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001-es BibID:BIBFORM099943
035-os BibID:(WOS)000469877700003 (Scopus)85066471327
Első szerző:Csípő Tamás
Cím:Age-related decline in peripheral vascular health predicts cognitive impairment / Csipo Tamas, Lipecz Agnes, Fulop Gabor A., Hand Rachel A., Ngo Bich-Thy N., Dzialendzik Mikita, Tarantini Stefano, Balasubramanian Priya, Kiss Tamas, Yabluchanska Valeriya, Silva-Palacios Federico, Courtney Donald L., Dasari Tarun W., Sorond Farzaneh, Sonntag William E., Csiszar Anna, Ungvari Zoltan, Yabluchanskiy Andriy
Dátum:2019
ISSN:2509-2715 2509-2723
Megjegyzések:Preclinical studies demonstrate that generalized endothelial cell dysfunction and microvascular impairment are potentially reversible causes of age-related vascular cognitive impairment and dementia (VCID). The present study was designed to test the hypothesis that severity of age-related macro- and microvascular dysfunction measured in the peripheral circulation is an independent predictor of cognitive performance in older adults. In this study, we enrolled 63 healthy individuals into young (< 45 years old) and aged (> 65 years old) groups. We used principal component analysis (PCA) to construct a comprehensive peripheral vascular health index (VHI) encompassing peripheral microvascular reactivity, arterial endothelial function, and vascular stiffness, as a marker of aging-induced generalized vascular dysfunction. Peripheral macrovascular and microvascular endothelial function were assessed using flow-mediated dilation (FMD) and laser speckle contrast imaging tests. Pulse waveform analysis was used to evaluate the augmentation index (AIx), a measure of arterial stiffness. Cognitive function was measured using a panel of CANTAB cognitive tests, and PCA was then applied to generate a cognitive impairment index (CII) for each participant. Aged subjects exhibited significantly impaired macrovascular endothelial function (FMD, 5.6 ? 0.7% vs. 8.3 ? 0.6% in young, p = 0.0061), increased arterial stiffness (AIx 29.3 ? 1.8% vs 4.5 ? 2.6% in young, p < 0.0001), and microvascular dysfunction (2.8 ? 0.2 vs 3.4 ? 0.1-fold change of perfusion in young, p = 0.032). VHI showed a significant negative correlation with age (r = - 0.54, p < 0.0001) and CII significantly correlated with age (r = 0.79, p < 0.0001). VHI significantly correlated with the CII (r = - 0.46, p = 0.0003). A decline in peripheral vascular health may reflect generalized vascular dysfunction and predict cognitive impairment in older adults.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Aging
Endothelial function
Cognitive impairment
Microvascular dysfunction
VCID
Megjelenés:GeroScience. - 41 : 2 (2019), p. 125-136. -
További szerzők:Lipécz Ágnes Fülöp Gábor Áron (1988-) (általános orvos) Hand, Rachel A. Ngo, Bich-Thy N. Dzialendzik, Mikita Tarantini, Stefano Balasubramanian, Priya Kiss Tamás (1950-) (vegyész) Yabluchanska, Valeriya Silva-Palacios, Federico Courtney, Donald L. Dasari, Tarun W. Sorond, Farzaneh A. Sonntag, William E. Csiszár Anna Ungvári Zoltán Yabluchanskiy, Andriy
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2.

001-es BibID:BIBFORM076737
035-os BibID:(WOS)000440106900010 (Scopus)85048661448
Első szerző:Csípő Tamás
Cím:Short-term weight loss reverses obesity-induced microvascular endothelial dysfunction / Tamas Csipo, Gabor A. Fulop, Agnes Lipecz, Stefano Tarantini, Tamas Kiss, Priya Balasubramanian, Anna Csiszar, Zoltan Ungvari, Andriy Yabluchanskiy
Dátum:2018
ISSN:2509-2715 2509-2723
Megjegyzések:Obesity is one of the major risk factors for cardiovascular diseases and its prevalence is increasing in all age groups, with the biggest impact observed in middle-aged and older adults. A critical mechanism by which obesity promotes vascular pathologies in these patients involves impairment of endothelial function. While endothelial dysfunction in large vessels promotes atherogenesis, obesity-induced microvascular endothelial dysfunction impairs organ perfusion and thereby is causally related to the pathogenesis of ischemic heart disease, chronic kidney disease, intermittent claudication, exercise intolerance, and exacerbates cognitive decline in aging. Reduction of weight via calorie-based diet and exercise in animal models of obesity results in significant improvement of endothelial function both in large vessels and in the microcirculation, primarily due to attenuation of oxidative stress and inflammation. Clinical data on the protective effects of weight loss on endothelial function is limited to studies of flow-mediated dilation assessed in brachial arteries. Currently, there is no guideline on testing the effects of different weight management strategies on microvascular endothelial function in obese patients. Here, we provide proof-of-concept that weight loss-induced improvement of microvascular endothelial function can be reliably assessed in the setting of a geriatric outpatient clinic using a fast, reproducible, non-invasive method: laser speckle contrast imaging-based measurement of endothelium-dependent microvascular responses during post-occlusive reactive hyperemia tests. Our study also provides initial evidence that short-term weight loss induced by consumption of a low-carbohydrate low-calorie diet can reverse microvascular endothelial dysfunction associated with obesity.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Weight loss
Obesity
Endothelial function
Aging
Megjelenés:GeroScience. - 40 : 3 (2018), p. 337-346. -
További szerzők:Fülöp Gábor Áron (1988-) (általános orvos) Lipécz Ágnes Tarantini, Stefano Kiss Tamás Balasubramanian, Priya Csiszár Anna Ungvári Zoltán Yabluchanskiy, Andriy
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3.

001-es BibID:BIBFORM108985
035-os BibID:(scopus)85065594719 (wos)000467562000011
Első szerző:Fülöp Gábor Áron (általános orvos)
Cím:Role of age-related alterations of the cerebral venous circulation in the pathogenesis of vascular cognitive impairment / Fulop Gabor A., Tarantini Stefano, Yabluchanskiy Andriy, Molnar Andrea, Prodan Calin I., Kiss Tamas, Csipo Tamas, Lipecz Agnes, Balasubramanian Priya, Farkas Eszter, Toth Peter, Sorond Farzaneh, Csiszar Anna, Ungvari Zoltan
Dátum:2019
ISSN:0363-6135
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:American Journal Of Physiology-Heart And Circulatory Physiology. - 316 : 5 (2019), p. H1124-H1140. -
További szerzők:Tarantini, Stefano Yabluchanskiy, Andriy Molnár Andrea (Budapest) Prodan, Calin I. Kiss Tamás Csípő Tamás (1990-) Lipécz Ágnes Balasubramanian, Priya Farkas Eszter Tóth Péter Sorond, Farzaneh A. Csiszár Anna Ungvári Zoltán
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4.

001-es BibID:BIBFORM099928
035-os BibID:(WOS)000516499100001 (Scopus)85078289607
Első szerző:Yabluchanskiy, Andriy
Cím:Pharmacological or genetic depletion of senescent astrocytes prevents whole brain irradiation-induced impairment of neurovascular coupling responses protecting cognitive function in mice / Yabluchanskiy Andriy, Tarantini Stefano, Balasubramanian Priya, Kiss Tamas, Csipo Tamas, Fülöp Gábor A., Lipecz Agnes, Ahire Chetan, DelFavero Jordan, Nyul-Toth Adam, Sonntag William E., Schwartzman Michal L., Campisi Judith, Csiszar Anna, Ungvari Zoltan
Dátum:2020
ISSN:2509-2715 2509-2723
Megjegyzések:Whole brain irradiation (WBI, also known as whole brain radiation therapy or WBRT) is a mainstream therapy for patients with identifiable brain metastases and as a prophylaxis for microscopic malignancies. WBI accelerates brain aging, causing progressive cognitive dysfunction in ~ 50% of surviving patients, thus compromising quality of life. The mechanisms responsible for this WBI side effect remain obscure, and there are no effective treatments or prevention strategies. Here, we test the hypothesis that WBI induces astrocyte senescence, which contributes to impaired astrocytic neurovascular coupling (NVC) responses and the genesis of cognitive decline. To achieve this goal, we used transgenic p16-3MR mice, which allows the detection and selective elimination of senescent cells. We subjected these mice to a clinically relevant protocol of fractionated WBI (5 Gy twice weekly for 4 weeks). WBI-treated and control mice were tested for spatial memory performance (radial arm water maze), astrocyte-dependent NVC responses (whisker-stimulation-induced increases in cerebral blood flow, assessed by laser speckle contrast imaging), NVC-related gene expression, astrocytic release of eicosanoid gliotransmitters and the presence of senescent astrocytes (by flow cytometry, immunohistochemistry and gene expression profiling) at 6 months post-irradiation. WBI induced senescence in astrocytes, which associated with NVC dysfunction and impaired performance on cognitive tasks. To establish a causal relationship between WBI-induced senescence and NVC dysfunction, senescent cells were depleted from WBI-treated animals (at 3 months post-WBI) by genetic (ganciclovir treatment) or pharmacological (treatment with the BCL-2/BCL-xL inhibitor ABT263/Navitoclax, a known senolytic drug) means. In WBI-treated mice, both treatments effectively eliminated senescent astrocytes, rescued NVC responses, and improved cognitive performance. Our findings suggest that the use of senolytic drugs can be a promising strategy for preventing the cognitive impairment associated with WBI.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Aging
Dementia
Functional hyperemia
Radiation
Senescence
Vascular cognitive impairment
WBI
WBRT
Whole brain radiation therapy
Megjelenés:GeroScience. - 42 : 2 (2020), p. 409-428. -
További szerzők:Tarantini, Stefano Balasubramanian, Priya Kiss Tamás (1950-) (vegyész) Csípő Tamás (1990-) Fülöp Gábor Áron (1988-) (általános orvos) Lipécz Ágnes Ahire, Chetan DelFavero, Jordan Nyúl-Tóth Ádám Sonntag, William E. Schwartzman, Michal L. Campisi, Judith Csiszár Anna Ungvári Zoltán
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