5774, Nj Usa
TI  - The impact of the cardiovascular component and somatic mutations on ageing.
JO  - Aging Cell
VL  - 22
IS  - 10
PB  - Wiley
PY  - 2023
SN  - 1474-9718
ER  - 

TY  - JOUR
AB  - Aging of the central nervous system (CNS) leads to motoric and cognitive decline and increases the probability for neurodegenerative disease development. Astrocytes fulfill central homeostatic functions in the CNS including regulation of immune responses and metabolic support of neurons and oligodendrocytes. In this study, we investigated the effect of redox imbalance in astrocytes by using a conditional astrocyte-specific SOD2-deficient mouse model (SOD2ako ) and analyzed these animals at different stages of their life. SOD2ako mice did not exhibit any overt phenotype within the first postnatal weeks. However, already as young adults, they displayed progressive motoric impairments. Moreover, as these mice grew older, they exhibited signs of a progeroid phenotype and early death. Histological analysis in moribund SOD2ako mice revealed the presence of age-related brain alterations, neuroinflammation, neuronal damage and myelin impairment in brain and spinal cord. Additionally, transcriptome analysis of primary astrocytes revealed that SOD2 deletion triggered a hypometabolic state and promoted polarization toward A1-neurotoxic status, possibly underlying the neuronal and myelin deficits. Conclusively, our study identifies maintenance of ROS homeostasis in astrocytes as a critical prerequisite for physiological CNS aging.
AU  - Tsesmelis, K.*
AU  - Maity-Kumar, G.
AU  - Croner, D.*
AU  - Sprissler, J.*
AU  - Tsesmelis, M.*
AU  - Hein, T.*
AU  - Baumann, B.*
AU  - Wirth, T.*
C1  - 67968
C2  - 54446
CY  - 111 River St, Hoboken 07030-5774, Nj Usa
TI  - Accelerated aging in mice with astrocytic redox imbalance as a consequence of SOD2 deletion.
JO  - Aging Cell
VL  - 22
IS  - 9
PB  - Wiley
PY  - 2023
SN  - 1474-9718
ER  - 

TY  - JOUR
AB  - DNA methylation (DNAm) has been reported to be associated with many diseases and with mortality. We hypothesized that the integration of DNAm with clinical risk factors would improve mortality prediction. We performed an epigenome-wide association study of whole blood DNAm in relation to mortality in 15 cohorts (n = 15,013). During a mean follow-up of 10 years, there were 4314 deaths from all causes including 1235 cardiovascular disease (CVD) deaths and 868 cancer deaths. Ancestry-stratified meta-analysis of all-cause mortality identified 163 CpGs in European ancestry (EA) and 17 in African ancestry (AA) participants at p < 1 × 10-7 , of which 41 (EA) and 16 (AA) were also associated with CVD death, and 15 (EA) and 9 (AA) with cancer death. We built DNAm-based prediction models for all-cause mortality that predicted mortality risk after adjusting for clinical risk factors. The mortality prediction model trained by integrating DNAm with clinical risk factors showed an improvement in prediction of cancer death with 5% increase in the C-index in a replication cohort, compared with the model including clinical risk factors alone. Mendelian randomization identified 15 putatively causal CpGs in relation to longevity, CVD, or cancer risk. For example, cg06885782 (in KCNQ4) was positively associated with risk for prostate cancer (Beta = 1.2, PMR  = 4.1 × 10-4 ) and negatively associated with longevity (Beta = -1.9, PMR  = 0.02). Pathway analysis revealed that genes associated with mortality-related CpGs are enriched for immune- and cancer-related pathways. We identified replicable DNAm signatures of mortality and demonstrated the potential utility of CpGs as informative biomarkers for prediction of mortality risk.
AU  - Huan, T.*
AU  - Nguyen, S.*
AU  - Colicino, E.*
AU  - Ochoa-Rosales, C.*
AU  - Hill, W.D.*
AU  - Brody, J.A.*
AU  - Soerensen, M.*
AU  - Zhang, Y.*
AU  - Baldassari, A.*
AU  - Elhadad, M.A.
AU  - Toshiko, T.*
AU  - Zheng, Y.*
AU  - Domingo-Relloso, A.*
AU  - Lee, D.H.*
AU  - Ma, J.*
AU  - Yao, C.*
AU  - Liu, C.*
AU  - Hwang, S.J.*
AU  - Joehanes, R.*
AU  - Fornage, M.*
AU  - Bressler, J.*
AU  - van Meurs, J.B.J.*
AU  - Debrabant, B.*
AU  - Mengel-From, J.*
AU  - Hjelmborg, J.B.H.*
AU  - Christensen, K.*
AU  - Vokonas, P.*
AU  - Schwartz, J.*
AU  - Gahrib, S.A.*
AU  - Sotoodehnia, N.*
AU  - Sitlani, C.M.*
AU  - Kunze, S.
AU  - Gieger, C.
AU  - Peters, A.
AU  - Waldenberger, M.
AU  - Deary, I.J.*
AU  - Ferrucci, L.*
AU  - Qu, Y.*
AU  - Greenland, P.*
AU  - Lloyd-Jones, D.M.*
AU  - Hou, L.*
AU  - Bandinelli, S.*
AU  - Voortman, T.*
AU  - Hermann, B.*
AU  - Baccarelli, A.*
AU  - Whitsel, E.A.*
AU  - Pankow, J.S.*
AU  - Levy, D.*
C1  - 65008
C2  - 52131
TI  - Integrative analysis of clinical and epigenetic biomarkers of mortality.
JO  - Aging Cell
PY  - 2022
SN  - 1474-9718
ER  - 

TY  - JOUR
AB  - One of the most fundamental challenges for all living organisms is to sense and respond to alternating nutritional conditions in order to adapt their metabolism and physiology to promote survival and achieve balanced growth. Here, we applied metabolomics and lipidomics to examine temporal regulation of metabolism during starvation in wild-type Caenorhabditis elegans and in animals lacking the transcription factor HLH-30. Our findings show for the first time that starvation alters the abundance of hundreds of metabolites and lipid species in a temporal- and HLH-30-dependent manner. We demonstrate that premature death of hlh-30 animals under starvation can be prevented by supplementation of exogenous fatty acids, and that HLH-30 is required for complete oxidation of long-chain fatty acids. We further show that RNAi-mediated knockdown of the gene encoding carnitine palmitoyl transferase I (cpt-1) only impairs survival of wild-type animals and not of hlh-30 animals. Strikingly, we also find that compromised generation of peroxisomes by prx-5 knockdown renders hlh-30 animals hypersensitive to starvation, which cannot be rescued by supplementation of exogenous fatty acids. Collectively, our observations show that mitochondrial functions are compromised in hlh-30 animals and that hlh-30 animals rewire their metabolism to largely depend on functional peroxisomes during starvation, underlining the importance of metabolic plasticity to maintain survival.
AU  - Dall, K.B.*
AU  - Havelund, J.F.*
AU  - Harvald, E.B.*
AU  - Witting,M.
AU  - Færgeman, N.J.*
C1  - 61621
C2  - 50355
CY  - 111 River St, Hoboken 07030-5774, Nj Usa
TI  - HLH-30-dependent rewiring of metabolism during starvation in C. elegans.
JO  - Aging Cell
VL  - 20
IS  - 4
PB  - Wiley
PY  - 2021
SN  - 1474-9718
ER  - 

TY  - JOUR
AB  - During aging, brain performances decline. Cellular senescence is one of the aging drivers and a key feature of a variety of human age-related disorders. The transcriptional repressor RE1-silencing transcription factor (REST) has been associated with aging and higher risk of neurodegenerative disorders. However, how REST contributes to the senescence program and functional impairment remains largely unknown. Here, we report that REST is essential to prevent the senescence phenotype in primary mouse neurons. REST deficiency causes failure of autophagy and loss of proteostasis, increased oxidative stress, and higher rate of cell death. Re-establishment of autophagy reverses the main hallmarks of senescence. Our data indicate that REST has a protective role in physiological aging by regulating the autophagic flux and the senescence program in neurons, with implications for neurological disorders associated with aging.
AU  - Rocchi, A.*
AU  - Carminati, E.*
AU  - De Fusco, A.*
AU  - Kowalska, J.A.*
AU  - Floss, T.
AU  - Benfenati, F.*
C1  - 63013
C2  - 51190
CY  - 111 River St, Hoboken 07030-5774, Nj Usa
TI  - REST/NRSF deficiency impairs autophagy and leads to cellular senescence in neurons.
JO  - Aging Cell
PB  - Wiley
PY  - 2021
SN  - 1474-9718
ER  - 

TY  - JOUR
AB  - The dauer larva ofCaenorhabditis elegans, destined to survive long periods of food scarcity and harsh environment, does not feed and has a very limited exchange of matter with the exterior. It was assumed that the survival time is determined by internal energy stores. Here, we show that ethanol can provide a potentially unlimited energy source for dauers by inducing a controlled metabolic shift that allows it to be metabolized into carbohydrates, amino acids, and lipids. Dauer larvae provided with ethanol survive much longer and have greater desiccation tolerance. On the cellular level, ethanol prevents the deterioration of mitochondria caused by energy depletion. By modeling the metabolism of dauers of wild-type and mutant strains with and without ethanol, we suggest that the mitochondrial health and survival of an organism provided with an unlimited source of carbon depends on the balance between energy production and toxic product(s) of lipid metabolism.
AU  - Kaptan, D.*
AU  - Penkov, S.
AU  - Zhang, X.*
AU  - Gade, V.R.*
AU  - Raghuraman, B.K.*
AU  - Galli, R.*
AU  - Sampaio, J.L.*
AU  - Haase, R.*
AU  - Koch, E.*
AU  - Shevchenko, A.*
AU  - Zaburdaev, V.*
AU  - Kurzchalia, T.V.*
C1  - 60052
C2  - 49196
CY  - 111 River St, Hoboken 07030-5774, Nj Usa
TI  - Exogenous ethanol induces a metabolic switch that prolongs the survival of Caenorhabditis elegans dauer larva and enhances its resistance to desiccation.
JO  - Aging Cell
VL  - 19
IS  - 10
PB  - Wiley
PY  - 2020
SN  - 1474-9718
ER  - 

TY  - JOUR
AB  - Remodeling of the extracellular matrix is a key component of the metabolic adaptations of adipose tissue in response to dietary and physiological challenges. Disruption of its integrity is a well-known aspect of adipose tissue dysfunction, for instance, during aging and obesity. Adipocyte regeneration from a tissue-resident pool of mesenchymal stem cells is part of normal tissue homeostasis. Among the pathophysiological consequences of adipogenic stem cell aging, characteristic changes in the secretory phenotype, which includes matrix-modifying proteins, have been described. Here, we show that the expression of the matricellular protein periostin, a component of the extracellular matrix produced and secreted by adipose tissue-resident interstitial cells, is markedly decreased in aged brown and white adipose tissue depots. Using a mouse model, we demonstrate that the adaptation of adipose tissue to adrenergic stimulation and high-fat diet feeding is impaired in animals with systemic ablation of the gene encoding for periostin. Our data suggest that loss of periostin attenuates lipid metabolism in adipose tissue, thus recapitulating one aspect of age-related metabolic dysfunction. In human white adipose tissue, periostin expression showed an unexpected positive correlation with age of study participants. This correlation, however, was no longer evident after adjusting for BMI or plasma lipid and liver function biomarkers. These findings taken together suggest that age-related alterations of the adipose tissue extracellular matrix may contribute to the development of metabolic disease by negatively affecting nutrient homeostasis.
AU  - Graja, A.*
AU  - Garcia-Carrizo, F.*
AU  - Jank, A.*
AU  - Gohlke, S.*
AU  - Ambrosi, T.H.*
AU  - Jonas, W.*
AU  - Ussar, S.
AU  - Kern, M.J.*
AU  - Schürmann, A.*
AU  - Aleksandrova, K.*
AU  - Blüher, M.*
AU  - Schulz, T.J.*
C1  - 54490
C2  - 45590
CY  - 111 River St, Hoboken 07030-5774, Nj Usa
TI  - Loss of periostin occurs in aging adipose tissue of mice and its genetic ablation impairs adipose tissue lipid metabolism.
JO  - Aging Cell
VL  - 17
IS  - 5
PB  - Wiley
PY  - 2018
SN  - 1474-9718
ER  - 

TY  - JOUR
AB  - Human longevity is characterized by a remarkable lack of confirmed genetic associations. Here, we report on the identification of a novel locus for longevity in the RAD50/IL13 region on chromosome 5q31.1 using a combined European sample of 3208 long-lived individuals (LLI) and 8919 younger controls. First, we performed a large-scale association study on 1458 German LLI (mean age 99.0 years) and 6368 controls (mean age 57.2 years) by targeting known immune-associated loci covered by the Immunochip. The analysis of 142 136 autosomal single nucleotide polymorphisms (SNPs) revealed an Immunochip-wide significant signal (PI mmunochip  = 7.01 × 10(-9) ) for the SNP rs2075650 in the TOMM40/APOE region, which has been previously described in the context of human longevity. To identify novel susceptibility loci, we selected 15 markers with PI mmunochip  < 5 × 10(-4) for replication in two samples from France (1257 LLI, mean age 102.4 years; 1811 controls, mean age 49.1 years) and Denmark (493 LLI, mean age 96.2 years; 740 controls, mean age 63.1 years). The association at SNP rs2706372 replicated in the French study collection and showed a similar trend in the Danish participants and was also significant in a meta-analysis of the combined French and Danish data after adjusting for multiple testing. In a meta-analysis of all three samples, rs2706372 reached a P-value of PI mmunochip+Repl  = 5.42 × 10(-7) (OR = 1.20; 95% CI = 1.12-1.28). SNP rs2706372 is located in the extended RAD50/IL13 region. RAD50 seems a plausible longevity candidate due to its involvement in DNA repair and inflammation. Further studies are needed to identify the functional variant(s) that predispose(s) to a long and healthy life.
AU  - Flachsbart, F.*
AU  - Ellinghaus, D.*
AU  - Gentschew, L.*
AU  - Heinsen, F.A.*
AU  - Caliebe, A.*
AU  - Christiansen, L.*
AU  - Nygaard, M.*
AU  - Christensen, K.*
AU  - Blanche, H.*
AU  - Deleuze, J.F.*
AU  - Derbois, C.*
AU  - Galan, P.*
AU  - Büning, C.*
AU  - Brand, S.*
AU  - Peters, A.
AU  - Strauch, K.
AU  - Müller-Nurasyid, M.
AU  - Hoffmann, P.*
AU  - Nöthen, M.M.*
AU  - Lieb, W.*
AU  - Franke, A.*
AU  - Schreiber, S.*
AU  - Nebel, A.*
C1  - 48429
C2  - 41101
CY  - Hoboken
SP  - 585-588
TI  - Immunochip analysis identifies association of the RAD50/IL13 region with human longevity.
JO  - Aging Cell
VL  - 15
IS  - 3
PB  - Wiley-blackwell
PY  - 2016
SN  - 1474-9718
ER  - 

TY  - JOUR
AB  - Alzheimer's disease (AD) is histopathologically characterized by neurodegeneration, the formation of intracellular neurofibrillary tangles and extracellular A* deposits that derive from proteolytic processing of the amyloid precursor protein (APP). As rodents do not normally develop A* pathology, various transgenic animal models of AD were designed to overexpress human APP with mutations favouring its amyloidogenic processing. However, these mouse models display tremendous differences in the spatial and temporal appearance of A* deposits, synaptic dysfunction, neurodegeneration and the manifestation of learning deficits which may be caused by age-related and brain region-specific differences in APP transgene levels. Consequentially, a comparative temporal and regional analysis of the pathological effects of A* in mouse brains is difficult complicating the validation of therapeutic AD treatment strategies in different mouse models. To date, no antibodies are available that properly discriminate endogenous rodent and transgenic human APP in brains of APP-transgenic animals. Here, we developed and characterized rat monoclonal antibodies by immunohistochemistry and Western blot that detect human but not murine APP in brains of three APP-transgenic mouse and one APP-transgenic rat model. We observed remarkable differences in expression levels and brain region-specific expression of human APP among the investigated transgenic mouse lines. This may explain the differences between APP-transgenic models mentioned above. Furthermore, we provide compelling evidence that our new antibodies specifically detect endogenous human APP in immunocytochemistry, FACS and immunoprecipitation. Hence, we propose these antibodies as standard tool for monitoring expression of endogenous or transfected APP in human cells and APP expression in transgenic animals.
AU  - Höfling, C.*
AU  - Morawski, M.*
AU  - Zeitschel, U.*
AU  - Zanier, E.R.*
AU  - Moschke, K.*
AU  - Serdaroglu, A.*
AU  - Canneva, F.*
AU  - von Hörsten, S.*
AU  - de Simoni, M.G.*
AU  - Forloni, G.*
AU  - Jäger, C.*
AU  - Kremmer, E.
AU  - Roßner, S.*
AU  - Lichtenthaler, S.F.*
AU  - Kuhn, P.H.*
C1  - 49189
C2  - 41701
CY  - Hoboken
SP  - 953-963
TI  - Differential transgene expression patterns in Alzheimer mouse models revealed by novel human amyloid precursor protein-specific antibodies.
JO  - Aging Cell
VL  - 15
IS  - 5
PB  - Wiley-blackwell
PY  - 2016
SN  - 1474-9718
ER  - 

TY  - JOUR
AB  - Age is the strongest risk factor for many diseases including neurodegenerative disorders, coronary heart disease, type 2 diabetes and cancer. Due to increasing life expectancy and low birth rates, the incidence of age-related diseases is increasing in industrialized countries. Therefore, understanding the relationship between diseases and aging and facilitating healthy aging are major goals in medical research. In the last decades, the dimension of biological data has drastically increased with high-throughput technologies now measuring thousands of (epi) genetic, expression and metabolic variables. The most common and so far successful approach to the analysis of these data is the so-called reductionist approach. It consists of separately testing each variable for association with the phenotype of interest such as age or age-related disease. However, a large portion of the observed phenotypic variance remains unexplained and a comprehensive understanding of most complex phenotypes is lacking. Systems biology aims to integrate data from different experiments to gain an understanding of the system as a whole rather than focusing on individual factors. It thus allows deeper insights into the mechanisms of complex traits, which are caused by the joint influence of several, interacting changes in the biological system. In this review, we look at the current progress of applying omics technologies to identify biomarkers of aging. We then survey existing systems biology approaches that allow for an integration of different types of data and highlight the need for further developments in this area to improve epidemiologic investigations.
AU  - Zierer, J.
AU  - Menni, C.*
AU  - Kastenmüller, G.
AU  - Spector, T.D.*
C1  - 46773
C2  - 37801
SP  - 933–944
TI  - Integration of 'omics' data in aging research: From biomarkers to systems biology.
JO  - Aging Cell
VL  - 14
IS  - 6
PY  - 2015
SN  - 1474-9718
ER  - 

TY  - JOUR
AB  - Understanding the complexity of aging is of utmost importance. This can now be addressed by the novel and powerful approach of metabolomics. However, to date, only a few metabolic studies based on large samples are available. Here, we provide novel and specific information on age-related metabolite concentration changes in human homeostasis. We report results from two population-based studies: the KORA F4 study from Germany as a discovery cohort, with 1038 female and 1124 male participants (32-81 years), and the TwinsUK study as replication, with 724 female participants. Targeted metabolomics of fasting serum samples quantified 131 metabolites by FIA-MS/MS. Among these, 71/34 metabolites were significantly associated with age in women/men (BMI adjusted). We further identified a set of 13 independent metabolites in women (with P values ranging from 4.6 × 10(-04) to 7.8 × 10(-42) , α(corr)  = 0.004). Eleven of these 13 metabolites were replicated in the TwinsUK study, including seven metabolite concentrations that increased with age (C0, C10:1, C12:1, C18:1, SM C16:1, SM C18:1, and PC aa C28:1), while histidine decreased. These results indicate that metabolic profiles are age dependent and might reflect different aging processes, such as incomplete mitochondrial fatty acid oxidation. The use of metabolomics will increase our understanding of aging networks and may lead to discoveries that help enhance healthy aging.
AU  - Yu, Z.
AU  - Zhai, G.*
AU  - Singmann, P.
AU  - He, Y.*
AU  - Xu, T.
AU  - Prehn, C.
AU  - Römisch-Margl, W.
AU  - Lattka, E.
AU  - Gieger, C.
AU  - Soranzo, N.*
AU  - Heinrich, J.
AU  - Standl, M.
AU  - Thiering, E.
AU  - Mittelstraß, K.
AU  - Wichmann, H.-E.
AU  - Peters, A.
AU  - Suhre, K.
AU  - Li, Y.*
AU  - Adamski, J.
AU  - Spector, T.D.*
AU  - Illig, T.
AU  - Wang-Sattler, R.
C1  - 10427
C2  - 30233
SP  - 960-967
TI  - Human serum metabolic profiles are age dependent.
JO  - Aging Cell
VL  - 11
IS  - 6
PB  - Wiley-Blackwell
PY  - 2012
SN  - 1474-9718
ER  -