@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},
	issn = {1932-6203},
	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},
	doi = {10.24364/MKL.2022.10},
	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}
}

@article{MTMT:32753550,
	title = {Impact of Two Neuronal Sigma-1 Receptor Modulators, PRE084 and DMT, on Neurogenesis and Neuroinflammation in an Aβ1–42-Injected, Wild-Type Mouse Model of AD},
	url = {https://m2.mtmt.hu/api/publication/32753550},
	author = {Borbély, Emőke and Varga, Viktória and Szögi, Titanilla and Schuster, Ildikó and Bozsó, Zsolt and Penke, Botond and Fülöp, Lívia},
	doi = {10.3390/ijms23052514},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {23},
	unique-id = {32753550},
	issn = {1661-6596},
	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}
}