TY  - JOUR
AU  - Kecskés, Szilvia
AU  - Mészáros, Mária
AU  - Dvorácskó, Szabolcs
AU  - Szabó, Írisz
AU  - Porkoláb, Gergő
AU  - Barna, Lilla
AU  - Harazin, András
AU  - Szecskó, Anikó
AU  - Menyhárt, Ákos
AU  - Bari, Ferenc
AU  - Deli, Mária Anna
AU  - Penke, Botond
AU  - Farkas, Eszter
AU  - Veszelka, Szilvia
TI  - The impact of the novel sigma1 receptor ligand (S)-L1 on brain endothelial cells and cerebrovascular reactivity challenged by ischemia
JF  - EUROPEAN JOURNAL OF PHARMACOLOGY
J2  - EUR J PHARMACOL
VL  - 1000
PY  - 2025
PG  - 10
SN  - 0014-2999
DO  - 10.1016/j.ejphar.2025.177724
UR  - https://m2.mtmt.hu/api/publication/36150231
ID  - 36150231
N1  - Funding Agency and Grant Number: National Research, Development and Innovation Office of Hungary [PD139012, FK143233, K146725]; EU's Horizon 2020 research and innovation program [739593]; Ministry of Innovation and Technology of Hungary; National Research, Development and Innovation Fund [TKP2021-EGA-28, TKP2021-EGA]; Janos Bolyai Research Scholarship of the Hungarian Academy of Sciences;  [GINOP-2.3.2-15-2016-00060];  [K134334]
            Funding text: This work was supported by the National Research, Development and Innovation Office of Hungary, (grant numbers GINOP-2.3.2-15-2016-00060, K134334, PD139012, FK143233, K146725) ; The EU's Horizon 2020 research and innovation program grant number 739593; the Ministry of Innovation and Technology of Hungary and the National Research, Development and Innovation Fund (grant number TKP2021-EGA-28 financed under the TKP2021-EGA funding scheme) , and the Janos Bolyai Research Scholarship of the Hungarian Academy of Sciences.
AB  - 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.
LA  - English
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  - 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  - Kristó, Katalin
AU  - Csík, Elvira
AU  - Sebők, Dániel
AU  - Kukovecz, Ákos
AU  - Sovány, Tamás
AU  - Regdon, Géza (ifj.)
AU  - Pannonhalminé Csóka, Ildikó
AU  - Penke, Botond
AU  - Hódi, Klára
TI  - Effects of the controlled temperature in the production of high-shear granulated protein-containing granules
JF  - POWDER TECHNOLOGY
J2  - POWDER TECHNOL
VL  - 395
PY  - 2022
SP  - 758
EP  - 765
PG  - 8
SN  - 0032-5910
DO  - 10.1016/j.powtec.2021.10.003
UR  - https://m2.mtmt.hu/api/publication/32473079
ID  - 32473079
N1  - Institute of Pharmaceutical Technology and Regulatory Affairs, University of Szeged, Eötvös u. 6., Szeged, H-6720, Hungary            
            Department of Applied and Environmental Chemistry, Interdisciplinary Excellence Centre, University of Szeged, Rerrich B tér 1, Szeged, H-6720, Hungary            
            Department of Medical Chemistry, University of Szeged, Dóm tér 8, Szeged, H-6720, Hungary            
            Export Date: 21 June 2022            
            CODEN: POTEB            
            Correspondence Address: Kristó, K.; Institute of Pharmaceutical Technology and Regulatory Affairs, Eötvös u. 6., Hungary; email: kristo.katalin@szte.hu
LA  - English
DB  - MTMT
ER  - 

TY  - JOUR
AU  - Váczi, Sándor
AU  - Barna, Lilla
AU  - Harazin, András
AU  - Mészáros, Mária
AU  - Porkoláb, Gergő
AU  - Zvara, Ágnes
AU  - Ónody, Rita
AU  - Földesi, Imre
AU  - Veszelka, Szilvia
AU  - Penke, Botond
AU  - Fülöp, Lívia
AU  - Deli, Mária Anna
AU  - Mezei, Zsófia
TI  - S1R agonist modulates rat platelet eicosanoid synthesis and aggregation
JF  - PLATELETS
J2  - PLATELETS
VL  - 33
PY  - 2022
IS  - 5
SP  - 709
EP  - 718
PG  - 10
SN  - 0953-7104
DO  - 10.1080/09537104.2021.1981843
UR  - https://m2.mtmt.hu/api/publication/32491017
ID  - 32491017
AB  - Sigma-1 receptor (S1R) is detected in different cell types and can regulate intracellular signaling pathways. S1R plays a role in the pathomechanism of diseases and the regulation of neurotransmitters. Fluvoxamine can bind to S1R and reduce the serotonin uptake of neurons and platelets. We therefore hypothesized that platelets express S1R, which can modify platelet function. The expression of the SIGMAR1 gene in rat platelets was examined with a reverse transcription polymerase chain reaction and a quantitative polymerase chain reaction. The receptor was also visualized by immunostaining and confocal laser scanning microscopy. The effect of S1R agonist PRE-084 on the eicosanoid synthesis of isolated rat platelets and ADP- and AA-induced platelet aggregation was examined. S1R was detected in rat platelets both at gene and protein levels. Pretreatment with PRE-084 of resting platelets induced elevation of eicosanoid synthesis. The rate of elevation in thromboxane B2 and prostaglandin D2 synthesis was similar, but the production of prostaglandin E2 was higher. The concentration-response curve showed a sigmoidal form. The most effective concentration of the agonist was 2 µM. PRE-084 increased the quantity of cyclooxygenase-1 as detected by ELISA. PRE-084 also elevated the ADP- and AA-induced platelet aggregation. S1R of platelets might regulate physiological or pathological functions. © 2021 Taylor & Francis Group, LLC.
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  - 

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  - 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  - 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  - 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  -