@article{MTMT:34796626,
	title = {Farmer involvement in agro-ecological research: organic on-farm wheat variety trials in Hungary and the Slovakian upland},
	url = {https://m2.mtmt.hu/api/publication/34796626},
	author = {Földi, Mihály and Bencze, Szilvia and Hertelendy, Péter and Veszter, Sara and Kovacs, Tina and Drexler, Dóra},
	doi = {10.1007/s13165-020-00335-x},
	journal-iso = {ORGANIC AGRICULTURE},
	journal = {ORGANIC AGRICULTURE},
	volume = {12},
	unique-id = {34796626},
	issn = {1879-4238},
	abstract = {The acreage of organic farming is constantly increasing in Hungary. The cultivation of cereals-and within it-the production of winter wheat is of main importance in organic field crop production. Besides the challenges of global climate change, various difficulties are known, such as the inadequate variety assortment, lack of knowledge on the performance of varieties under organic conditions and often low quality of the seeds sown. As official post-registration variety trials only exist under conventional farming conditions in Hungary, the Hungarian Research Institute of Organic Agriculture (oMKi) started participatory organic on-farm variety tests in 2012, with the involvement of volunteer farmers all over the country. Over the past 7 years, nearly 60 wheat varieties and more than 20 farms have been included in the tests. The aim of the study was to find the most suitable varieties for high-quality organic wheat production and exclude inappropriate varieties for respective production regions. Results demonstrated that there is great potential in choosing varieties best suited to regional environmental conditions and that it is possible to achieve both high yield and excellent quality also in organic farming when adopting the appropriate varieties. The use of varieties, which were proven to be disease tolerant or resistant, can significantly contribute to safer organic production. The comparisons between the performance of varieties indicated that organic breeding has a great role in all of the above matters.},
	keywords = {Winter wheat; organic farming; Agriculture, Multidisciplinary; Participatory research; On-farm; Organic variety tests},
	year = {2022},
	eissn = {1879-4246},
	pages = {293-305}
}

@mastersthesis{MTMT:31267847,
	title = {The impact of age on the elicitation of spreading depolarization and the implication of prostanoids in the associated cerebral blood flow response Hertelendy Péter},
	url = {https://m2.mtmt.hu/api/publication/31267847},
	author = {Hertelendy, Péter},
	doi = {10.14232/phd.10277},
	publisher = {SZTE},
	unique-id = {31267847},
	year = {2019}
}

@article{MTMT:30646506,
	title = {Nicotinamide mononucleotide (NMN) supplementation rescues cerebromicrovascular endothelial function and neurovascular coupling responses and improves cognitive function in aged mice},
	url = {https://m2.mtmt.hu/api/publication/30646506},
	author = {Tarantini, Stefano and Valcarcel-Ares, Marta Noa and Tóth, Péter József and Yabluchanskiy, Andriy and Tucsek, Zsuzsanna and Kiss, Tamás and Hertelendy, Péter and Kinter, Michael and Ballabh, Praveen and Süle, Zoltán and Farkas, Eszter and Baur, Joseph A and Sinclair, David A and Csiszar, Anna and Ungvári, Zoltán István},
	doi = {10.1016/j.redox.2019.101192},
	journal-iso = {REDOX BIOL},
	journal = {REDOX BIOLOGY},
	volume = {24},
	unique-id = {30646506},
	issn = {2213-2317},
	abstract = {Adjustment of cerebral blood flow (CBF) to neuronal activity via neurovascular coupling (NVC) has an essential role in maintenance of healthy cognitive function. In aging increased oxidative stress and cerebromicrovascular endothelial dysfunction impair NVC, contributing to cognitive decline. There is increasing evidence showing that a decrease in NAD+ availability with age plays a critical role in a range of age-related cellular impairments but its role in impaired NVC responses remains unexplored. The present study was designed to test the hypothesis that restoring NAD+ concentration may exert beneficial effects on NVC responses in aging. To test this hypothesis 24-month-old C57BL/6 mice were treated with nicotinamide mononucleotide (NMN), a key NAD+ intermediate, for 2 weeks. NVC was assessed by measuring CBF responses (laser Doppler flowmetry) evoked by contralateral whisker stimulation. We found that NVC responses were significantly impaired in aged mice. NMN supplementation rescued NVC responses by increasing endothelial NO-mediated vasodilation, which was associated with significantly improved spatial working memory and gait coordination. These findings are paralleled by the sirtuin-dependent protective effects of NMN on mitochondrial production of reactive oxygen species and mitochondrial bioenergetics in cultured cerebromicrovascular endothelial cells derived from aged animals. Thus, a decrease in NAD+ availability contributes to age-related cerebromicrovascular dysfunction, exacerbating cognitive decline. The cerebromicrovascular protective effects of NMN highlight the preventive and therapeutic potential of NAD+ intermediates as effective interventions in patients at risk for vascular cognitive impairment (VCI).},
	keywords = {MICROCIRCULATION; endothelial dysfunction; ROS; Functional hyperemia; Oxidative stress},
	year = {2019},
	eissn = {2213-2317},
	orcid-numbers = {Tarantini, Stefano/0000-0001-5627-1430; Kiss, Tamás/0000-0001-5339-5227; Süle, Zoltán/0000-0003-1304-0207; Farkas, Eszter/0000-0002-8478-9664; Ungvári, Zoltán István/0000-0002-6035-6039}
}

@article{MTMT:30345331,
	title = {Susceptibility of the cerebral cortex to spreading depolarization in neurological disease states: The impact of aging},
	url = {https://m2.mtmt.hu/api/publication/30345331},
	author = {Hertelendy, Péter and Varga, Dániel Péter and Menyhárt, Ákos and Bari, Ferenc and Farkas, Eszter},
	doi = {10.1016/j.neuint.2018.10.010},
	journal-iso = {NEUROCHEM INT},
	journal = {NEUROCHEMISTRY INTERNATIONAL},
	volume = {127},
	unique-id = {30345331},
	issn = {0197-0186},
	year = {2019},
	eissn = {1872-9754},
	pages = {125-136},
	orcid-numbers = {Varga, Dániel Péter/0000-0001-5797-9334; Menyhárt, Ákos/0000-0002-1355-3208; Farkas, Eszter/0000-0002-8478-9664}
}

@article{MTMT:30461805,
	title = {Ischemic Stroke and Kynurenines: Medicinal Chemistry Aspects},
	url = {https://m2.mtmt.hu/api/publication/30461805},
	author = {Hertelendy, Péter and Toldi, József and Fülöp, Ferenc and Vécsei, László},
	doi = {10.2174/0929867325666180313113411},
	journal-iso = {CURR MED CHEM},
	journal = {CURRENT MEDICINAL CHEMISTRY},
	volume = {25},
	unique-id = {30461805},
	issn = {0929-8673},
	abstract = {Ischemic stroke is one of the leading causes of mortality and permanent disability in developed countries, Stroke induces massive glutamate release, which in turn causes N-Methyl-D-aspartate (NMDA) receptor over-excitation and thus, calcium overload in neurons leading to cell death via apoptotic cascades, The kynurenine pathway is a complex enzymatic cascade of tryptophan catabolism, generating various neuroactive metabolites. One metabolite, kynurenic acid (KYNA), is a potent endogenous NMDA glutamate receptor antagonist, making it a possible therapeutic tool to decrease excitotoxicity and neuroinflammation. Recently, clinical investigations have shown that during the acute phase of ischemic stroke, kynurenine pathway is activated and peripheral levels of metabolites correlated with worse outcome. In this review, we set out to summarize the current literature on the connection of the kynurenine pathway and ischemic stroke and set a course for future investigations and potential drug development.},
	keywords = {ISCHEMIA; CENTRAL-NERVOUS-SYSTEM; IMMUNOMODULATION; QUINOLINIC ACID; KYNURENINE; stroke; INDOLEAMINE 2,3-DIOXYGENASE; Cortical spreading depression; REGULATORY T-CELLS; PATHWAY METABOLISM; Biochemistry & Molecular Biology; Chemistry, Medicinal; GLOBAL CEREBRAL-ISCHEMIA; Kynurenine analogue; BRAIN-BARRIER BREAKDOWN; Oxidative stress},
	year = {2018},
	eissn = {1875-533X},
	pages = {5945-5957},
	orcid-numbers = {Toldi, József/0000-0001-7355-0503; Fülöp, Ferenc/0000-0003-1066-5287; Vécsei, László/0000-0001-8037-3672}
}

@article{MTMT:30452343,
	title = {Corretion to: Pharmacologically induced impairment of neurovascular coupling responses alters gait coordination in mice},
	url = {https://m2.mtmt.hu/api/publication/30452343},
	author = {Tarantini, Stefano and Yabluchanskiy, Andriy and Fülöp, Gábor Áron and Hertelendy, Péter and Valcarcel-Ares, M. Noa and Kiss, Tamás and Bagwell, Jonathan M. and O'Connor, Daniel and Farkas, Eszter and Sorond, Farzaneh and Csiszar, Anna and Ungvári, Zoltán István},
	doi = {10.1007/s11357-018-0012-4},
	journal-iso = {GEROSCIENCE},
	journal = {GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE)},
	volume = {40},
	unique-id = {30452343},
	issn = {2509-2715},
	year = {2018},
	eissn = {2509-2723},
	pages = {219-219},
	orcid-numbers = {Tarantini, Stefano/0000-0001-5627-1430; Yabluchanskiy, Andriy/0000-0002-9648-7161; Kiss, Tamás/0000-0001-5339-5227; Farkas, Eszter/0000-0002-8478-9664; Ungvári, Zoltán István/0000-0002-6035-6039}
}

@article{MTMT:30452341,
	title = {Pharmacologically-induced impairment of neurovascular coupling responses alters gait coordination in mice},
	url = {https://m2.mtmt.hu/api/publication/30452341},
	author = {Tarantini, Stefano and Yabluchanskiy, Andriy and Fulop, Gabor Aaron and Hertelendy, Péter and Valcarcel-Ares, Marta Noa and Kiss, Tamás and Bagwell, Jonathan M. and O'Connor, Daniel and Farkas, Eszter and Sorond, Farzaneh and Csiszar, Anna and Ungvári, Zoltán István},
	journal-iso = {FASEB J},
	journal = {FASEB JOURNAL},
	volume = {32},
	unique-id = {30452341},
	issn = {0892-6638},
	keywords = {Biology; Biochemistry & Molecular Biology},
	year = {2018},
	eissn = {1530-6860},
	pages = {711.9-711.9},
	orcid-numbers = {Tarantini, Stefano/0000-0001-5627-1430; Kiss, Tamás/0000-0001-5339-5227; Ungvári, Zoltán István/0000-0002-6035-6039}
}

@article{MTMT:3413924,
	title = {Nrf2 Deficiency Exacerbates Obesity-Induced Oxidative Stress, Neurovascular Dysfunction, Blood-Brain Barrier Disruption, Neuroinflammation, Amyloidogenic Gene Expression, and Cognitive Decline in Mice, Mimicking the Aging Phenotype},
	url = {https://m2.mtmt.hu/api/publication/3413924},
	author = {Tarantini, Stefano and Valcarcel-Ares, MN and Yabluchanskiy, A and Tucsek, Z and Hertelendy, Péter and Kiss, Tamás and Gautam, T and Zhang, XA and Sonntag, WE and de Cabo, R and Farkas, Eszter and Elliott, MH and Kinter, MT and Deak, F and Ungvári, Zoltán István and Csiszar, Anna},
	doi = {10.1093/gerona/glx177},
	journal-iso = {J GERONTOL A-BIOL MED SCI},
	journal = {JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES},
	volume = {73},
	unique-id = {3413924},
	issn = {1079-5006},
	abstract = {Obesity has deleterious effects on cognitive function in the elderly adults. In mice, aging exacerbates obesity-induced oxidative stress, microvascular dysfunction, blood-brain barrier (BBB) disruption, and neuroinflammation, which compromise cognitive health. However, the specific mechanisms through which aging and obesity interact to remain elusive. Previously, we have shown that Nrf2 signaling plays a critical role in microvascular resilience to obesity and that aging is associated with progressive Nrf2 dysfunction, promoting microvascular impairment. To test the hypothesis that Nrf2 deficiency exacerbates cerebromicrovascular dysfunction induced by obesity Nrf2(+/+) and Nrf2(-/-), mice were fed an adipogenic high-fat diet (HFD). Nrf2 deficiency significantly exacerbated HFD-induced oxidative stress and cellular senescence, impairment of neurovascular coupling responses, BBB disruption, and microglia activation, mimicking the aging phenotype. Obesity in Nrf2(-/-) mice elicited complex alterations in the amyloidogenic gene expression profile, including upregulation of amyloid precursor protein. Nrf2 deficiency and obesity additively reduced long-term potentiation in the CAI area of the hippocampus. Collectively, Nrf2 dysfunction exacerbates the deleterious effects of obesity, compromising cerebromicrovascular and brain health by impairing neurovascular coupling mechanisms, BBB integrity and synaptic function and promoting neuroinflammation. These results support a possible role for age-related Nrf2 dysfunction in the pathogenesis of vascular cognitive impairment and Alzheimer's disease.},
	keywords = {ALZHEIMERS-DISEASE; LONG-TERM POTENTIATION; high-fat diet; mouse somatosensory cortex; HIGH-FAT/SUCROSE DIET; Vascular cognitive impairment; Vascular cognitive impairment; Geriatrics & Gerontology; PRIMATE MACACA-MULATTA; AUTOREGULATORY DYSFUNCTION; RESVERATROL TREATMENT; CEREBROMICROVASCULAR ENDOTHELIAL-CELLS; Vascular contributions to cognitive impairment and dementia; ANTIOXIDANT RESPONSE},
	year = {2018},
	eissn = {1758-535X},
	pages = {853-863},
	orcid-numbers = {Tarantini, Stefano/0000-0001-5627-1430; Kiss, Tamás/0000-0001-5339-5227; Farkas, Eszter/0000-0002-8478-9664; Ungvári, Zoltán István/0000-0002-6035-6039}
}

@article{MTMT:3367042,
	title = {Treatment with the mitochondrial-targeted antioxidant peptide SS-31 rescues neurovascular coupling responses and cerebrovascular endothelial function and improves cognition in aged mice},
	url = {https://m2.mtmt.hu/api/publication/3367042},
	author = {Tarantini, Stefano and Valcarcel-Ares, NM and Yabluchanskiy, A and Fülöp, Gábor Áron and Hertelendy, Péter and Gautam, T and Farkas, Eszter and Perz, A and Rabinovitch, PS and Sonntag, WE and Csiszar, Anna and Ungvári, Zoltán István},
	doi = {10.1111/acel.12731},
	journal-iso = {AGING CELL},
	journal = {AGING CELL},
	volume = {17},
	unique-id = {3367042},
	issn = {1474-9718},
	year = {2018},
	eissn = {1474-9726},
	orcid-numbers = {Tarantini, Stefano/0000-0001-5627-1430; Farkas, Eszter/0000-0002-8478-9664; Ungvári, Zoltán István/0000-0002-6035-6039}
}

@article{MTMT:30452358,
	title = {Neurovascular uncoupling predicts cognitive decline and gait abnormalities in a clinically relevant mouse model of whole brain irradiation},
	url = {https://m2.mtmt.hu/api/publication/30452358},
	author = {Yabluchanskiy, Andriy and Tarantini, Stefano and Hertelendy, Péter and Valcarcel-Ares, Marta Noa and Gautam, Tripti and Farkas, Eszter and Sonntag, William E. and Csiszar, Anna and Ungvári, Zoltán István},
	journal-iso = {FASEB J},
	journal = {FASEB JOURNAL},
	volume = {31},
	unique-id = {30452358},
	issn = {0892-6638},
	keywords = {Biology; Biochemistry & Molecular Biology},
	year = {2017},
	eissn = {1530-6860},
	orcid-numbers = {Tarantini, Stefano/0000-0001-5627-1430; Ungvári, Zoltán István/0000-0002-6035-6039}
}