@article{MTMT:34147524,
	title = {MEAL ESTIMATION ACCURACY IN MODEL PREDICTIVE CONTROL-MOVING HORIZON ESTIMATION CONTROL STRATEGY},
	url = {https://m2.mtmt.hu/api/publication/34147524},
	author = {Siket, Máté and Novak, K. and Eigner, György and Kovács, László Ákos},
	journal-iso = {DIABETES TECHNOL THE},
	journal = {DIABETES TECHNOLOGY AND THERAPEUTICS},
	volume = {25},
	unique-id = {34147524},
	issn = {1520-9156},
	year = {2023},
	eissn = {1557-8593},
	pages = {A112-A112}
}

@article{MTMT:34147477,
	title = {THE IMPACT OF MINIMED (TM) 780G INSULIN PUMP SYSTEM - A SINGLE CENTRE PROSPECTIVE STUDY},
	url = {https://m2.mtmt.hu/api/publication/34147477},
	author = {Kocsis, G. and Garam, Nóra and Javorfi, T. and Svebis, M. and Toth, B. and Ferenci, Tamás and Eigner, György and Barkai, L. and Kovács, László Ákos},
	journal-iso = {DIABETES TECHNOL THE},
	journal = {DIABETES TECHNOLOGY AND THERAPEUTICS},
	volume = {25},
	unique-id = {34147477},
	issn = {1520-9156},
	year = {2023},
	eissn = {1557-8593},
	pages = {A70-A70},
	orcid-numbers = {Garam, Nóra/0000-0002-1959-4473; Ferenci, Tamás/0000-0001-6791-3080}
}

@article{MTMT:34074467,
	title = {Downregulation of PACAP and the PAC1 Receptor in the Basal Ganglia, Substantia Nigra and Centrally Projecting Edinger–Westphal Nucleus in the Rotenone model of Parkinson’s Disease},
	url = {https://m2.mtmt.hu/api/publication/34074467},
	author = {Fehér, Máté and Márton, Zsombor and Szabó, Ákos and Kocsa, János and Kormos, Viktória and Hunyady, Ágnes and Kovács, László Ákos and Ujvári, Balázs and Berta, Gergely and Farkas, József and Füredi, Nóra and Gaszner, Tamás and Pytel, Bence and Reglődi, Dóra and Gaszner, Balázs},
	doi = {10.3390/ijms241411843},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {24},
	unique-id = {34074467},
	issn = {1661-6596},
	abstract = {Numerous in vitro and in vivo models of Parkinson’s disease (PD) demonstrate that pituitary adenylate cyclase-activating polypeptide (PACAP) conveys its strong neuroprotective actions mainly via its specific PAC1 receptor (PAC1R) in models of PD. We recently described the decrease in PAC1R protein content in the basal ganglia of macaques in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) model of PD that was partially reversed by levodopa therapy. In this work, we tested whether these observations occur also in the rotenone model of PD in the rat. The rotarod test revealed motor skill deterioration upon rotenone administration, which was reversed by benserazide/levodopa (B/L) treatment. The sucrose preference test suggested increased depression level while the open field test showed increased anxiety in rats rendered parkinsonian, regardless of the received B/L therapy. Reduced dopaminergic cell count in the substantia nigra pars compacta (SNpc) diminished the dopaminergic fiber density in the caudate-putamen (CPu) and decreased the peptidergic cell count in the centrally projecting Edinger–Westphal nucleus (EWcp), supporting the efficacy of rotenone treatment. RNAscope in situ hybridization revealed decreased PACAP mRNA (Adcyap1) and PAC1R mRNA (Adcyap1r1) expression in the CPu, globus pallidus, dopaminergic SNpc and peptidergic EWcp of rotenone-treated rats, but no remarkable downregulation occurred in the insular cortex. In the entopeduncular nucleus, only the Adcyap1r1 mRNA was downregulated in parkinsonian animals. B/L therapy attenuated the downregulation of Adcyap1 in the CPu only. Our current results further support the evolutionarily conserved role of the PACAP/PAC1R system in neuroprotection and its recruitment in the development/progression of neurodegenerative states such as PD.},
	year = {2023},
	eissn = {1422-0067},
	orcid-numbers = {Gaszner, Balázs/0000-0003-2830-2732}
}

@article{MTMT:33163285,
	title = {Epigenetic and Neuronal Activity Markers Suggest the Recruitment of the Prefrontal Cortex and Hippocampus in the Three-Hit Model of Depression in Male PACAP Heterozygous Mice.},
	url = {https://m2.mtmt.hu/api/publication/33163285},
	author = {Gaszner, Tamás and Farkas, József and Kun, Dániel and Ujvári, Balázs and Füredi, Nóra and Kovács, László Ákos and Hashimoto, Hitoshi and Reglődi, Dóra and Kormos, Viktória and Gaszner, Balázs},
	doi = {10.3390/ijms231911739},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {23},
	unique-id = {33163285},
	issn = {1661-6596},
	abstract = {Depression and its increasing prevalence challenge patients, the healthcare system, and the economy. We recently created a mouse model based on the three-hit concept of depression. As genetic predisposition (first hit), we applied pituitary adenylate cyclase-activating polypeptide heterozygous mice on CD1 background. Maternal deprivation modeled the epigenetic factor (second hit), and the chronic variable mild stress was the environmental factor (third hit). Fluoxetine treatment was applied to test the predictive validity of our model. We aimed to examine the dynamics of the epigenetic marker acetyl-lysine 9 H3 histone (H3K9ac) and the neuronal activity marker FOSB in the prefrontal cortex (PFC) and hippocampus. Fluoxetine decreased H3K9ac in PFC in non-deprived animals, but a history of maternal deprivation abolished the effect of stress and SSRI treatment on H3K9ac immunoreactivity. In the hippocampus, stress decreased, while SSRI increased H3K9ac immunosignal, unlike in the deprived mice, where the opposite effect was detected. FOSB in stress was stimulated by fluoxetine in the PFC, while it was inhibited in the hippocampus. The FOSB immunoreactivity was almost completely abolished in the hippocampus of the deprived mice. This study showed that FOSB and H3K9ac were modulated in a territory-specific manner by early life adversities and later life stress interacting with the effect of fluoxetine therapy supporting the reliability of our model.},
	keywords = {Maternal Deprivation; Chronic stress; Histone acetylation; H3K9Ac; FosB},
	year = {2022},
	eissn = {1422-0067},
	orcid-numbers = {Gaszner, Balázs/0000-0003-2830-2732}
}

@article{MTMT:33123834,
	title = {Fluoxetine treatment supports predictive validity of the three hit model of depression in male PACAP heterozygous mice and underpins the impact of early life adversity on therapeutic efficacy},
	url = {https://m2.mtmt.hu/api/publication/33123834},
	author = {Gaszner, Tamás and Farkas, József and Kun, Dániel and Ujvári, Balázs and Berta, Gergely and Csernus, Valér and Füredi, Nóra and Kovács, László Ákos and Hashimoto, Hitoshi and Reglődi, Dóra and Kormos, Viktória and Gaszner, Balázs},
	doi = {10.3389/fendo.2022.995900},
	journal-iso = {FRONT ENDOCRINOL},
	journal = {FRONTIERS IN ENDOCRINOLOGY},
	volume = {13},
	unique-id = {33123834},
	issn = {1664-2392},
	abstract = {According to the three hit concept of depression, interaction of genetic predisposition altered epigenetic programming and environmental stress factors contribute to the disease. Earlier we demonstrated the construct and face validity of our three hit concept-based mouse model. In the present work, we aimed to examine the predictive validity of our model, the third willnerian criterion. Fluoxetine treatment was applied in chronic variable mild stress (CVMS)-exposed (environmental hit) CD1 mice carrying one mutated allele of pituitary adenylate cyclase-activating polypeptide gene (genetic hit) that were previously exposed to maternal deprivation (epigenetic hit) vs. controls. Fluoxetine reduced the anxiety level in CVMS-exposed mice in marble burying test, and decreased the depression level in tail suspension test if mice were not deprived maternally. History of maternal deprivation caused fundamental functional-morphological changes in response to CVMS and fluoxetine treatment in the corticotropin-releasing hormone-producing cells of the bed nucleus of the stria terminalis and central amygdala, in tyrosine-hydroxylase content of ventral tegmental area, in urocortin 1-expressing cells of the centrally projecting Edinger-Westphal nucleus, and serotonergic cells of the dorsal raphe nucleus. The epigenetic background of alterations was approved by altered acetylation of histone H3. Our findings further support the validity of both the three hit concept and that of our animal model. Reversal of behavioral and functional-morphological anomalies by fluoxetine treatment supports the predictive validity of the model. This study highlights that early life stress does not only interact with the genetic and environmental factors, but has strong influence also on therapeutic efficacy.},
	year = {2022},
	eissn = {1664-2392},
	orcid-numbers = {Gaszner, Balázs/0000-0003-2830-2732}
}

@article{MTMT:32804334,
	title = {Age-Dependent FOSB/ΔFOSB Response to Acute and Chronic Stress in the Extended Amygdala, Hypothalamic Paraventricular, Habenular, Centrally-Projecting Edinger-Westphal, and Dorsal Raphe Nuclei in Male Rats},
	url = {https://m2.mtmt.hu/api/publication/32804334},
	author = {Kovács, László Ákos and Füredi, Nóra and Ujvári, Balázs and Golgol, Abolfazl and Gaszner, Balázs},
	doi = {10.3389/fnagi.2022.862098},
	journal-iso = {FRONT AGING NEUROSCI},
	journal = {FRONTIERS IN AGING NEUROSCIENCE},
	volume = {14},
	unique-id = {32804334},
	issn = {1663-4365},
	abstract = {FOS proteins are early-responding gene products that contribute to the formation of activator protein-1. Several acute and chronic stimuli lead to Fos gene expression, accompanied by an increase of nuclear FOS, which appears to decline with aging. FOSB is another marker to detect acute cellular response, while ΔFOSB mirrors long-lasting changes in neuronal activity upon chronic stress. The notion that the occurrence of stress-related mood disorders shows some age dependence suggests that the brain's stress sensitivity is also a function of age. To study age-dependent stress vulnerability at the immediate-early gene level, we aimed to describe how the course of aging affects the neural responses of FOSB/ΔFOSB in the acute restraint stress (ARS), and chronic variable mild stress (CVMS) in male rats. Fourteen brain areas [central, medial, basolateral (BLA) amygdala; dorsolateral- (BNSTdl), oval- (BNSTov), dorsomedial-, ventral- (BNSTv), and fusiform- (BNSTfu) divisions of the bed nucleus of the stria terminalis; medial and lateral habenula, hypothalamic paraventricular nucleus (PVN), centrally-projecting Edinger-Westphal nucleus, dorsal raphe nucleus, barrel field of somatosensory cortex (S1)] were examined in the course of aging. Eight age groups [1-month-old (M), 1.5 M, 2 M, 3 M, 6 M, 12 M, 18 M, and 24 M] of rats were exposed to a single ARS vs. controls. In addition, rats in six age groups (2, 3, 6, 12, 18, and 24 M) were subjected to CVMS. The FOSB/ΔFOSB immunoreactivity (IR) was a function of age in both controls, ARS- and CVMS-exposed rats. ARS increased the FOSB/ΔFOSB in all nuclei (except in BLA), but only BNSTfu, BNSTv, and PVN reacted throughout the examined lifespan. The CVMS did not increase the FOSB/ΔFOSB in BLA, BNSTov, BNSTdl, and S1. PVN showed a constantly maintained FOSB/ΔFOSB IR during the examined life period. The maximum stress-evoked FOSB/ΔFOSB signal was detected at 2-3 M periods in the ARS- and at 6 M, 18 M in CVMS- model. Corresponding to our previous observations on FOS, the FOSB/ΔFOSB response to stress decreased with age in most of the examined nuclei. Only the PVN exerted a sustained age-independent FOSB/ΔFOSB, which may reflect the long-lasting adaptation response and plasticity of neurons that maintain the hypothalamus-pituitary-adrenal axis response throughout the lifespan.},
	year = {2022},
	eissn = {1663-4365},
	orcid-numbers = {Gaszner, Balázs/0000-0003-2830-2732}
}

@article{MTMT:32640720,
	title = {Neurodegeneration in the centrally-projecting Edinger–Westphal nucleus contributes to the non-motor symptoms of Parkinson’s disease in the rat},
	url = {https://m2.mtmt.hu/api/publication/32640720},
	author = {Ujvári, Balázs and Pytel, Bence and Márton, Zsombor and Bognár, Máté and Kovács, László Ákos and Farkas, József and Gaszner, Tamás and Berta, Gergely and Kecskés, Angéla and Kormos, Viktória and Farkas, Boglárka and Füredi, Nóra and Gaszner, Balázs},
	doi = {10.1186/s12974-022-02399-w},
	journal-iso = {J NEUROINFLAMM},
	journal = {JOURNAL OF NEUROINFLAMMATION},
	volume = {19},
	unique-id = {32640720},
	abstract = {The neuropathological background of major depression and anxiety as non-motor symptoms of Parkinson's disease is much less understood than classical motor symptoms. Although, neurodegeneration of the Edinger-Westphal nucleus in human Parkinson's disease is a known phenomenon, its possible significance in mood status has never been elucidated. In this work we aimed at investigating whether neuron loss and alpha-synuclein accumulation in the urocortin 1 containing (UCN1) cells of the centrally-projecting Edinger-Westphal (EWcp) nucleus is associated with anxiety and depression-like state in the rat.Systemic chronic rotenone administration as well as targeted leptin-saporin-induced lesions of EWcp/UCN1 neurons were conducted. Rotarod, open field and sucrose preference tests were performed to assess motor performance and mood status. Multiple immunofluorescence combined with RNAscope were used to reveal the functional-morphological changes. Two-sample Student's t test, Spearman's rank correlation analysis and Mann-Whitney U tests were used for statistics.In the rotenone model, besides motor deficit, an anxious and depression-like phenotype was detected. Well-comparable neuron loss, cytoplasmic alpha-synuclein accumulation as well as astro- and microglial activation were observed both in the substantia nigra pars compacta and EWcp. Occasionally, UCN1-immunoreactive neuronal debris was observed in phagocytotic microglia. UCN1 peptide content of viable EWcp cells correlated with dopaminergic substantia nigra cell count. Importantly, other mood status-related dopaminergic (ventral tegmental area), serotonergic (dorsal and median raphe) and noradrenergic (locus ceruleus and A5 area) brainstem centers did not show remarkable morphological changes. Targeted partial selective EWcp/UCN1 neuron ablation induced similar mood status without motor symptoms.Our findings collectively suggest that neurodegeneration of urocortinergic EWcp contributes to the mood-related non-motor symptoms in toxic models of Parkinson's disease in the rat.},
	year = {2022},
	eissn = {1742-2094},
	orcid-numbers = {Gaszner, Balázs/0000-0003-2830-2732}
}

@book{MTMT:32804723,
	title = {VÍZ ALATTI SPORTOK VILÁGA I.. AZ USZONYOSÚSZÁS},
	url = {https://m2.mtmt.hu/api/publication/32804723},
	isbn = {9786150139937},
	author = {Kovács, Zsófia and Kovács, László Ákos and Paic, Róbert and Solymossy, Mária and Kovács, László},
	publisher = {Wunderlich Production Kft.},
	unique-id = {32804723},
	keywords = {oktatásmódszertan; Úszás; anatómia; sportmotiváció; uszonyosúszás},
	year = {2021}
}

@article{MTMT:30935538,
	title = {Lack of Pituitary Adenylate Cyclase–Activating Polypeptide (PACAP) Disturbs Callus Formation},
	url = {https://m2.mtmt.hu/api/publication/30935538},
	author = {Józsa, Gergő and Fülöp, Balázs Dániel and Kovács, László Ákos and Czibere, Bernadett and Szegeczki, Vince and Kiss, Tamás and Hajdú, Tibor and Tamás, Andrea and Helyes, Zsuzsanna and Zákány, Róza and Reglődi, Dóra and Juhász, Tamás},
	doi = {10.1007/s12031-019-01448-z},
	journal-iso = {J MOL NEUROSCI},
	journal = {JOURNAL OF MOLECULAR NEUROSCIENCE},
	volume = {71},
	unique-id = {30935538},
	issn = {0895-8696},
	abstract = {Pituitary adenylate cyclase–activating polypeptide (PACAP) is a naturally secreted signaling peptide and has important regulatory roles in the differentiation of the central nervous system and its absence results in disorders in femur development. PACAP has an important function in prevention of oxidative stress or mechanical stress in chondrogenesis but little is known about its function in bone regeneration. A new callus formation model was set to investigate its role in bone remodeling. Fracturing was 5 mm distal from the proximal articular surface of the tibia and the depth was 0.5 mm. Reproducibility of callus formation was investigated with CT 3, 7, and 21 days after the operation. Absence of PACAP did not alter the alkaline phosphatase (ALP) activation in PACAP KO healing process. In developing callus, the expression of collagen type I increased in wild-type (WT) and PACAP KO mice decreased to the end of healing process. Expression of the elements of BMP signaling was disturbed in the callus formation of PACAP KO mice, as bone morphogenic protein 4 (BMP4) and 6 showed an early reduction in bone regeneration. However, elevated Smad1 expression was demonstrated in PACAP KO mice. Our results indicate that PACAP KO mice show various signs of disturbed bone healing and suggest PACAP compensatory and fine tuning effects in proper bone regeneration.},
	year = {2021},
	eissn = {1559-1166},
	pages = {1543-1555}
}

@mastersthesis{MTMT:31664192,
	title = {Limbikus és középagyi stressz-asszociált magok korfüggő aktivitásának vizsgálata az akut és krónikus stressz patkánymodelljében},
	url = {https://m2.mtmt.hu/api/publication/31664192},
	author = {Kovács, László Ákos},
	unique-id = {31664192},
	year = {2020}
}