TY - JOUR AU - Penke, Botond AU - Szűcs, Mária AU - Bogár, Ferenc TI - Alzheimer-kór: le tudjuk-e lassítani a betegséget, lesz-e oki terápia? JF - BIOKÉMIA: A MAGYAR BIOKÉMIAI EGYESÜLET FOLYÓIRATA J2 - BIOKÉMIA VL - 47 PY - 2023 IS - 2 SP - 10 EP - 29 PG - 20 SN - 0133-8455 UR - https://m2.mtmt.hu/api/publication/34030642 ID - 34030642 LA - Hungarian DB - MTMT ER - TY - JOUR AU - Penke, Botond AU - Szűcs, Mária AU - Bogár, Ferenc TI - New Pathways Identify Novel Drug Targets for the Prevention and Treatment of Alzheimer’s Disease JF - INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES J2 - INT J MOL SCI VL - 24 PY - 2023 IS - 6 PG - 23 SN - 1661-6596 DO - 10.3390/ijms24065383 UR - https://m2.mtmt.hu/api/publication/33702944 ID - 33702944 N1 - ELKH-SZTE Biomimetic Systems Research Group, Eötvös Loránd Research Funding details: Nemzeti Kutatási Fejlesztési és Innovációs Hivatal, NKFIH, GINOP-2.3.2-15-2016-00034, GINOP-2.3.2-15-2016-00060 Funding text 1: This research was funded by National Research Development and Innovation Office (NKFIH), grant numbers GINOP-2.3.2-15-2016-00060 and GINOP-2.3.2-15-2016-00034. AB - 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. LA - English DB - MTMT ER - TY - JOUR AU - Perczel, András AU - Nagyné László, Krisztina AU - Penke, Botond AU - Vancsó, Gyula AU - Peter, J. Stang TI - Kiemelt publikációk JF - MAGYAR KÉMIKUSOK LAPJA J2 - MAGY KEM LAP VL - 77 PY - 2022 IS - 9 SP - 263 EP - 265 PG - 3 SN - 0025-0163 UR - https://m2.mtmt.hu/api/publication/33549036 ID - 33549036 LA - Hungarian DB - MTMT ER - TY - JOUR AU - Váczi, Sándor AU - Barna, Lilla AU - Laczi, Krisztián AU - Tömösi, Ferenc AU - Rákhely, Gábor AU - Penke, Botond AU - Fülöp, Lívia AU - Bogár, Ferenc AU - Janáky, Tamás AU - Deli, Mária Anna AU - Mezei, Zsófia TI - Effects of sub-chronic, in vivo administration of sigma-1 receptor ligands on platelet and aortic arachidonate cascade in streptozotocin-induced diabetic rats JF - PLOS ONE J2 - PLOS ONE VL - 17 PY - 2022 IS - 11 PG - 23 SN - 1932-6203 DO - 10.1371/journal.pone.0265854 UR - https://m2.mtmt.hu/api/publication/33265905 ID - 33265905 LA - English DB - MTMT ER - TY - JOUR AU - Perczel, András AU - Nagyné László, Krisztina AU - Penke, Botond AU - Vancsó, Gyula AU - Peter, J. Stang TI - Válogatás JF - MAGYAR KÉMIKUSOK LAPJA J2 - MAGY KEM LAP VL - 77 PY - 2022 IS - 10 SP - 316 EP - 317 PG - 1 SN - 0025-0163 DO - 10.24364/MKL.2022.10 UR - https://m2.mtmt.hu/api/publication/33134539 ID - 33134539 LA - Hungarian DB - MTMT ER - TY - JOUR AU - Szögi, Titanilla AU - Borbély, Emőke AU - Schuster, Ildikó AU - Bozsó, Zsolt AU - Sántha, Miklós AU - Tóth, Erzsébet Melinda AU - Penke, Botond AU - Fülöp, Lívia TI - 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 JF - INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES J2 - INT J MOL SCI VL - 23 PY - 2022 IS - 18 PG - 17 SN - 1661-6596 DO - 10.3390/ijms231810364 UR - https://m2.mtmt.hu/api/publication/33111245 ID - 33111245 N1 - Funding Agency and Grant Number: National Research, Development and Innovation Office [GINOP-2.3.2-15-2016-00060]; Hungarian Brain Research Program I and II [KTIA_13_NAP-A-III/7, 2017-1.2.1-NKP-2017-00002]; Ministry of Human Capacities, Hungary [20391-3/2018/FEKUSTRAT]; Ministry of Innovation and Technology of Hungary from the National Research, Development and Innovation Fund [TKP2021-EGA-32] Funding text: This project was supported by the National Research, Development and Innovation Office (GINOP-2.3.2-15-2016-00060) and by the Hungarian Brain Research Program I and II (Grant No. KTIA_13_NAP-A-III/7, and 2017-1.2.1-NKP-2017-00002). Support by the Ministry of Human Capacities, Hungary (grant 20391-3/2018/FEKUSTRAT) and the Ministry of Innovation and Technology of Hungary from the National Research, Development and Innovation Fund (TKP2021-EGA-32) is acknowledged. AB - 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. LA - English DB - MTMT ER - TY - CONF AU - Dukay, Brigitta AU - Bódai, Zsófia AU - Csefová, Alexandra AU - Hajdu, Petra AU - Ruppert, Zsófia AU - Penke, Botond AU - Fülöp, Lívia AU - Szabó, Kitti AU - Keller-Pintér, Anikó AU - Dux, László AU - Gombos, Imre AU - Török, Zsolt AU - Sántha, Miklós AU - Tóth, E. Melinda TI - A rendszeres testmozgás izom- és agyszövetre kifejtett nem-függő hatásainak vizsgálata a hiperlipidémia egérmodelljében T2 - 51. Membrán-Transzport Konferencia PY - 2022 PG - 1 UR - https://m2.mtmt.hu/api/publication/32908630 ID - 32908630 LA - Hungarian DB - MTMT ER - TY - JOUR AU - Váczi, Sándor AU - Barna, Lilla AU - Laczi, Krisztián AU - Tömösi, Ferenc AU - Rákhely, Gábor AU - Penke, Botond AU - Fülöp, Lívia AU - Bogár, Ferenc AU - Janáky, Tamás AU - Deli, Mária Anna AU - Mezei, Zsófia TI - Effects of sub-chronic, in vivo administration of sigma non-opioid intracellular receptor 1 ligands on platelet and aortic arachidonate cascade in rats JF - EUROPEAN JOURNAL OF PHARMACOLOGY J2 - EUR J PHARMACOL VL - 925 PY - 2022 PG - 10 SN - 0014-2999 DO - 10.1016/j.ejphar.2022.174983 UR - https://m2.mtmt.hu/api/publication/32801748 ID - 32801748 N1 - További támogatások: ÚNKP-20-3-SZTE-503; Richter Gedeon Nyrt. Centenáriumi Alapítvány 2020/K/21/2503 LA - English DB - MTMT ER - TY - JOUR AU - Bogár, Ferenc AU - Fülöp, Lívia AU - Penke, Botond TI - Novel Therapeutic Target for Prevention of Neurodegenerative Diseases: Modulation of Neuroinflammation with Sig-1R Ligands JF - BIOMOLECULES J2 - BIOMOLECULES VL - 12 PY - 2022 IS - 3 PG - 16 SN - 2218-273X DO - 10.3390/biom12030363 UR - https://m2.mtmt.hu/api/publication/32753552 ID - 32753552 LA - English DB - MTMT ER - TY - JOUR AU - Borbély, Emőke AU - Varga, Viktória AU - Szögi, Titanilla AU - Schuster, Ildikó AU - Bozsó, Zsolt AU - Penke, Botond AU - Fülöp, Lívia TI - 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 JF - INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES J2 - INT J MOL SCI VL - 23 PY - 2022 IS - 5 PG - 20 SN - 1661-6596 DO - 10.3390/ijms23052514 UR - https://m2.mtmt.hu/api/publication/32753550 ID - 32753550 N1 - Funding Agency and Grant Number: National Research, Development, and Innovation Office [GINOP-2.3.2-15-2016-00060]; Hungarian Brain Research Program I [KTIA_13_NAP-A-III/7, 2017-1.2.1-NKP-2017-00002]; Ministry of Innovation and Technology of Hungary from the National Research, Development and Innovation Fund [TKP2021EGA-32]; Hungarian Brain Research Program II [KTIA_13_NAP-A-III/7, 2017-1.2.1-NKP-2017-00002] Funding text: This project was supported by the National Research, Development, and Innovation Office (GINOP-2.3.2-15-2016-00060) and by the Hungarian Brain Research Program I and II-Grant No. KTIA_13_NAP-A-III/7, and 2017-1.2.1-NKP-2017-00002. Support by the Ministry of Innovation and Technology of Hungary from the National Research, Development and Innovation Fund (TKP2021EGA-32) is acknowledged. LA - English DB - MTMT ER -