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1.

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
Internet cím:DOI
Intézményi repozitóriumban (DEA) tárolt változat
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2.

001-es BibID:BIBFORM082128
035-os BibID:(WOS)000494370900001 (Scopus)85074926339
Első szerző:Fülöp Gábor Áron (általános orvos)
Cím:Cerebral venous congestion promotes blood-brain barrier disruption and neuroinflammation, impairing cognitive function in mice / Gabor A. Fulop, Chetan Ahire, Tamas Csipo, Stefano Tarantini, Tamas Kiss, Priya Balasubramanian, Andriy Yabluchanskiy, Eszter Farkas, Attila Toth, Ádám Nyúl-Tóth, Peter Toth, Anna Csiszar, Zoltan Ungvari
Dátum:2019
ISSN:2509-2715 2509-2723
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:GeroScience. - 41 : 5 (2019), p. 575-589. -
További szerzők:Ahire, Chetan Csípő Tamás (1990-) Tarantini, Stefano Kiss Tamás Balasubramanian, Priya Yabluchanskiy, Andriy Farkas Eszter Tóth Attila (1971-) (biológus) Nyúl-Tóth Ádám Tóth Péter Csiszár Anna Ungvári Zoltán
Pályázati támogatás:EFOP-3.6.1-16-2016-00008, 20765-3/2018/FEKUTSTRAT
EFOP
EFOP-3.6.2.-16-2017-00008
EFOP
GINOP-2.3.2-15-2016-00048
GINOP
GINOP-2.3.3-15-2016-00032
GINOP
NKFI-FK123798
NKFIH
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Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM076738
035-os BibID:(WOS)000453351000007 (Scopus)85057166811
Első szerző:Fülöp Gábor Áron (általános orvos)
Cím:Nrf2 deficiency in aged mice exacerbates cellular senescence promoting cerebrovascular inflammation / Gabor A. Fulop, Tamas Kiss, Stefano Tarantini, Priya Balasubramanian, Andriy Yabluchanskiy, Eszter Farkas, Ferenc Bari, Zoltan Ungvari, Anna Csiszar
Dátum:2018
ISSN:2509-2715 2509-2723
Megjegyzések:Aging-induced pro-inflammatory phenotypic alterations of the cerebral vasculature critically contribute to the pathogenesis of vascular cognitive impairment. Cellular senescence is a fundamental aging process that promotes inflammation; however, its role in cerebrovascular aging remains unexplored. The present study was undertaken to test the hypothesis that advanced aging promotes cellular senescence in the cerebral vasculature. We found that in cerebral arteries of 24-month-old mice, expression of molecular markers of senescence (p16INK4a, p21) is upregulated as compared to that in young controls. Induction of senescence programs in cerebral arteries is associated by an upregulation of a wide range of inflammatory cytokines and chemokines, which are known to contribute to the senescence-associated secretory phenotype (SASP) in vascular cells. Age-related cerebrovascular senescence and inflammation are associated with neuroinflammation, as shown by the molecular footprint of microglia activation in the hippocampus. Genetic depletion of the pro-survival/anti-aging transcriptional regulator Nrf2 exacerbated age-related induction of senescence markers and inflammatory SASP factors and resulted in a heightened inflammatory status of the hippocampus. In conclusion, our studies provide evidence that aging and Nrf2 dysfunction promote cellular senescence in cerebral vessels, which may potentially cause or exacerbate age-related pathology.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Endothelial dysfunction
Senescence
VCID
Vascular aging
Vascular cognitive impairment
Megjelenés:GeroScience. - 40 : 5-6 (2018), p. 513-521. -
További szerzők:Kiss Tamás Tarantini, Stefano Balasubramanian, Priya Yabluchanskiy, Andriy Farkas Eszter Bari Ferenc Ungvári Zoltán Csiszár Anna
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Intézményi repozitóriumban (DEA) tárolt változat
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4.

001-es BibID:BIBFORM099949
035-os BibID:(WOS)000433040100011 (Scopus)85042217471
Első szerző:Tarantini, Stefano
Cím:Correction to : pharmacologically induced impairment of neurovascular coupling responses alters gait coordination in mice / Tarantini Stefano, Yabluchanskiy Andriy, Fülöp Gábor A., Hertelendy Peter, Noa Valcarcel-Ares M., Kiss Tamas, Bagwell Jonathan M., O'Connor Daniel, Farkas Eszter, Sorond Farzaneh, Csiszar Anna, Ungvari Zoltan
Dátum:2018
ISSN:2509-2715 2509-2723
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:GeroScience. - 40 : 2 (2018), p. 219-219. -
További szerzők:Yabluchanskiy, Andriy Fülöp Gábor Áron (1988-) (általános orvos) Hertelendy Péter Valcarcel Ares, Marta Noa Kiss Tamás (1950-) (vegyész) Bagwell, Jonathan M. O'Connor, Daniel Farkas Eszter Sorond, Farzaneh A. Csiszár Anna Ungvári Zoltán
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Intézményi repozitóriumban (DEA) tárolt változat
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5.

001-es BibID:BIBFORM085462
035-os BibID:(WOS)000418822500008 (Scopus)85038095208
Első szerző:Tarantini, Stefano
Cím:Pharmacologically induced impairment of neurovascular coupling responses alters gait coordination in mice / Tarantini Stefano, Yabluchanksiy Andriy, Fülöp Gábor A., Hertelendy Peter, Valcarcel-Ares M. Noa, Kiss Tamas, Bagwell Jonathan M., O'Connor Daniel. Farkas Eszter, Sorond Farzaneh, Csiszar Anna, Ungvari Zoltan
Dátum:2017
ISSN:2509-2715 2509-2723
Megjegyzések:There is correlative evidence that impaired cerebral blood flow (CBF) regulation, in addition to promoting cognitive impairment, is also associated with alterations in gait and development of falls in elderly people. CBF is adjusted to neuronal activity via neurovascular coupling (NVC) and this mechanism becomes progressively impaired with age. To establish a direct cause-andeffect relationship between impaired NVC and gait abnormalities, we induced neurovascular uncoupling pharmacologically in young C57BL/6 mice by inhibiting the synthesis of vasodilator mediators involved in NVC. Treatment of mice with the epoxygenase inhibitor MSPPOH, the NO synthase inhibitor L-NAME, and the COX inhibitor indomethacin significantly decreased NVC mimicking the aging phenotype. Pharmacologically induced neurovascular uncoupling significantly decreased the dynamic gait parameter duty cycle, altered footfall patterns, and significantly increased phase dispersion, indicating impaired interlimb coordination. Impaired NVC also tended to increase gait variability. Thus, selective experimental disruption of NVC causes subclinical gait abnormalities, supporting the importance of CBF in both cognitive function and gait regulation.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Neurovascular coupling
Gait
Catwalk
Neurovascular uncoupling
Megjelenés:GeroScience. - 39 : 5-6 (2017), p. 601-614. -
További szerzők:Yabluchanskiy, Andriy Fülöp Gábor Áron (1988-) (általános orvos) Hertelendy Péter Valcarcel Ares, Marta Noa Kiss Tamás Bagwell, Jonathan M. O'Connor, Daniel Farkas Eszter Sorond, Farzaneh A. Csiszár Anna Ungvári Zoltán
Pályázati támogatás:EFOP-3.6.1-16-2016-00008
EFOP
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DOI
Intézményi repozitóriumban (DEA) tárolt változat
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6.

001-es BibID:BIBFORM085460
035-os BibID:(WOS)000412737500010 (Scopus)85020091346
Első szerző:Tarantini, Stefano
Cím:Demonstration of impaired neurovascular coupling responses in TG2576 mouse model of Alzheimer's disease using functional laser speckle contrast imaging / Tarantini Stefano, Fulop Gabor A., Kiss Tamas, Farkas Eszter, Zölei-Szénási Dániel, Galvan Veronica, Toth Peter, Csiszar Anna, Ungvari Zoltan, Yabluchanskiy Andriy
Dátum:2017
ISSN:2509-2715 2509-2723
Megjegyzések:Increasing evidence from epidemiological, clinical, and experimental studies indicates that cerebromicrovascular dysfunction and microcirculatory damage play critical roles in the pathogenesis of many types of dementia in the elderly, including both vascular cognitive impairment (VCI) and Alzheimer's disease. Vascular contributions to cognitive impairment and dementia (VCID) include impairment of neurovascular coupling responses/functional hyperemia (Bneurovascular uncoupling^). Due to the growing interest in understanding and pharmacologically targeting pathophysiological mechanisms of VCID, there is an increasing need for sensitive, easy-to-establish methods to assess neurovascular coupling responses. Laser speckle contrast imaging (LSCI) is a technique that allows rapid and minimally invasive visualization of changes in regional cerebromicrovascular blood perfusion. This type of imaging technique combines high resolution and speed to provide great spatiotemporal accuracy to measure moment-to-moment changes in cerebral blood flow induced by neuronal activation. Here, we provide detailed protocols for the successful measurement in neurovascular coupling responses in anesthetized mice equipped with a thinned-skull cranial window using LSCI. This method can be used to evaluate the effects of anti-aging or anti-AD treatments on cerebromicrovascular health.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Neurovascular coupling
Functional hyperemia
Laser speckle contrast imaging
Laser speckle contrast analysis
LASCA
Laser speckle imaging
LSI
Megjelenés:GeroScience. - 39 : 4 (2017), p. 465-473. -
További szerzők:Fülöp Gábor Áron (1988-) (általános orvos) Kiss Tamás Farkas Eszter Zölei-Szénási Dániel Galvan, Veronica Tóth Péter (sebész) Csiszár Anna Ungvári Zoltán Yabluchanskiy, Andriy
Pályázati támogatás:K111923
OTKA
EFOP-3.6.1-16- 2016-00008
EFOP
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Intézményi repozitóriumban (DEA) tárolt változat
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7.

001-es BibID:BIBFORM082129
035-os BibID:(WOS)000493693900001 (Scopus)85074812973
Első szerző:Tarantini, Stefano
Cím:Treatment with the poly(ADP-ribose) polymerase inhibitor PJ-34 improves cerebromicrovascular endothelial function, neurovascular coupling responses and cognitive performance in aged mice, supporting the NAD+ depletion hypothesis of neurovascular aging / Tarantini Stefano, Yabluchanskiy Andriy, Csipo Tamas, Fulop Gabor, Kiss Tamas, Balasubramanian Priya, DelFavero Jordan, Ahire Chetan, Ungvari Anna, Nyúl-Tóth Ádám, Farkas Eszter, Benyo Zoltan, Tóth Attila, Csiszar Anna, Ungvari Zoltan
Dátum:2019
ISSN:2509-2715 2509-2723
Megjegyzések:Adjustment of cerebral blood flow (CBF) to neuronal activity via neurovascular coupling (NVC) plays an important role in the maintenance of healthy cognitive function. Strong evidence demonstrates that age-related cerebromicrovascular endothelial dysfunction and consequential impairment of NVC responses contribute importantly to cognitive decline. Recent studies demonstrate that NAD(+) availability decreases with age in the vasculature and that supplemental NAD(+) precursors can ameliorate cerebrovascular dysfunction, rescuing NVC responses and improving cognitive performance in aged mice. The mechanisms underlying the age-related decline in [NAD(+)] in cells of the neurovascular unit are likely multifaceted and may include increased utilization of NAD(+) by activated poly (ADP-ribose) polymerase (PARP-1). The present study was designed to test the hypothesis that inhibition of PARP-1 activity may confer protective effects on neurovascular function in aging, similar to the recently demonstrated protective effects of treatment with the NAD+ precursor nicotinamide mononucleotide (NMN). To test this hypothesis, 24-month-old C57BL/6 mice were treated with PJ-34, a potent PARP inhibitor, for 2 weeks. NVC was assessed by measuring CBF responses (laser speckle contrast imaging) in the somatosensory whisker barrel cortex evoked by contralateral whisker stimulation. We found that NVC responses were significantly impaired in aged mice. Treatment with PJ-34 improved NVC responses by increasing endothelial NO-mediated vasodilation, which was associated with significantly improved spatial working memory. PJ-34 treatment also improved endothelium-dependent acetylcholine-induced relaxation of aorta rings. Thus, PARP-1 activation, likely by decreasing NAD(+) availability, contributes to age-related endothelial dysfunction and neurovascular uncoupling, exacerbating cognitive decline. The cerebromicrovascular protective effects of pharmacological inhibition of PARP-1 highlight the preventive and therapeutic potential of treatments that restore NAD+ homeostasis as effective interventions in patients at risk for vascular cognitive impairment (VCI).
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Cellular energetics
Oxidative stress
ROS
Endothelial dysfunction
Functional hyperemia
Microcirculation
Senescence
Megjelenés:GeroScience. - 41 : 5 (2019), p. 533-542. -
További szerzők:Yabluchanskiy, Andriy Csípő Tamás (1990-) Fülöp Gábor Áron (1988-) (általános orvos) Kiss Tamás Balasubramanian, Priya DelFavero, Jordan Ahire, Chetan Ungvári Anna Nyúl-Tóth Ádám Farkas Eszter Benyó Zoltán Tóth Attila (1971-) (biológus) Csiszár Anna Ungvári Zoltán
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Intézményi repozitóriumban (DEA) tárolt változat
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8.

001-es BibID:BIBFORM076739
035-os BibID:(cikkazonosító)e12731 (WoS)000427234300020 (Scopus)85041585148
Első szerző:Tarantini, Stefano
Cím:Treatment with the mitochondrial-targeted antioxidant peptide SS-31 rescues neurovascular coupling responses and cerebrovascular endothelial function and improves cognition in aged mice / Stefano Tarantini, Noa M. Valcarcel-Ares, Andriy Yabluchanskiy, Gabor A. Fulop, Peter Hertelendy, Tripti Gautam, Eszter Farkas, Aleksandra Perz, Peter S. Rabinovitch, William E. Sonntag, Anna Csiszar, Zoltan Ungvari
Dátum:2018
ISSN:1474-9718
Megjegyzések: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. This study was designed to test the hypothesis that attenuation of mitochondrial oxidative stress may exert beneficial effects on neurovascular coupling responses in aging. To test this hypothesis, 24-month-old C57BL/6 mice were treated with a cell-permeable, mitochondria-targeted antioxidant peptide (SS-31; 10 mg kg-1 day-1 , i.p.) or vehicle for 2 weeks. Neurovascular coupling was assessed by measuring CBF responses (laser speckle contrast imaging) evoked by contralateral whisker stimulation. We found that neurovascular coupling responses were significantly impaired in aged mice. Treatment with SS-31 significantly improved neurovascular coupling responses by increasing NO-mediated cerebromicrovascular dilation, which was associated with significantly improved spatial working memory, motor skill learning, and gait coordination. These findings are paralleled by the protective effects of SS-31 on mitochondrial production of reactive oxygen species and mitochondrial respiration in cultured cerebromicrovascular endothelial cells derived from aged animals. Thus, mitochondrial oxidative stress contributes to age-related cerebromicrovascular dysfunction, exacerbating cognitive decline. We propose that mitochondria-targeted antioxidants may be considered for pharmacological microvascular protection for the prevention/treatment of age-related vascular cognitive impairment (VCI).
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
aging
cerebral circulation
endothelial dysfunction
oxidative stress
vascular cognitive impairment
Megjelenés:Aging Cell. - 17 : 2 (2018), p. 1-12. -
További szerzők:Valcarcel Ares, Marta Noa Yabluchanskiy, Andriy Fülöp Gábor Áron (1988-) (általános orvos) Hertelendy Péter Gautam, Tripti Farkas Eszter Perz, Aleksandra Rabinovitch, Peter S. Sonntag, William E. Csiszár Anna Ungvári Zoltán
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Intézményi repozitóriumban (DEA) tárolt változat
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9.

001-es BibID:BIBFORM085446
035-os BibID:(WOS)000401331200004 (Scopus)85017238534
Első szerző:Ungvári Zoltán
Cím:Cerebromicrovascular dysfunction predicts cognitive decline and gait abnormalities in a mouse model of whole brain irradiation-induced accelerated brain senescence / Ungvari Zoltan, Tarantini Stefano, Hertelendy Peter, Valcarcel-Ares M. Noa, Fülöp Gabor A., Logan Sreemathi, Kiss Tamas, Farkas Eszter, Csiszar Anna, Yabluchanskiy Andriy
Dátum:2017
ISSN:2509-2715 2509-2723
Megjegyzések:Whole brain irradiation (WBI) is a mainstream therapy for patients with both identifiable brain metastases and prophylaxis for microscopic malignancies. However, it also promotes accelerated senescence in healthy tissues and leads to progressive cognitive dysfunction in up to 50% of tumor patients surviving long term after treatment, due to ?-irradiation-induced cerebromicrovascular injury. Moment-to-moment adjustment of cerebral blood flow (CBF) via neuronal activity-dependent cerebromicrovascular dilation (functional hyperemia) has a critical role in maintenance of healthy cognitive function. To determine whether cognitive decline induced by WBI associates with impaired cerebromicrovascular function, C56BL/6 mice (3 months) subjected to a clinically relevant protocol of fractionated WBI (5 Gy twice weekly for 4 weeks) and control mice were compared. Mice were tested for spatial memory performance (radial arm water maze), sensorimotor coordination (computerized gait analysis, CatWalk), and cerebromicrovascular function (whisker-stimulation-induced increases in CBF, measured by laser Doppler flowmetry) at 3 to 6 months post-irradiation. We found that mice with WBI exhibited impaired cerebromicrovascular function at 3 months post-irradiation, which was associated with impaired performance in the radial arm water maze. At 6 months, post-irradiation progressive impairment in gait coordination (including changes in the regularity index and phase dispersion) was also evident. Collectively, our findings provide evidence for early and persisting neurovascular impairment after a clinically relevant protocol of fractionated WBI, which predict early manifestations of cognitive impairment.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Whole brain irradiation
Neurovascular coupling
Functional hyperemia
Dementia
Gait dysfunction
Neurovascular unit
Cellular senescence
DNA damage
Megjelenés:GeroScience. - 39 : 1 (2017), p. 33-42. -
További szerzők:Tarantini, Stefano Hertelendy Péter Valcarcel Ares, Marta Noa Fülöp Gábor Áron (1988-) (általános orvos) Logan, Sreemathi Kiss Tamás Farkas Eszter Csiszár Anna Yabluchanskiy, Andriy
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DOI
Intézményi repozitóriumban (DEA) tárolt változat
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