@article{MTMT:34804161,
	title = {Atherosclerotic burden and cerebral small vessel disease : exploring the link through microvascular aging and cerebral microhemorrhages},
	url = {https://m2.mtmt.hu/api/publication/34804161},
	author = {Csiszar, Anna and Ungvári, Anna Sára and Patai, Roland and Gulej, Rafal and Yabluchanskiy, Andriy and Benyó, Zoltán and Kovács, Illés and Sótonyi, Péter and Kirkpartrick, Angelia C and Prodan, Calin I and Liotta, Eric M and Zhang, Xin A and Tóth, Péter József and Tarantini, Stefano and Sorond, Farzaneh A and Ungvári, Zoltán István},
	doi = {10.1007/s11357-024-01139-7},
	journal-iso = {GEROSCIENCE},
	journal = {GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE)},
	volume = {in press},
	unique-id = {34804161},
	issn = {2509-2715},
	abstract = {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.},
	keywords = {ATHEROSCLEROSIS; Aging; Blood-Brain Barrier; Arteriosclerosis; stroke; Leukoaraiosis; Peripheral artery disease; VASCULAR DEMENTIA; Microbleed; White matter hyperintensities; white matter injury},
	year = {2024},
	eissn = {2509-2723},
	orcid-numbers = {Benyó, Zoltán/0000-0001-6015-0359; Kovács, Illés/0000-0001-5763-0482; Sótonyi, Péter/0000-0002-2216-4298; Tarantini, Stefano/0000-0001-5627-1430; Ungvári, Zoltán István/0000-0002-6035-6039}
}

@article{MTMT:34773870,
	title = {Accelerated Aging Induced by an Unhealthy High-Fat Diet: Initial Evidence for the Role of Nrf2 Deficiency and Impaired Stress Resilience in Cellular Senescence},
	url = {https://m2.mtmt.hu/api/publication/34773870},
	author = {Balasubramanian, Priya and Kiss, Tamás and Gulej, Rafal and Nyúl-Tóth, Ádám and Tarantini, Stefano and Yabluchanskiy, Andriy and Ungvári, Zoltán István and Csiszar, Anna},
	doi = {10.3390/nu16070952},
	journal-iso = {NUTRIENTS},
	journal = {NUTRIENTS},
	volume = {16},
	unique-id = {34773870},
	abstract = {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.},
	year = {2024},
	eissn = {2072-6643},
	orcid-numbers = {Kiss, Tamás/0000-0001-5339-5227; Gulej, Rafal/0000-0002-9958-707X; Tarantini, Stefano/0000-0001-5627-1430; Ungvári, Zoltán István/0000-0002-6035-6039}
}

@article{MTMT:34756276,
	title = {Neurovascular coupling impairment as a mechanism for cognitive deficits in COVID-19},
	url = {https://m2.mtmt.hu/api/publication/34756276},
	author = {Owens, Cameron D and Bonin Pinto, Camila and Detwiler, Sam and Olay, Lauren and Pinaffi-Langley, Ana Clara da C and Mukli, Péter and Péterfi, Anna and Szarvas, Zsófia and James, Judith A and Galvan, Veronica and Tarantini, Stefano and Csiszar, Anna and Ungvári, Zoltán István and Kirkpatrick, Angelia C and Prodan, Calin I and Yabluchanskiy, Andriy},
	doi = {10.1093/braincomms/fcae080},
	journal-iso = {BRAIN COMMUN},
	journal = {BRAIN COMMUNICATIONS},
	volume = {6},
	unique-id = {34756276},
	abstract = {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.},
	year = {2024},
	eissn = {2632-1297},
	orcid-numbers = {Owens, Cameron D/0000-0002-5020-2810; Mukli, Péter/0000-0003-4355-8103; Szarvas, Zsófia/0000-0002-0022-5053; Tarantini, Stefano/0000-0001-5627-1430; Ungvári, Zoltán István/0000-0002-6035-6039; Yabluchanskiy, Andriy/0000-0002-9648-7161}
}

@article{MTMT:34506904,
	title = {Dimension-based quantification of aging-associated cerebral microvasculature determined by optical coherence tomography and two-photon microscopy},
	url = {https://m2.mtmt.hu/api/publication/34506904},
	author = {Yan, F. and Alhajeri, Z.A. and Nyúl-Tóth, Ádám and Wang, C. and Zhang, Q. and Mercyshalinie, E.R.S. and Delfavero, J. and Ahire, C. and Mutembei, B.M. and Tarantini, S. and Csiszar, Anna and Tang, Q.},
	doi = {10.1002/jbio.202300409},
	journal-iso = {J BIOPHOTONICS},
	journal = {JOURNAL OF BIOPHOTONICS},
	volume = {17},
	unique-id = {34506904},
	issn = {1864-063X},
	year = {2024},
	eissn = {1864-0648}
}

@article{MTMT:34500888,
	title = {Irradiation-induced hair graying in mice: an experimental model to evaluate the effectiveness of interventions targeting oxidative stress, DNA damage prevention, and cellular senescence},
	url = {https://m2.mtmt.hu/api/publication/34500888},
	author = {Ungvári, Anna Sára and Kiss, Tamás and Gulej, R. and Tarantini, Stefano and Csik, B. and Yabluchanskiy, A. and Mukli, Péter and Csiszar, Anna and Harris, M.L. and Ungvári, Zoltán István},
	doi = {10.1007/s11357-023-01042-7},
	journal-iso = {GEROSCIENCE},
	journal = {GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE)},
	volume = {46},
	unique-id = {34500888},
	issn = {2509-2715},
	year = {2024},
	eissn = {2509-2723},
	pages = {3105-3122},
	orcid-numbers = {Kiss, Tamás/0000-0001-5339-5227; Tarantini, Stefano/0000-0001-5627-1430; Mukli, Péter/0000-0003-4355-8103; Ungvári, Zoltán István/0000-0002-6035-6039}
}

@article{MTMT:34477401,
	title = {Impaired Neurovascular Coupling and Increased Functional Connectivity in the Frontal Cortex Predict Age-Related Cognitive Dysfunction},
	url = {https://m2.mtmt.hu/api/publication/34477401},
	author = {Mukli, Péter and Pinto, Camila B and Owens, Cameron D and Csípő, Tamás and Lipécz, Ágnes and Szarvas, Zsófia and Péterfi, Anna and Langley, Ana Clara da Costa Pinaffi and Hoffmeister, Jordan and Rácz, Frigyes Sámuel and Perry, Jonathan W and Tarantini, Stefano and Nyúl-Tóth, Ádám and Sorond, Farzaneh A and Yang, Yuan and James, Judith A and Kirkpatrick, Angelia C and Prodan, Calin I and Tóth, Péter József and Galindo, Juliette and Gardner, Andrew W and Sonntag, William E and Csiszar, Anna and Ungvári, Zoltán István and Yabluchanskiy, Andriy},
	doi = {10.1002/advs.202303516},
	journal-iso = {ADV SCI},
	journal = {ADVANCED SCIENCE},
	volume = {11},
	unique-id = {34477401},
	abstract = {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.},
	keywords = {Aging; cognitive decline; functional connectivity; Neurovascular coupling; functional near-infrared spectroscopy},
	year = {2024},
	eissn = {2198-3844},
	orcid-numbers = {Mukli, Péter/0000-0003-4355-8103; Szarvas, Zsófia/0000-0002-0022-5053; Rácz, Frigyes Sámuel/0000-0001-9077-498X; Tarantini, Stefano/0000-0001-5627-1430; Ungvári, Zoltán István/0000-0002-6035-6039}
}

@article{MTMT:34474845,
	title = {Rejuvenation of cerebromicrovascular function in aged mice through heterochronic parabiosis: insights into neurovascular coupling and the impact of young blood factors},
	url = {https://m2.mtmt.hu/api/publication/34474845},
	author = {Gulej, R. and Nyúl-Tóth, Ádám and Csik, B. and Petersen, B. and Faakye, J. and Negri, S. and Chandragiri, S.S. and Mukli, Péter and Yabluchanskiy, A. and Conley, S. and Huffman, D.M. and Csiszar, Anna and Tarantini, Stefano and Ungvári, Zoltán István},
	doi = {10.1007/s11357-023-01039-2},
	journal-iso = {GEROSCIENCE},
	journal = {GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE)},
	volume = {46},
	unique-id = {34474845},
	issn = {2509-2715},
	year = {2024},
	eissn = {2509-2723},
	pages = {327-347},
	orcid-numbers = {Mukli, Péter/0000-0003-4355-8103; Tarantini, Stefano/0000-0001-5627-1430; Ungvári, Zoltán István/0000-0002-6035-6039}
}

@article{MTMT:34452959,
	title = {PCSK9: an emerging player in cardiometabolic aging and its potential as a therapeutic target and biomarker},
	url = {https://m2.mtmt.hu/api/publication/34452959},
	author = {Csiszar, Anna and Tarantini, Stefano and Yabluchanskiy, A. and Ungvári, Zoltán István},
	doi = {10.1007/s11357-023-01003-0},
	journal-iso = {GEROSCIENCE},
	journal = {GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE)},
	volume = {46},
	unique-id = {34452959},
	issn = {2509-2715},
	year = {2024},
	eissn = {2509-2723},
	pages = {257-263},
	orcid-numbers = {Tarantini, Stefano/0000-0001-5627-1430; Ungvári, Zoltán István/0000-0002-6035-6039}
}

@article{MTMT:34444878,
	title = {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},
	url = {https://m2.mtmt.hu/api/publication/34444878},
	author = {Gulej, Rafal and Csik, B. and Faakye, J. and Tarantini, Stefano and Shanmugarama, S. and Chandragiri, S.S. and Mukli, P. and Conley, S. and Csiszar, Anna and Ungvári, Zoltán István and Yabluchanskiy, A. and Nyúl-Tóth, Ádám},
	doi = {10.1111/micc.12840},
	journal-iso = {MICROCIRCULATION},
	journal = {MICROCIRCULATION},
	volume = {31},
	unique-id = {34444878},
	issn = {1073-9688},
	year = {2024},
	eissn = {1549-8719},
	orcid-numbers = {Tarantini, Stefano/0000-0001-5627-1430; Ungvári, Zoltán István/0000-0002-6035-6039}
}

@article{MTMT:34425939,
	title = {The Semmelweis Study: a longitudinal occupational cohort study within the framework of the Semmelweis Caring University Model Program for supporting healthy aging},
	url = {https://m2.mtmt.hu/api/publication/34425939},
	author = {Ungvári, Zoltán István and Tabák, Ádám and Ádány, Róza and Purebl, György and Kaposvári, Csilla and Fazekas-Pongor, Vince and Csípő, Tamás and Szarvas, Zsófia and Horváth, Krisztián and Mukli, Péter and Balog, Piroska and Bódizs, Róbert and Ujma, Przemyslaw Péter and Stauder, Adrienne and Belsky, Daniel W. and Kovács, Illés and Yabluchanskiy, Andriy and Maier, Andrea B. and Moizs, Mariann and Östlin, Piroska and Yon, Yongjie and Varga, Péter and Vokó, Zoltán and Papp, Magor Csongor and Takács, István and Vásárhelyi, Barna and Torzsa, Péter and Ferdinandy, Péter and Csiszar, Anna and Benyó, Zoltán and Szabó, Attila and Bednárikné Dörnyei, Gabriella and Kivimäki, Mika and Kellermayer, Miklós and Merkely, Béla Péter},
	doi = {10.1007/s11357-023-01018-7},
	journal-iso = {GEROSCIENCE},
	journal = {GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE)},
	volume = {46},
	unique-id = {34425939},
	issn = {2509-2715},
	abstract = {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.},
	year = {2024},
	eissn = {2509-2723},
	pages = {191-218},
	orcid-numbers = {Ungvári, Zoltán István/0000-0002-6035-6039; Tabák, Ádám/0000-0002-6234-3936; Purebl, György/0000-0002-9750-2001; Fazekas-Pongor, Vince/0000-0002-6405-4003; Szarvas, Zsófia/0000-0002-0022-5053; Mukli, Péter/0000-0003-4355-8103; Balog, Piroska/0000-0001-5025-8649; Bódizs, Róbert/0000-0001-5341-060X; Ujma, Przemyslaw Péter/0000-0002-7981-3009; Stauder, Adrienne/0000-0002-0358-3657; Kovács, Illés/0000-0001-5763-0482; Vokó, Zoltán/0000-0002-1004-1848; Takács, István/0000-0002-7810-4833; Vásárhelyi, Barna/0000-0003-0055-7346; Torzsa, Péter/0000-0002-8148-4961; Ferdinandy, Péter/0000-0002-6424-6806; Benyó, Zoltán/0000-0001-6015-0359; Szabó, Attila/0000-0001-7321-9861; Bednárikné Dörnyei, Gabriella/0000-0001-7007-6252; Kellermayer, Miklós/0000-0002-5553-6553; Merkely, Béla Péter/0000-0001-6514-0723}
}