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1.
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
Internet cím:
Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Saját polcon:
2.
001-es BibID:
BIBFORM085246
Első szerző:
Tarantini, Stefano
Cím:
Insulin-like growth factor 1 deficiency exacerbates hypertension-induced cerebral microhemorrhages in mice, mimicking the aging phenotype / Tarantini Stefano, Valcarcel-Ares Noa M., Yabluchanskiy Andriy, Springo Zsolt, Fulop Gabor A., Ashpole Nicole, Gautam Tripti, Giles Cory B., Wren Jonathan D., Sonntag William E., Csiszar Anna, Ungvari Zoltan
Dátum:
2017
ISSN:
1474-9718 1474-9726
Megjegyzések:
Clinical and experimental studies show that aging exacerbates hypertension-induced cerebral microhemorrhages (CMHs), which progressively impair neuronal function. There is growing evidence that aging promotes insulin-like growth factor 1 (IGF-1) deficiency, which compromises multiple aspects of cerebromicrovascular and brain health. To determine the role of IGF-1 deficiency in the pathogenesis of CMHs, we induced hypertension in mice with liver-specific knockdown of IGF-1 (Igf1f/f + TBGCre-AAV8) and control mice by angiotensin II plus L-NAME treatment. In IGF-1-deficient mice, the same level of hypertension led to significantly earlier onset and increased incidence and neurological consequences of CMHs, as compared to control mice, as shown by neurological examination, gait analysis, and histological assessment of CMHs in serial brain sections. Previous studies showed that in aging, increased oxidative stressmediated matrix metalloprotease (MMP) activation importantly contributes to the pathogenesis of CMHs. Thus, it is significant that hypertension-induced cerebrovascular oxidative stress and MMP activation were increased in IGF-1-deficient mice. We found that IGF-1 deficiency impaired hypertension-induced adaptive media hypertrophy and extracellular matrix remodeling, which together with the increased MMP activation likely also contributes to increased fragility of intracerebral arterioles. Collectively, IGF-1 deficiency promotes the pathogenesis of CMHs, mimicking the aging phenotype, which likely contribute to its deleterious effect on cognitive function. Therapeutic strategies that upregulate IGF-1 signaling in the cerebral vessels and/or reduce microvascular oxidative stress, and MMP activation may be useful for the prevention of CMHs, protecting cognitive function in high-risk elderly patients.
Tárgyszavak:
Orvostudományok
Elméleti orvostudományok
idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
arteriole
dementia
gait dysfunction
microbleed
oxidative stress
Megjelenés:
Aging Cell. - 16 : 3 (2017), p. 469-479. -
További szerzők:
Valcarcel Ares, Marta Noa
Yabluchanskiy, Andriy
Springó Zsolt
Fülöp Gábor Áron (1988-) (általános orvos)
Ashpole, Nicole
Gautam, Tripti
Giles, Cory B.
Wren, Jonathan D.
Sonntag, William E.
Csiszár Anna
Ungvári Zoltán
Internet cím:
Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Saját polcon:
3.
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
Internet cím:
Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Saját polcon:
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
Internet cím:
Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Saját polcon:
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