@article{MTMT:33688118,
	title = {Role of interleukin-6 and interleukin-10 in morphological and functional changes of the blood–brain barrier in hypertriglyceridemia},
	url = {https://m2.mtmt.hu/api/publication/33688118},
	author = {Barabási, Beáta and Barna, Lilla and Santa Maria, Anaraquel and Harazin, András and Molnár, Réka and Kincses, András and Vigh, Judit Piroska and Dukay, Brigitta and Sántha, Miklós and Tóth, Erzsébet Melinda and Walter, Fruzsina and Deli, Mária Anna and Hoyk, Zsófia},
	doi = {10.1186/s12987-023-00418-3},
	journal-iso = {FLUIDS BARRIERS CNS},
	journal = {FLUIDS AND BARRIERS OF THE CNS},
	volume = {20},
	unique-id = {33688118},
	issn = {2045-8118},
	year = {2023},
	eissn = {2045-8118},
	orcid-numbers = {Santa Maria, Anaraquel/0000-0003-3505-5477; Harazin, András/0000-0002-0904-5606; Molnár, Réka/0000-0002-3128-825X; Walter, Fruzsina/0000-0001-8145-2823; Deli, Mária Anna/0000-0001-6084-6524}
}

@article{MTMT:33111245,
	title = {Examination of Longitudinal Alterations in Alzheimer’s Disease-Related Neurogenesis in an APP/PS1 Transgenic Mouse Model, and the Effects of P33, a Putative Neuroprotective Agent Thereon},
	url = {https://m2.mtmt.hu/api/publication/33111245},
	author = {Szögi, Titanilla and Borbély, Emőke and Schuster, Ildikó and Bozsó, Zsolt and Sántha, Miklós and Tóth, Erzsébet Melinda and Penke, Botond and Fülöp, Lívia},
	doi = {10.3390/ijms231810364},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {23},
	unique-id = {33111245},
	issn = {1661-6596},
	abstract = {Neurogenesis plays a crucial role in cognitive processes. During aging and in Alzheimer’s disease (AD), altered neurogenesis and neuroinflammation are evident both in C57BL/6J, APPSwe/PS1dE9 (Tg) mice and humans. AD pathology may slow down upon drug treatment, for example, in a previous study of our group P33, a putative neuroprotective agent was found to exert advantageous effects on the elevated levels of APP, Aβ, and neuroinflammation. In the present study, we aimed to examine longitudinal alterations in neurogenesis, neuroinflammation and AD pathology in a transgenic (Tg) mouse model, and assessed the putative beneficial effects of long-term P33 treatment on AD-specific neurological alterations. Hippocampal cell proliferation and differentiation were significantly reduced between 8 and 12 months of age. Regarding neuroinflammation, significantly elevated astrogliosis and microglial activation were observed in 6- to 7-month-old Tg animals. The amounts of the molecules involved in the amyloidogenic pathway were altered from 4 months of age in Tg animals. P33-treatment led to significantly increased neurogenesis in 9-month-old animals. Our data support the hypothesis that altered neurogenesis may be a consequence of AD pathology. Based on our findings in the transgenic animal model, early pharmacological treatment before the manifestation of AD symptoms might ameliorate neurological decline.},
	year = {2022},
	eissn = {1422-0067},
	orcid-numbers = {Szögi, Titanilla/0000-0002-9854-7340; Schuster, Ildikó/0000-0001-9997-5729; Bozsó, Zsolt/0000-0002-5713-3096; Penke, Botond/0000-0003-0938-0567; Fülöp, Lívia/0000-0002-8010-0129}
}

@article{MTMT:32637299,
	title = {Exercise training worsens cardiac performance in males but does not change ejection fraction and improves hypertrophy in females in a mouse model of metabolic syndrome},
	url = {https://m2.mtmt.hu/api/publication/32637299},
	author = {Tóth, Erzsébet Melinda and Sárközy, Márta and Szűcs, Gergő and Dukay, Brigitta and Hajdu, Petra and Zvara, Ágnes and Puskás, László and Szebeni, Gábor and Ruppert, Zsófia and Csonka, Csaba and Kovács, Ferenc and Kriston, András and Horváth, Péter and Kővári, Bence and Cserni, Gábor and Csont, Tamás Bálint and Sántha, Miklós},
	doi = {10.1186/s13293-022-00414-6},
	journal-iso = {BIOL SEX DIFFER},
	journal = {BIOLOGY OF SEX DIFFERENCES},
	volume = {13},
	unique-id = {32637299},
	year = {2022},
	eissn = {2042-6410},
	orcid-numbers = {Sárközy, Márta/0000-0002-5929-2146; Szűcs, Gergő/0000-0003-1874-2718; Szebeni, Gábor/0000-0002-6998-5632; Csonka, Csaba/0000-0003-2532-6261; Kővári, Bence/0000-0002-4498-8781; Cserni, Gábor/0000-0003-1344-7744; Csont, Tamás Bálint/0000-0001-5792-2768}
}

@article{MTMT:32113140,
	title = {Age-Related Inflammatory Balance Shift, Nasal Barrier Function, and Cerebro-Morphological Status in Healthy and Diseased Rodents},
	url = {https://m2.mtmt.hu/api/publication/32113140},
	author = {Varga-Medveczky, Zsófia and Stelczerné Kovács, Noémi and Tóth, Erzsébet Melinda and Sántha, Miklós and Horváth, Ildikó and Bors, Luca Anna and Fónagy, Katalin and Imre, Timea and Szabó, Pál Tamás and Máthé, Domokos and Erdő, Franciska},
	doi = {10.3389/fnins.2021.700729},
	journal-iso = {FRONT NEUROSCI-SWITZ},
	journal = {FRONTIERS IN NEUROSCIENCE},
	volume = {15},
	unique-id = {32113140},
	issn = {1662-4548},
	year = {2021},
	eissn = {1662-453X},
	orcid-numbers = {Szabó, Pál Tamás/0000-0003-2260-4641}
}

@article{MTMT:32078131,
	title = {Q134R: Small chemical compound with NFAT inhibitory properties improves behavioral performance and synapse function in mouse models of amyloid pathology},
	url = {https://m2.mtmt.hu/api/publication/32078131},
	author = {Sompol, Pradoldej and Gollihue, Jenna L. and Kraner, Susan D. and Artiushin, Irina A. and Cloyd, Ryan A. and Chishti, Emad A. and Koren, Shon A. and Nation, Grant K. and Abisambra, Jose F. and Huzian, Orsolya and Nagy, Lajos I. and Sántha, Miklós and Hackler, Laszlo Jr. and Puskás, László and Norris, Christopher M.},
	doi = {10.1111/acel.13416},
	journal-iso = {AGING CELL},
	journal = {AGING CELL},
	volume = {20},
	unique-id = {32078131},
	issn = {1474-9718},
	abstract = {Inhibition of the protein phosphatase calcineurin (CN) ameliorates pathophysiologic and cognitive changes in aging rodents and mice with aging-related Alzheimer's disease (AD)-like pathology. However, concerns over adverse effects have slowed the transition of common CN-inhibiting drugs to the clinic for the treatment of AD and AD-related disorders. Targeting substrates of CN, like the nuclear factor of activated T cells (NFATs), has been suggested as an alternative, safer approach to CN inhibitors. However, small chemical inhibitors of NFATs have only rarely been described. Here, we investigate a newly developed neuroprotective hydroxyquinoline derivative (Q134R) that suppresses NFAT signaling, without inhibiting CN activity. Q134R partially inhibited NFAT activity in primary rat astrocytes, but did not prevent CN-mediated dephosphorylation of a non-NFAT target, either in vivo, or in vitro. Acute (<= 1 week) oral delivery of Q134R to APP/PS1 (12 months old) or wild-type mice (3-4 months old) infused with oligomeric A beta peptides led to improved Y maze performance. Chronic (>= 3 months) oral delivery of Q134R appeared to be safe, and, in fact, promoted survival in wild-type (WT) mice when given for many months beyond middle age. Finally, chronic delivery of Q134R to APP/PS1 mice during the early stages of amyloid pathology (i.e., between 6 and 9 months) tended to reduce signs of glial reactivity, prevented the upregulation of astrocytic NFAT4, and ameliorated deficits in synaptic strength and plasticity, without noticeably altering parenchymal A beta plaque pathology. The results suggest that Q134R is a promising drug for treating AD and aging-related disorders.},
	year = {2021},
	eissn = {1474-9726},
	orcid-numbers = {Abisambra, Jose F./0000-0001-6341-679X}
}

@article{MTMT:31970009,
	title = {Male and Female Animals Respond Differently to High-Fat Diet and Regular Exercise Training in a Mouse Model of Hyperlipidemia},
	url = {https://m2.mtmt.hu/api/publication/31970009},
	author = {Tóth, Erzsébet Melinda and Dukay, Brigitta and Péter, Mária and Balogh, Gábor and Szűcs, Gergő and Zvara, Ágnes and Szebeni, Gábor and Hajdu, Petra and Sárközy, Márta and Puskás, László and Török, Zsolt and Csont, Tamás Bálint and Vigh, László and Sántha, Miklós},
	doi = {10.3390/ijms22084198},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {22},
	unique-id = {31970009},
	issn = {1661-6596},
	abstract = {Inappropriate nutrition and a sedentary lifestyle can lead to obesity, one of the most common risk factors for several chronic diseases. Although regular physical exercise is an efficient approach to improve cardiometabolic health, the exact cellular processes are still not fully understood. We aimed to analyze the morphological, gene expression, and lipidomic patterns in the liver and adipose tissues in response to regular exercise. Healthy (wild type on a normal diet) and hyperlipidemic, high-fat diet-fed (HFD-fed) apolipoprotein B-100 (APOB-100)-overexpressing mice were trained by treadmill running for 7 months. The serum concentrations of triglyceride and tumor necrosis factor alpha (TNF alpha), as well as the level of lipid accumulation in the liver, were significantly higher in HFD-fed APOB-100 males compared to females. However, regular exercise almost completely abolished lipid accumulation in the liver of hyperlipidemic animals. The expression level of the thermogenesis marker, uncoupling protein-1 (Ucp1), was significantly higher in the subcutaneous white adipose tissue of healthy females, as well as in the brown adipose tissue of HFD-fed APOB-100 females, compared to males. Lipidomic analyses revealed that hyperlipidemia essentially remodeled the lipidome of brown adipose tissue, affecting both the membrane and storage lipid fractions, which was partially restored by exercise in both sexes. Our results revealed more severe metabolic disturbances in HFD-fed APOB-100 males compared to females. However, exercise efficiently reduced the body weight, serum triglyceride levels, expression of pro-inflammatory factors, and hepatic lipid accumulation in our model.},
	year = {2021},
	eissn = {1422-0067},
	orcid-numbers = {Szűcs, Gergő/0000-0003-1874-2718; Szebeni, Gábor/0000-0002-6998-5632; Sárközy, Márta/0000-0002-5929-2146; Török, Zsolt/0000-0003-0836-3247; Csont, Tamás Bálint/0000-0001-5792-2768}
}

@article{MTMT:31807147,
	title = {Neuroinflammatory processes are augmented in mice overexpressing human heat-shock protein B1 following ethanol-induced brain injury},
	url = {https://m2.mtmt.hu/api/publication/31807147},
	author = {Dukay, Brigitta and Walter, Fruzsina and Vigh, Judit Piroska and Barabási, Beáta and Hajdu, Petra and Balassa, Tamás and Migh, Ede and Kincses, András and Hoyk, Zsófia and Szögi, Titanilla and Borbély, Emőke and Csoboz, Bálint and Horváth, Péter and Fülöp, Lívia and Penke, Botond and Vigh, László and Deli, Mária Anna and Sántha, Miklós and Tóth, Erzsébet Melinda},
	doi = {10.1186/s12974-020-02070-2},
	journal-iso = {J NEUROINFLAMM},
	journal = {JOURNAL OF NEUROINFLAMMATION},
	volume = {18},
	unique-id = {31807147},
	year = {2021},
	eissn = {1742-2094},
	orcid-numbers = {Walter, Fruzsina/0000-0001-8145-2823; Szögi, Titanilla/0000-0002-9854-7340; Fülöp, Lívia/0000-0002-8010-0129; Penke, Botond/0000-0003-0938-0567; Deli, Mária Anna/0000-0001-6084-6524}
}

@article{MTMT:31670054,
	title = {Biologia futura: animal testing in drug development-the past, the present and the future},
	url = {https://m2.mtmt.hu/api/publication/31670054},
	author = {Sántha, Miklós},
	doi = {10.1007/s42977-020-00050-4},
	journal-iso = {BIOL FUTURA},
	journal = {BIOLOGIA FUTURA},
	volume = {71},
	unique-id = {31670054},
	issn = {2676-8615},
	abstract = {Animal experiments have served to improve our knowledge on diseases and treatment approaches since ancient times. Today, animal experiments are widely used in medical, biomedical and veterinary research, and are essential means of drug development and preclinical testing, including toxicology and safety studies. Recently, great efforts have been made to replace animal experiments with in vitro organoid culture methods and in silico predictions, in agreement with the 3R strategy to "reduce, refine and replace" animals in experimental testing, as outlined by the European Commission. Here we present a mini-review on the development of animal testing, as well as on alternative in vitro and in silico methods, that may at least partly replace animal experiments in the near future.},
	year = {2020},
	eissn = {2676-8607},
	pages = {443-452}
}

@article{MTMT:31599677,
	title = {Editorial: The Role of Heat Shock Proteins in Neuroprotection},
	url = {https://m2.mtmt.hu/api/publication/31599677},
	author = {Sántha, Miklós and Durham, Heather D. and Vigh, László and Prodromou, Chrisostomos},
	doi = {10.3389/fphar.2020.01227},
	journal-iso = {FRONT PHARMACOL},
	journal = {FRONTIERS IN PHARMACOLOGY},
	volume = {11},
	unique-id = {31599677},
	year = {2020},
	eissn = {1663-9812}
}

@article{MTMT:31195696,
	title = {Cerebrovascular Changes and Neurodegeneration Related to Hyperlipidemia. Characteristics of the Human ApoB-100 Transgenic Mice.},
	url = {https://m2.mtmt.hu/api/publication/31195696},
	author = {Tóth, Erzsébet Melinda and Dukay, Brigitta and Hoyk, Zsófia and Sántha, Miklós},
	doi = {10.2174/1381612826666200218101818},
	journal-iso = {CURR PHARM DESIGN},
	journal = {CURRENT PHARMACEUTICAL DESIGN},
	volume = {26},
	unique-id = {31195696},
	issn = {1381-6128},
	abstract = {Serum lipid levels are closely related to the structure and function of blood vessels. Chronic hyperlipidemia may lead to damage in both the cardio- and the cerebrovascular systems. Vascular dysfunctions, including impairments of the blood-brain barrier, are known to be associated with neurodegenerative diseases. A growing number of evidence suggests that cardiovascular risk factors, such as hyperlipidemia, may increase the likelihood of developing dementia. Due to differences in lipoprotein metabolism, wild-type mice are protected against diet-induced hypercholesterolemia, and their serum lipid profile is different from that observed in humans. Therefore, several transgenic mouse models have been established to study the role of different apolipoproteins and their receptors in lipid metabolism, as well as the complications related to pathological lipoprotein levels. This mini-review will focus on a transgenic mouse model overexpressing an apolipoprotein, the human ApoB-100. We will discuss literature data and current advancements on the understanding of ApoB-100 induced cardio- and cerebrovascular lesions in order to demonstrate the involvement of this type of apolipoprotein in a wide range of pathologies, and a link between hyperlipidemia and neurodegeneration.},
	keywords = {TRANSGENIC MICE; ATHEROSCLEROSIS; DEMENTIA; endothelial dysfunction; cerebrovascular disease; neurodegeneration; hyperlipidemia; Blood-brain barrier (BBB); ApoB-100 lipoprotein},
	year = {2020},
	eissn = {1873-4286},
	pages = {1486-1494}
}