@article{MTMT:36150231,
	title = {The impact of the novel sigma1 receptor ligand (S)-L1 on brain endothelial cells and cerebrovascular reactivity challenged by ischemia.},
	url = {https://m2.mtmt.hu/api/publication/36150231},
	author = {Kecskés, Szilvia and Meszaros, Maria and Dvoracsko, Szabolcs and Szabó, Írisz and Porkolab, Gergo and Barna, Lilla and Harazin, Andras and Szecsko, Aniko and Menyhárt, Ákos and Bari, Ferenc and Deli, Maria A and Penke, Botond and Farkas, Eszter and Veszelka, Szilvia},
	doi = {10.1016/j.ejphar.2025.177724},
	journal-iso = {EUR J PHARMACOL},
	journal = {EUROPEAN JOURNAL OF PHARMACOLOGY},
	unique-id = {36150231},
	issn = {0014-2999},
	abstract = {Intracellular sigma-1 receptors (sigma1 receptors) have a versatile function through the regulation of lipid rafts, neuroreceptors and ion channels, and can influence signal transduction and neuronal plasticity. Since decreased activity of sigma1 receptors is a common pathological feature in the early stages of many neurological diseases, sigma1 receptor agonists may represent a promising therapeutic tool for the treatment of these disorders. In this study, we aimed to comprehensively investigate the potential protective effects of the novel synthetic sigma1 receptor agonist (S)-L1 against endothelial endoplasmic reticulum (ER) stress and cerebral ischemia. In binding affinity experiments, we showed that (S)-L1 has a high affinity and selectivity for sigma1 receptor with virtually no affinity for any of the other receptors tested. Next, (S)-L1 exerted protection against endoplasmic reticulum stress in human brain endothelial cells, consistent with the localization of sigma1 receptor in endothelial cells. Furthermore, (S)-L1 penetration was demonstrated across the cell culture model of the blood-brain barrier, providing a rationale for neuronal action in addition to endothelial protection. Finally, (S)-L1 inhibited spreading depolarization, suppressed apoptosis and rescued astrocytes in a rat model of cerebral ischemia. Based on our results, (S)-L1 exerts a protective effect on both brain endothelial cells and neural tissue. Moreover, since these experiments revealed no affinity for serotonergic receptors, the compound holds promise as an adjuvant therapy for the treatment of cerebrovascular disease without potential psychedelic side effects. Copyright © 2025. Published by Elsevier B.V.},
	keywords = {Blood-Brain Barrier; Cerebral ischemia; Neurovascular coupling; Brain endothelial cells; sigma-1 receptor ligand},
	year = {2025},
	eissn = {1879-0712},
	orcid-numbers = {Menyhárt, Ákos/0000-0002-1355-3208; Penke, Botond/0000-0003-0938-0567; Farkas, Eszter/0000-0002-8478-9664}
}

@article{MTMT:34030642,
	title = {Alzheimer-kór: le tudjuk-e lassítani a betegséget, lesz-e oki terápia?},
	url = {https://m2.mtmt.hu/api/publication/34030642},
	author = {Penke, Botond and Szűcs, Mária and Bogár, Ferenc},
	journal-iso = {BIOKÉMIA},
	journal = {BIOKÉMIA: A MAGYAR BIOKÉMIAI EGYESÜLET FOLYÓIRATA},
	volume = {47},
	unique-id = {34030642},
	issn = {0133-8455},
	year = {2023},
	eissn = {2060-8152},
	pages = {10-29},
	orcid-numbers = {Penke, Botond/0000-0003-0938-0567; Bogár, Ferenc/0000-0002-0611-1452}
}

@article{MTMT:33702944,
	title = {New Pathways Identify Novel Drug Targets for the Prevention and Treatment of Alzheimer’s Disease},
	url = {https://m2.mtmt.hu/api/publication/33702944},
	author = {Penke, Botond and Szűcs, Mária and Bogár, Ferenc},
	doi = {10.3390/ijms24065383},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {24},
	unique-id = {33702944},
	issn = {1661-6596},
	abstract = {Alzheimer’s disease (AD) is an incurable, progressive neurodegenerative disorder. AD is a complex and multifactorial disease that is responsible for 60–80% of dementia cases. Aging, genetic factors, and epigenetic changes are the main risk factors for AD. Two aggregation-prone proteins play a decisive role in AD pathogenesis: β-amyloid (Aβ) and hyperphosphorylated tau (pTau). Both of them form deposits and diffusible toxic aggregates in the brain. These proteins are the biomarkers of AD. Different hypotheses have tried to explain AD pathogenesis and served as platforms for AD drug research. Experiments demonstrated that both Aβ and pTau might start neurodegenerative processes and are necessary for cognitive decline. The two pathologies act in synergy. Inhibition of the formation of toxic Aβ and pTau aggregates has been an old drug target. Recently, successful Aβ clearance by monoclonal antibodies has raised new hopes for AD treatments if the disease is detected at early stages. More recently, novel targets, e.g., improvements in amyloid clearance from the brain, application of small heat shock proteins (Hsps), modulation of chronic neuroinflammation by different receptor ligands, modulation of microglial phagocytosis, and increase in myelination have been revealed in AD research.},
	year = {2023},
	eissn = {1422-0067},
	orcid-numbers = {Penke, Botond/0000-0003-0938-0567; Bogár, Ferenc/0000-0002-0611-1452}
}

@article{MTMT:33549036,
	title = {Kiemelt publikációk},
	url = {https://m2.mtmt.hu/api/publication/33549036},
	author = {Perczel, András and Nagyné László, Krisztina and Penke, Botond and Vancsó, Gyula and Peter, J. Stang},
	journal-iso = {MAGY KEM LAP},
	journal = {MAGYAR KÉMIKUSOK LAPJA},
	volume = {77},
	unique-id = {33549036},
	issn = {0025-0163},
	year = {2022},
	eissn = {1588-1199},
	pages = {263-265},
	orcid-numbers = {Perczel, András/0000-0003-1252-6416; Nagyné László, Krisztina/0000-0003-4499-3983; Penke, Botond/0000-0003-0938-0567}
}

@article{MTMT:33265905,
	title = {Effects of sub-chronic, in vivo administration of sigma-1 receptor ligands on platelet and aortic arachidonate cascade in streptozotocin-induced diabetic rats},
	url = {https://m2.mtmt.hu/api/publication/33265905},
	author = {Váczi, Sándor and Barna, Lilla and Laczi, Krisztián and Tömösi, Ferenc and Rákhely, Gábor and Penke, Botond and Fülöp, Lívia and Bogár, Ferenc and Janáky, Tamás and Deli, Mária Anna and Mezei, Zsófia},
	doi = {10.1371/journal.pone.0265854},
	journal-iso = {PLOS ONE},
	journal = {PLOS ONE},
	volume = {17},
	unique-id = {33265905},
	abstract = {Diabetes mellitus is a chronic metabolic disorder which induces endothelial dysfunction and platelet activation. Eicosanoids produced from arachidonic acid regulate cellular and vascular functions. Sigma-1 receptors (S1R) are expressed in platelets and endothelial cells and S1R expression is protective in diabetes.},
	year = {2022},
	eissn = {1932-6203},
	orcid-numbers = {Váczi, Sándor/0000-0002-9642-7126; Laczi, Krisztián/0000-0002-9399-7406; Tömösi, Ferenc/0000-0002-6657-5777; Rákhely, Gábor/0000-0003-2557-3641; Penke, Botond/0000-0003-0938-0567; Fülöp, Lívia/0000-0002-8010-0129; Bogár, Ferenc/0000-0002-0611-1452; Janáky, Tamás/0000-0002-6466-8283; Deli, Mária Anna/0000-0001-6084-6524}
}

@article{MTMT:33134539,
	title = {Válogatás},
	url = {https://m2.mtmt.hu/api/publication/33134539},
	author = {Perczel, András and Nagyné László, Krisztina and Penke, Botond and Vancsó, Gyula and Peter, J. Stang},
	journal-iso = {MAGY KEM LAP},
	journal = {MAGYAR KÉMIKUSOK LAPJA},
	volume = {77},
	unique-id = {33134539},
	issn = {0025-0163},
	year = {2022},
	eissn = {1588-1199},
	pages = {316-317},
	orcid-numbers = {Perczel, András/0000-0003-1252-6416; Nagyné László, Krisztina/0000-0003-4499-3983; Penke, Botond/0000-0003-0938-0567}
}

@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}
}

@CONFERENCE{MTMT:32908630,
	title = {A rendszeres testmozgás izom- és agyszövetre kifejtett nem-függő hatásainak vizsgálata a hiperlipidémia egérmodelljében},
	url = {https://m2.mtmt.hu/api/publication/32908630},
	author = {Dukay, Brigitta and Bódai, Zsófia and Csefová, Alexandra and Hajdu, Petra and Ruppert, Zsófia and Penke, Botond and Fülöp, Lívia and Szabó, Kitti and Keller-Pintér, Anikó and Dux, László and Gombos, Imre and Török, Zsolt and Sántha, Miklós and Tóth, E. Melinda},
	booktitle = {51. Membrán-Transzport Konferencia},
	unique-id = {32908630},
	year = {2022},
	orcid-numbers = {Penke, Botond/0000-0003-0938-0567; Fülöp, Lívia/0000-0002-8010-0129; Szabó, Kitti/0000-0002-1177-2036; Keller-Pintér, Anikó/0000-0002-4105-8458; Dux, László/0000-0002-1270-1678}
}

@article{MTMT:32801748,
	title = {Effects of sub-chronic, in vivo administration of sigma non-opioid intracellular receptor 1 ligands on platelet and aortic arachidonate cascade in rats},
	url = {https://m2.mtmt.hu/api/publication/32801748},
	author = {Váczi, Sándor and Barna, Lilla and Laczi, Krisztián and Tömösi, Ferenc and Rákhely, Gábor and Penke, Botond and Fülöp, Lívia and Bogár, Ferenc and Janáky, Tamás and Deli, Mária Anna and Mezei, Zsófia},
	doi = {10.1016/j.ejphar.2022.174983},
	journal-iso = {EUR J PHARMACOL},
	journal = {EUROPEAN JOURNAL OF PHARMACOLOGY},
	volume = {925},
	unique-id = {32801748},
	issn = {0014-2999},
	year = {2022},
	eissn = {1879-0712},
	orcid-numbers = {Váczi, Sándor/0000-0002-9642-7126; Laczi, Krisztián/0000-0002-9399-7406; Tömösi, Ferenc/0000-0002-6657-5777; Rákhely, Gábor/0000-0003-2557-3641; Penke, Botond/0000-0003-0938-0567; Fülöp, Lívia/0000-0002-8010-0129; Bogár, Ferenc/0000-0002-0611-1452; Janáky, Tamás/0000-0002-6466-8283; Deli, Mária Anna/0000-0001-6084-6524}
}

@article{MTMT:32753552,
	title = {Novel Therapeutic Target for Prevention of Neurodegenerative Diseases: Modulation of Neuroinflammation with Sig-1R Ligands},
	url = {https://m2.mtmt.hu/api/publication/32753552},
	author = {Bogár, Ferenc and Fülöp, Lívia and Penke, Botond},
	doi = {10.3390/biom12030363},
	journal-iso = {BIOMOLECULES},
	journal = {BIOMOLECULES},
	volume = {12},
	unique-id = {32753552},
	issn = {2218-273X},
	year = {2022},
	eissn = {2218-273X},
	orcid-numbers = {Bogár, Ferenc/0000-0002-0611-1452; Fülöp, Lívia/0000-0002-8010-0129; Penke, Botond/0000-0003-0938-0567}
}