TY - JOUR AU - Csiszar, Anna AU - Ungvári, Anna Sára AU - Patai, Roland AU - Gulej, Rafal AU - Yabluchanskiy, Andriy AU - Benyó, Zoltán AU - Kovács, Illés AU - Sótonyi, Péter AU - Kirkpartrick, Angelia C AU - Prodan, Calin I AU - Liotta, Eric M AU - Zhang, Xin A AU - Tóth, Péter József AU - Tarantini, Stefano AU - Sorond, Farzaneh A AU - Ungvári, Zoltán István TI - Atherosclerotic burden and cerebral small vessel disease : exploring the link through microvascular aging and cerebral microhemorrhages JF - GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE) J2 - GEROSCIENCE VL - in press PY - 2024 PG - 30 SN - 2509-2715 DO - 10.1007/s11357-024-01139-7 UR - https://m2.mtmt.hu/api/publication/34804161 ID - 34804161 N1 - * Megosztott szerzőség AB - Cerebral microhemorrhages (CMHs, also known as cerebral microbleeds) are a critical but frequently underestimated aspect of cerebral small vessel disease (CSVD), bearing substantial clinical consequences. Detectable through sensitive neuroimaging techniques, CMHs reveal an extensive pathological landscape. They are prevalent in the aging population, with multiple CMHs often being observed in a given individual. CMHs are closely associated with accelerated cognitive decline and are increasingly recognized as key contributors to the pathogenesis of vascular cognitive impairment and dementia (VCID) and Alzheimer's disease (AD). This review paper delves into the hypothesis that atherosclerosis, a prevalent age-related large vessel disease, extends its pathological influence into the cerebral microcirculation, thereby contributing to the development and progression of CSVD, with a specific focus on CMHs. We explore the concept of vascular aging as a continuum, bridging macrovascular pathologies like atherosclerosis with microvascular abnormalities characteristic of CSVD. We posit that the same risk factors precipitating accelerated aging in large vessels (i.e., atherogenesis), primarily through oxidative stress and inflammatory pathways, similarly instigate accelerated microvascular aging. Accelerated microvascular aging leads to increased microvascular fragility, which in turn predisposes to the formation of CMHs. The presence of hypertension and amyloid pathology further intensifies this process. We comprehensively overview the current body of evidence supporting this interconnected vascular hypothesis. Our review includes an examination of epidemiological data, which provides insights into the prevalence and impact of CMHs in the context of atherosclerosis and CSVD. Furthermore, we explore the shared mechanisms between large vessel aging, atherogenesis, microvascular aging, and CSVD, particularly focusing on how these intertwined processes contribute to the genesis of CMHs. By highlighting the role of vascular aging in the pathophysiology of CMHs, this review seeks to enhance the understanding of CSVD and its links to systemic vascular disorders. Our aim is to provide insights that could inform future therapeutic approaches and research directions in the realm of neurovascular health. LA - English DB - MTMT ER - TY - JOUR AU - Balasubramanian, Priya AU - Kiss, Tamás AU - Gulej, Rafal AU - Nyúl-Tóth, Ádám AU - Tarantini, Stefano AU - Yabluchanskiy, Andriy AU - Ungvári, Zoltán István AU - Csiszar, Anna TI - Accelerated Aging Induced by an Unhealthy High-Fat Diet: Initial Evidence for the Role of Nrf2 Deficiency and Impaired Stress Resilience in Cellular Senescence JF - NUTRIENTS J2 - NUTRIENTS VL - 16 PY - 2024 IS - 7 PG - 18 SN - 2072-6643 DO - 10.3390/nu16070952 UR - https://m2.mtmt.hu/api/publication/34773870 ID - 34773870 AB - High-fat diets (HFDs) have pervaded modern dietary habits, characterized by their excessive saturated fat content and low nutritional value. Epidemiological studies have compellingly linked HFD consumption to obesity and the development of type 2 diabetes mellitus. Moreover, the synergistic interplay of HFD, obesity, and diabetes expedites the aging process and prematurely fosters age-related diseases. However, the underlying mechanisms driving these associations remain enigmatic. One of the most conspicuous hallmarks of aging is the accumulation of highly inflammatory senescent cells, with mounting evidence implicating increased cellular senescence in the pathogenesis of age-related diseases. Our hypothesis posits that HFD consumption amplifies senescence burden across multiple organs. To scrutinize this hypothesis, we subjected mice to a 6-month HFD regimen, assessing senescence biomarker expression in the liver, white adipose tissue, and the brain. Aging is intrinsically linked to impaired cellular stress resilience, driven by dysfunction in Nrf2-mediated cytoprotective pathways that safeguard cells against oxidative stress-induced senescence. To ascertain whether Nrf2-mediated pathways shield against senescence induction in response to HFD consumption, we explored senescence burden in a novel model of aging: Nrf2-deficient (Nrf2+/−) mice, emulating the aging phenotype. Our initial findings unveiled significant Nrf2 dysfunction in Nrf2+/− mice, mirroring aging-related alterations. HFD led to substantial obesity, hyperglycemia, and impaired insulin sensitivity in both Nrf2+/− and Nrf2+/+ mice. In control mice, HFD primarily heightened senescence burden in white adipose tissue, evidenced by increased Cdkn2a senescence biomarker expression. In Nrf2+/− mice, HFD elicited a significant surge in senescence burden across the liver, white adipose tissue, and the brain. We postulate that HFD-induced augmentation of senescence burden may be a pivotal contributor to accelerated organismal aging and the premature onset of age-related diseases. LA - English DB - MTMT ER - TY - JOUR AU - Owens, Cameron D AU - Bonin Pinto, Camila AU - Detwiler, Sam AU - Olay, Lauren AU - Pinaffi-Langley, Ana Clara da C AU - Mukli, Péter AU - Péterfi, Anna AU - Szarvas, Zsófia AU - James, Judith A AU - Galvan, Veronica AU - Tarantini, Stefano AU - Csiszar, Anna AU - Ungvári, Zoltán István AU - Kirkpatrick, Angelia C AU - Prodan, Calin I AU - Yabluchanskiy, Andriy TI - Neurovascular coupling impairment as a mechanism for cognitive deficits in COVID-19 JF - BRAIN COMMUNICATIONS J2 - BRAIN COMMUN VL - 6 PY - 2024 IS - 2 PG - 23 SN - 2632-1297 DO - 10.1093/braincomms/fcae080 UR - https://m2.mtmt.hu/api/publication/34756276 ID - 34756276 N1 - Oklahoma Center for Geroscience and Healthy Brain Aging, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73117, United States Vascular Cognitive Impairment, Neurodegeneration and Healthy Brain Aging Program, Department of Neurosurgery, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, United States International Training Program in Geroscience, Doctoral School of Basic and Translational Medicine/Departments of Public Health, Translational Medicine and Physiology, Semmelweis University, Budapest, 1089, Hungary Arthritis & Clinical Immunology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104, United States Department of Internal Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, United States Department of Pathology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, United States Department of Biochemistry and Molecular Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, United States Veterans Affairs Medical Center, Oklahoma City, OK 73104, United States The Peggy and Charles Stephenson Cancer Center, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, United States Department of Health Promotion Sciences, College of Public Health, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, United States Cardiovascular Section, Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73117, United States Department of Neurology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, United States Export Date: 5 April 2024 Correspondence Address: Yabluchanskiy, A.; Department of Neurosurgery, 975 NE 10th Street, United States; email: andriy-yabluchanskiy@ouhsc.edu AB - Components that comprise our brain parenchymal and cerebrovascular structures provide a homeostatic environment for proper neuronal function to ensure normal cognition. Cerebral insults (e.g. ischaemia, microbleeds and infection) alter cellular structures and physiologic processes within the neurovascular unit and contribute to cognitive dysfunction. COVID-19 has posed significant complications during acute and convalescent stages in multiple organ systems, including the brain. Cognitive impairment is a prevalent complication in COVID-19 patients, irrespective of severity of acute SARS-CoV-2 infection. Moreover, overwhelming evidence from in vitro, preclinical and clinical studies has reported SARS-CoV-2-induced pathologies in components of the neurovascular unit that are associated with cognitive impairment. Neurovascular unit disruption alters the neurovascular coupling response, a critical mechanism that regulates cerebromicrovascular blood flow to meet the energetic demands of locally active neurons. Normal cognitive processing is achieved through the neurovascular coupling response and involves the coordinated action of brain parenchymal cells (i.e. neurons and glia) and cerebrovascular cell types (i.e. endothelia, smooth muscle cells and pericytes). However, current work on COVID-19-induced cognitive impairment has yet to investigate disruption of neurovascular coupling as a causal factor. Hence, in this review, we aim to describe SARS-CoV-2's effects on the neurovascular unit and how they can impact neurovascular coupling and contribute to cognitive decline in acute and convalescent stages of the disease. Additionally, we explore potential therapeutic interventions to mitigate COVID-19-induced cognitive impairment. Given the great impact of cognitive impairment associated with COVID-19 on both individuals and public health, the necessity for a coordinated effort from fundamental scientific research to clinical application becomes imperative. This integrated endeavour is crucial for mitigating the cognitive deficits induced by COVID-19 and its subsequent burden in this especially vulnerable population. LA - English DB - MTMT ER - TY - JOUR AU - Yan, F. AU - Alhajeri, Z.A. AU - Nyúl-Tóth, Ádám AU - Wang, C. AU - Zhang, Q. AU - Mercyshalinie, E.R.S. AU - Delfavero, J. AU - Ahire, C. AU - Mutembei, B.M. AU - Tarantini, S. AU - Csiszar, Anna AU - Tang, Q. TI - Dimension-based quantification of aging-associated cerebral microvasculature determined by optical coherence tomography and two-photon microscopy JF - JOURNAL OF BIOPHOTONICS J2 - J BIOPHOTONICS VL - 17 PY - 2024 IS - 3 PG - 14 SN - 1864-063X DO - 10.1002/jbio.202300409 UR - https://m2.mtmt.hu/api/publication/34506904 ID - 34506904 N1 - Stephenson School of Biomedical Engineering, University of Oklahoma, Norman, OK, United States Vascular Cognitive Impairment, Neurodegeneration, and Healthy Brain Aging Program, Department of Neurosurgery, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States Oklahoma Center for Geroscience and Healthy Brain Aging, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States International Training Program in Geroscience, Doctoral School of Basic and Translational Medicine/Department of Public Health, Semmelweis University, Budapest, Hungary International Training Program in Geroscience, Institute of Biophysics, Biological Research Centre, Eötvös Loránd Research Network, Szeged, Hungary Stephenson Cancer Center, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States International Training Program in Geroscience, Doctoral School of Basic and Translational Medicine/Department of Translational Medicine, Semmelweis University, Budapest, Hungary Institute for Biomedical Engineering, Science, and Technology (IBEST), University of Oklahoma, Norman, OK, United States Cited By :1 Export Date: 6 April 2024 Correspondence Address: Tang, Q.; Stephenson School of Biomedical Engineering, United States; email: qtang@ou.edu Funding details: National Science Foundation, NSF, 2238648, OIA‐2132161 Funding details: National Science Foundation, NSF Funding details: National Institutes of Health, NIH, 5U01HL152410‐04, R01CA255840, R01DK133717 Funding details: National Institutes of Health, NIH Funding details: American Cancer Society, ACS Funding details: National Cancer Institute, NCI Funding details: National Institute of General Medical Sciences, NIGMS, P20GM103639, U54GM104938 Funding details: National Institute of General Medical Sciences, NIGMS Funding details: University of Oklahoma, OU, IRG‐19‐142‐01 Funding details: University of Oklahoma, OU Funding details: University of Oklahoma Health Sciences Center, OUHSC, P30CA225520 Funding details: University of Oklahoma Health Sciences Center, OUHSC Funding details: Oklahoma Center for the Advancement of Science and Technology, OCAST, HR23‐071, P20 GM135009 Funding details: Oklahoma Center for the Advancement of Science and Technology, OCAST Funding text 1: This work was supported by grants from the University of Oklahoma Health Sciences Center (P30CA225520), Faculty Investment Program from University of Oklahoma, Institutional Research Grant number IRG‐19‐142‐01 from the American Cancer Society, National Science Foundation (OIA‐2132161, 2238648), National Institute of Health (R01DK133717, R01CA255840, 5U01HL152410‐04), Oklahoma Shared Clinical and Translational Resources (NIGMS U54GM104938), Oklahoma Center for the Advancement of Science and Technology (HR23‐071), and the medical imaging COBRE (P20 GM135009). Histology service provided by the Tissue Pathology Shared Resource was supported in part by the National Institute of General Medical Sciences COBRE Grant P20GM103639 and National Cancer Institute Grant P30CA225520 of the National Institutes of Health. American Heart Association (ANT: AHA834339), the Oklahoma Center for the Advancement of Science and Technology, the National Institute on Aging (RF1AG072295, R01AG055395, R01AG068295; R01AG070915, K01AG073614), the National Institute of Neurological Disorders and Stroke (R01NS100782). Financial support was provided by the OU Libraries' Open Access Fund. LA - English DB - MTMT ER - TY - JOUR AU - Ungvári, Anna Sára AU - Kiss, Tamás AU - Gulej, R. AU - Tarantini, Stefano AU - Csik, B. AU - Yabluchanskiy, A. AU - Mukli, Péter AU - Csiszar, Anna AU - Harris, M.L. AU - Ungvári, Zoltán István TI - Irradiation-induced hair graying in mice: an experimental model to evaluate the effectiveness of interventions targeting oxidative stress, DNA damage prevention, and cellular senescence JF - GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE) J2 - GEROSCIENCE VL - 46 PY - 2024 IS - 3 SP - 3105 EP - 3122 PG - 18 SN - 2509-2715 DO - 10.1007/s11357-023-01042-7 UR - https://m2.mtmt.hu/api/publication/34500888 ID - 34500888 LA - English DB - MTMT ER - TY - JOUR AU - Mukli, Péter AU - Pinto, Camila B AU - Owens, Cameron D AU - Csípő, Tamás AU - Lipécz, Ágnes AU - Szarvas, Zsófia AU - Péterfi, Anna AU - Langley, Ana Clara da Costa Pinaffi AU - Hoffmeister, Jordan AU - Rácz, Frigyes Sámuel AU - Perry, Jonathan W AU - Tarantini, Stefano AU - Nyúl-Tóth, Ádám AU - Sorond, Farzaneh A AU - Yang, Yuan AU - James, Judith A AU - Kirkpatrick, Angelia C AU - Prodan, Calin I AU - Tóth, Péter József AU - Galindo, Juliette AU - Gardner, Andrew W AU - Sonntag, William E AU - Csiszar, Anna AU - Ungvári, Zoltán István AU - Yabluchanskiy, Andriy TI - Impaired Neurovascular Coupling and Increased Functional Connectivity in the Frontal Cortex Predict Age-Related Cognitive Dysfunction JF - ADVANCED SCIENCE J2 - ADV SCI VL - 11 PY - 2024 IS - 10 PG - 18 SN - 2198-3844 DO - 10.1002/advs.202303516 UR - https://m2.mtmt.hu/api/publication/34477401 ID - 34477401 AB - Impaired cerebrovascular function contributes to the genesis of age-related cognitive decline. In this study, the hypothesis is tested that impairments in neurovascular coupling (NVC) responses and brain network function predict cognitive dysfunction in older adults. Cerebromicrovascular and working memory function of healthy young (n = 21, 33.2±7.0 years) and aged (n = 30, 75.9±6.9 years) participants are assessed. To determine NVC responses and functional connectivity (FC) during a working memory (n-back) paradigm, oxy- and deoxyhemoglobin concentration changes from the frontal cortex using functional near-infrared spectroscopy are recorded. NVC responses are significantly impaired during the 2-back task in aged participants, while the frontal networks are characterized by higher local and global connection strength, and dynamic FC (p < 0.05). Both impaired NVC and increased FC correlate with age-related decline in accuracy during the 2-back task. These findings suggest that task-related brain states in older adults require stronger functional connections to compensate for the attenuated NVC responses associated with working memory load. LA - English DB - MTMT ER - TY - JOUR AU - Gulej, R. AU - Nyúl-Tóth, Ádám AU - Csik, B. AU - Petersen, B. AU - Faakye, J. AU - Negri, S. AU - Chandragiri, S.S. AU - Mukli, Péter AU - Yabluchanskiy, A. AU - Conley, S. AU - Huffman, D.M. AU - Csiszar, Anna AU - Tarantini, Stefano AU - Ungvári, Zoltán István TI - Rejuvenation of cerebromicrovascular function in aged mice through heterochronic parabiosis: insights into neurovascular coupling and the impact of young blood factors JF - GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE) J2 - GEROSCIENCE VL - 46 PY - 2024 SP - 327 EP - 347 PG - 21 SN - 2509-2715 DO - 10.1007/s11357-023-01039-2 UR - https://m2.mtmt.hu/api/publication/34474845 ID - 34474845 N1 - Vascular Cognitive Impairment, Neurodegeneration, and Healthy Brain Aging Program, Department of Neurosurgery, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States Oklahoma Center for Geroscience and Healthy Brain Aging, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States International Training Program in Geroscience, Doctoral School of Basic and Translational Medicine/Department of Public Health, Semmelweis University, Budapest, Hungary Stephenson Cancer Center, University of Oklahoma, Oklahoma City, OK, United States Department of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States Department of Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, NY, United States Department of Medicine, Albert Einstein College of Medicine, Bronx, NY, United States International Training Program in Geroscience, Doctoral School of Basic and Translational Medicine/Department of Translational Medicine, Semmelweis University, Budapest, Hungary Export Date: 19 March 2024 Correspondence Address: Ungvari, Z.; Vascular Cognitive Impairment, United States; email: zoltan-ungvari@ouhsc.edu Funding details: P20GM125528 Funding details: 101004093/ EUniWell/EAC-A02-2019 / EAC-A02-2019–1 Funding details: 135784, RRF-2.3.1–21-2022–00003 Funding details: P30AG050911 Funding details: U54GM104938 Funding details: National Institute on Aging, NIA, K01AG073613, K01AG073614, R01AG055395, R01AG068295, R01AG070915, R03AG070479, RF1AG072295 Funding details: National Cancer Institute, NCI, P30 CA225520, R01CA255840 Funding details: National Institute of General Medical Sciences, NIGMS Funding details: National Institute of Neurological Disorders and Stroke, NINDS, R01NS100782 Funding details: American Heart Association, AHA, 916225, AHA CDA941290, AHA834339 Funding details: Presbyterian Health Foundation, PHF Funding details: University of Oklahoma Health Sciences Center, OUHSC Funding details: Oklahoma Center for the Advancement of Science and Technology, OCAST Funding details: Richard S. Reynolds Foundation Funding details: Oklahoma Tobacco Settlement Endowment Trust, TSET, P30AG038072, TKP2021-NKTA-47 Funding details: Nemzeti Kutatási Fejlesztési és Innovációs Hivatal, NKFI Funding details: Nemzeti Kutatási, Fejlesztési és Innovaciós Alap, NKFIA Funding text 1: We sincerely thank the Division of Comparative Medicine team at the University of Oklahoma Health Sciences Center for their invaluable support in supervising animal care and sharing their extensive expertise. Special recognition is extended to Dr. Shawn Lane, DVM, for his invaluable guidance and expertise in surgical and postsurgical care. We are grateful to Dr. Wendy Williams, DVM, for her instrumental role in designing appropriate pre- and postsurgical treatments. We also acknowledge Ms. Carlye Yancey, BS, for her exceptional animal husbandry knowledge and contributions to parabiosis housing. Furthermore, we wish to express our gratitude to Mr. Chad Cunningham, Electronic & Instrument Shop Supervisor Building Manager of the University of Oklahoma’ s Department of Physics and Engineering for his essential assistance in fabricating the parabiont-adjusted components of the stereotactic frame, which was instrumental in facilitating simultaneous measurements of neurovascular coupling in parabionts. Funding text 2: This work was supported by grants from the American Heart Association (R.G.: 916225, ANT: AHA834339, and S.T.: AHA CDA941290), the Oklahoma Center for the Advancement of Science and Technology, the National Institute on Aging (RF1AG072295, R01AG055395, R01AG068295; R01AG070915, K01AG073614, K01AG073613, R03AG070479), the National Institute of Neurological Disorders and Stroke (R01NS100782), the National Cancer Institute (R01CA255840), the Oklahoma Shared Clinical and Translational Resources (U54GM104938) with an Institutional Development Award (IDeA) from NIGMS, the Presbyterian Health Foundation, the Reynolds Foundation, the Oklahoma Nathan Shock Center (P30AG050911), and the Cellular and Molecular GeroScience CoBRE (P20GM125528), the NCI Cancer Center Support Grant (P30 CA225520) and the Oklahoma Tobacco Settlement Endowment Trust. ANT was supported by Project no. DMH is supported by P30AG038072. TKP2021-NKTA-47, implemented with the support provided by the Ministry of Innovation and Technology of Hungary from the National Research, Development and Innovation Fund, financed under the TKP2021-NKTA funding scheme; by funding through the National Cardiovascular Laboratory Program (RRF-2.3.1–21-2022–00003) provided by the Ministry of Innovation and Technology of Hungary from the National Research, Development and Innovation Fund; Project no. 135784 implemented with the support provided from the National Research, Development and Innovation Fund of Hungary, financed under the K_20 funding scheme and the European University for Well-Being (EUniWell) program (grant agreement number: 101004093/ EUniWell/EAC-A02-2019 / EAC-A02-2019–1). The funding sources had no role in the study design; in the collection, analysis and interpretation of data; in the writing of the report; and in the decision to submit the article for publication. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health, the American Heart Association, or the Presbyterian Health Foundation. The 3.5 version of ChatGPT, developed by OpenAI, was used as a language tool to refine our writing, enhancing the clarity of our work. LA - English DB - MTMT ER - TY - JOUR AU - Csiszar, Anna AU - Tarantini, Stefano AU - Yabluchanskiy, A. AU - Ungvári, Zoltán István TI - PCSK9: an emerging player in cardiometabolic aging and its potential as a therapeutic target and biomarker JF - GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE) J2 - GEROSCIENCE VL - 46 PY - 2024 IS - 1 SP - 257 EP - 263 PG - 7 SN - 2509-2715 DO - 10.1007/s11357-023-01003-0 UR - https://m2.mtmt.hu/api/publication/34452959 ID - 34452959 N1 - Export Date: 2 May 2024 Correspondence Address: Ungvari, Z.; OUHSC-SE International Training Program in Geroscience, Hungary; email: zoltan-ungvari@ouhsc.edu LA - English DB - MTMT ER - TY - JOUR AU - Gulej, Rafal AU - Csik, B. AU - Faakye, J. AU - Tarantini, Stefano AU - Shanmugarama, S. AU - Chandragiri, S.S. AU - Mukli, P. AU - Conley, S. AU - Csiszar, Anna AU - Ungvári, Zoltán István AU - Yabluchanskiy, A. AU - Nyúl-Tóth, Ádám TI - Endothelial deficiency of insulin-like growth factor-1 receptor leads to blood–brain barrier disruption and accelerated endothelial senescence in mice, mimicking aspects of the brain aging phenotype JF - MICROCIRCULATION J2 - MICROCIRCULATION VL - 31 PY - 2024 IS - 2 PG - 13 SN - 1073-9688 DO - 10.1111/micc.12840 UR - https://m2.mtmt.hu/api/publication/34444878 ID - 34444878 N1 - Vascular Cognitive Impairment, Neurodegeneration, and Healthy Brain Aging Program, Department of Neurosurgery, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States Oklahoma Center for Geroscience and Healthy Brain Aging, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States International Training Program in Geroscience, Doctoral School of Basic and Translational Medicine/Department of Public Health, Semmelweis University, Budapest, Hungary Stephenson Cancer Center, University of Oklahoma, Oklahoma City, OK, United States Department of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States International Training Program in Geroscience, Doctoral School of Basic and Translational Medicine/Department of Translational Medicine, Semmelweis University, Budapest, Hungary Export Date: 18 March 2024 CODEN: MROCE Correspondence Address: Yabluchanskiy, A.; Department of Neurosurgery, United States; email: andriy-yabluchanskiy@ouhsc.edu Correspondence Address: Nyúl-Tóth, Á.; Vascular Cognitive Impairment, United States; email: adam-nyultoth@ouhsc.edu Chemicals/CAS: somatomedin C, 67763-96-6; Insulin-Like Growth Factor I; Insulin-Like Peptides LA - English DB - MTMT ER - TY - JOUR AU - Ungvári, Zoltán István AU - Tabák, Ádám AU - Ádány, Róza AU - Purebl, György AU - Kaposvári, Csilla AU - Fazekas-Pongor, Vince AU - Csípő, Tamás AU - Szarvas, Zsófia AU - Horváth, Krisztián AU - Mukli, Péter AU - Balog, Piroska AU - Bódizs, Róbert AU - Ujma, Przemyslaw Péter AU - Stauder, Adrienne AU - Belsky, Daniel W. AU - Kovács, Illés AU - Yabluchanskiy, Andriy AU - Maier, Andrea B. AU - Moizs, Mariann AU - Östlin, Piroska AU - Yon, Yongjie AU - Varga, Péter AU - Vokó, Zoltán AU - Papp, Magor Csongor AU - Takács, István AU - Vásárhelyi, Barna AU - Torzsa, Péter AU - Ferdinandy, Péter AU - Csiszar, Anna AU - Benyó, Zoltán AU - Szabó, Attila AU - Bednárikné Dörnyei, Gabriella AU - Kivimäki, Mika AU - Kellermayer, Miklós AU - Merkely, Béla Péter TI - The Semmelweis Study: a longitudinal occupational cohort study within the framework of the Semmelweis Caring University Model Program for supporting healthy aging JF - GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE) J2 - GEROSCIENCE VL - 46 PY - 2024 IS - 1 SP - 191 EP - 218 PG - 28 SN - 2509-2715 DO - 10.1007/s11357-023-01018-7 UR - https://m2.mtmt.hu/api/publication/34425939 ID - 34425939 N1 - International Training Program in Geroscience/Healthy Aging Program, Doctoral School of Basic and Translational Medicine/Department of Public Health, Semmelweis University, Budapest, Hungary Vascular Cognitive Impairment, Neurodegeneration and Healthy Brain Aging Program, Department of Neurosurgery, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States Department of Health Promotion Sciences, The Hudson College of Public Health, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States Department of Public Health, Faculty of Medicine, Semmelweis University, Budapest, Hungary UCL Brain Sciences, University College London, London, United Kingdom Department of Internal Medicine and Oncology, Semmelweis University, Faculty of Medicine, Budapest, Hungary HUN-REN-UD Public Health Research Group, Department of Public Health and Epidemiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary Institute of Behavioral Sciences, Faculty of Medicine, Semmelweis University, Budapest, Hungary Robert N. Butler Columbia Aging Center, Columbia University, New York, NY, United States Department of Epidemiology, Columbia University Mailman School of Public Health, New York, NY, United States Department of Ophthalmology, Faculty of Medicine, Semmelweis University, Budapest, Hungary Department of Ophthalmology, Weill Cornell Medical College, New York City, NY, United States Department of Clinical Ophthalmology, Faculty of Health Sciences, Semmelweis University, Budapest, Hungary Healthy Longevity Translational Research Program, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore Centre for Healthy Longevity, National University Health System, Singapore, Singapore Department of Human Movement Sciences, @AgeAmsterdam, Vrije Universiteit, Amsterdam Movement Sciences, Amsterdam, Netherlands Ministry of Interior of Hungary, Budapest, Hungary WHO Regional Office for Europe, Copenhagen, Denmark Clinical Center, Semmelweis University, Budapest, Hungary Center for Health Technology Assessment, Semmelweis University, Budapest, Hungary Department of Laboratory Medicine, Faculty of Medicine, Semmelweis University, Budapest, Hungary Department of Family Medicine, Faculty of Medicine, Semmelweis University, Budapest, Hungary Department of Pharmacology and Pharmacotherapy, Faculty of Medicine, Semmelweis University, Budapest, Hungary Department of Translational Medicine, Faculty of Medicine, Semmelweis University, Budapest, Hungary HUN-REN-SU Cerebrovascular and Neurocognitive Diseases Research Group, Budapest, Hungary First Department of Pediatrics, Faculty of Medicine, Semmelweis University, Budapest, Hungary HUN-REN-SU Pediatrics and Nephrology Research Group, Semmelweis University, Budapest, Hungary Department of Morphology and Physiology, Faculty of Health Sciences, Semmelweis University, Budapest, Hungary Department of Biophysics and Radiation Biology, Faculty of Medicine, Semmelweis University, Budapest, Hungary Heart and Vascular Center, Semmelweis University, Budapest, Hungary Cited By :1 Export Date: 29 February 2024 Correspondence Address: Ungvari, Z.; International Training Program in Geroscience/Healthy Aging Program, Hungary; email: Zoltan-Ungvari@ouhsc.edu Correspondence Address: Adany, R.; International Training Program in Geroscience/Healthy Aging Program, Hungary AB - The Semmelweis Study is a prospective occupational cohort study that seeks to enroll all employees of Semmelweis University (Budapest, Hungary) aged 25 years and older, with a population of 8866 people, 70.5% of whom are women. The study builds on the successful experiences of the Whitehall II study and aims to investigate the complex relationships between lifestyle, environmental, and occupational risk factors, and the development and progression of chronic age-associated diseases. An important goal of the Semmelweis Study is to identify groups of people who are aging unsuccessfully and therefore have an increased risk of developing age-associated diseases. To achieve this, the study takes a multidisciplinary approach, collecting economic, social, psychological, cognitive, health, and biological data. The Semmelweis Study comprises a baseline data collection with open healthcare data linkage, followed by repeated data collection waves every 5 years. Data are collected through computer-assisted self-completed questionnaires, followed by a physical health examination, physiological measurements, and the assessment of biomarkers. This article provides a comprehensive overview of the Semmelweis Study, including its origin, context, objectives, design, relevance, and expected contributions. LA - English DB - MTMT ER -