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July 2-6, 2016 | Copenhagen, Denmark Organised by the Federation of European Neuroscience Societies (FENS) Hosted by the Danish Society for Neuroscience Where European Neuroscience meets the world 91298_FENS 2016_COVER.indd 2 8/06/16 11:15 POSTER PRESENTATION I Sunday July 3, 2016
89 POSTER PRESENTATION I – SUNDAY JULY 3, 2016 | POSTER PRESENTATION I SUNDAY JULY 3, 2016 BOARD NO INDEX NUMBER SESSION TIME: 09:30 - 13:00 PRESENTATION TIME: 11:30 - 13:00 Poster Area C012 EPOTHILONE-D RESCUES COGNITION AND ATTENUATES ALZHEIMER’S DISEASE-LIKE PATHOLOGY IN APP/PS1 MICE 301 J.J. Fernandez-Valenzuela, R. Sanchez-Varo, V. De Castro, F.J. Moyano, M.L. Vizuete, J.C. Davila, J. Vitorica, A. Gutierrez (Málaga, Spain) C013 AMYLOID-PLAQUES TOXICITY INCREASES DURING THE PROGRESSION OF ALZHEIMER'S DISEASE 302 C. Nunez Diaz, E. Sanchez-Mejias, R. Sanchez-Varo, L. Trujillo-Estrada, A. Gomez-Arboledas, J.C. Davila, J. Vitorica, A. Gutierrez (Málaga, Spain) C014 RECIPROCAL INFLUENCE BETWEEN APP EXPRESSION AND GLUCOSE METABOLISM IN THE HIPPOCAMPUS 303 M. Gloire, L. Ris, A. Villers (Mons, Belgium) C015 PICOMOLAR AMYLOID-BETA MODULATES SYNAPTIC PLASTICITY BY ACTING ON THE NO/CGMP/CREB PATHWAY 304 W. Gulisano, M. Melone, S. Giunta, C. Ripoli, D. Li Puma, C. Loreto, O. Arancio, C. Grassi, F. Conti, A. Palmeri, D. Puzzo (Catania, Italy) C016 AMYLOID-BETA PEPTIDE IS NEEDED FOR CGMP-INDUCED LONG-TERM POTENTIATION AND MEMORY 305 D. Puzzo, R. Ricciarelli, W. Gulisano, M.R. Tropea, C. Rebosio, O. Arancio, E. Fedele, A. Palmeri (Catania, Italy) C017 SORTILINS IN CELLULAR TRAFFICKING OF APOE 306 M. Holm, S. Glerup, K. Weyer (Aarhus, Denmark) C018 HEPARAN SULFATES ARE INVOLVED IN AMYLOIDOSIS AND NEUROINFLAMMATION IN TRANSGENIC MOUSE MODELS OF ALZHEIMER DISEASE 307 C. Jendresen, H. Cui, X. Zhang, I. Vlodavsky, L. Nilsson, J. Li (Oslo, Norway) DISORDERS OF THE NERVOUS SYSTEM: C.2.A PARKINSON’S DISEASE - GENETIC DETERMINANTS C019 MUTATIONS IN PARKINSON’S DISEASE COMMON GENES ARE RARE IN A POPULATION OF SAUDI PATIENTS AS REVEALED BY WHOLE-EXOME SEQUENCING 308 B. Al-Mubarak, E. Alyemni, D. Monies, M. Abouelhoda, S. Bohlega, T. Alkhairallah, E. Goljan, M. Al Breacan, R. Albar, A. Magrashi, M. AlTurki, B. AlTawil, B. Alsaffar, A. Almusaiab, S. Bin Ghadir, L. Bahour, L. Alshakmobarak, H. Abou Al-Shaar, M. ElKalioby, N. Al Tassan (Riyadh, Kingdom of Saudi Arabia) C020 GENOME WIDE ASSESSMENT OF PARKINSON’S DISEASE IN A SOUTHERN SPANISH POPULATION 309 R. Duran Ogalla, S. Bandres-ciga, T.R. Price, F. Barrero, F. Escamilla-sevilla, J. Pelegrina, S. Arepalli, D. Hernandez, B. Gutierrez, J. Cervilla, M. Rivera, A. Rivera, J. Ding, M. Nalls, A. Singleton, F. Vives (Granada, Spain) C021 DOMINANT NEGATIVE VARIANT OF THE DOPAMINE TRANSPORTER ASSOCIATE WITH EARLY-ONSET PARKINSONISM AND PSYCHIATRIC DISEASE 310 F. Hansen, T. Skjørringe, N. Arends, K. Erreger, L. Friberg, A. Galli, L. Møller, L. Hjermind, U. Gether (København, Denmark) C022 NON-CODING RNAS AND THEIR REGULATION OF ALPHA-SYNUCLEIN IN VIVO IN A PARKINSON’S DISEASE MODEL 311 M. Jakobsen, T.B. Hansen, J. Jakobsson, N. Casadei, O. Riess, M. Romero-Ramos, J. Kjems (Aarhus, Denmark) C023 IDENTIFICATION OF MULTIPLE QTLS LINKED TO NEUROPATHOLOGY IN THE ENGRAILED1 HETEROZYGOUS MOUSE MODEL OF PARKINSON'S DISEASE 312 M. Jewett, Z. Kurowska, P.L. Brattås, I.J. Ferrer, X. Kenez, T. Björklund, U. Nordstöm, P. Brundin, M. Swanberg (Lund, Sweden) C024 MHCIIMEDIATED EFFECTS ON MICROGLIAL ACTIVATION AND DOPAMINERGIC NEURODEGENERATION INDUCED BY OVEREXPRESSION OF ALPHA-SYNUCLEIN 313 I. Jimenez Ferrer, M. Jewett, A. Tontanahal, M. Romero-Ramos, M. Swanberg (Lund, Sweden) C025 HOW DOES THE LOSS OF FBXO7 IN MYELINATING CELLS CONTIBUTE TO PARKINSONISM? 314 S. Joseph, S. Vingil, W. Möbius, K.A. Nave, J. Stegmüller (Göttingen, Germany) C026 VALIDATION OF CIRS-7 AS A TARGET FOR REGULATION OF ALPHA-SYNUCLEIN EXPRESSION IN PRIMARY NEURONS IN VITRO 315 R. Mouridsen, M. Jakobsen, T.B. Hansen, J. Kjems (Aarhus, Denmark) C027 ANALYSIS OF THE ROLE OF MICRORNAS IN AN ALPHA-SYNUCLEIN OVEREXPRESSION MOUSE MODEL 316 R. Petri, K. Pircs, M. Matusiak-Brueckner, J. Malmevik, J. Jakobsson (Lund, Sweden) C028 PARKIN REGULATES KAINATE RECEPTORS CONTAINING THE GLUK2 SUBUNIT 317 G.M. Serratto, J. Sassone, M. Passafaro, A. Ciammola (Milano, Italy) C029 GENE EXPRESSION CHANGES WITHIN THE HUMAN SUBTHALAMIC NUCLEUS DURING PARKINSON'S DISEASE 318 X.H. Wu, S. Reid, H. Waldvogel, R. Faull (Auckland, New Zealand)
EPOTHILONE-D RESCUES COGNITION AND ATTENUATES ALZHEIMER’S DISEASE-LIKE PATHOLOGY IN APP/PS1 MICE Fernandez-Valenzuela JJ.1, Sanchez-Varo R.1, De Castro V.1, Moyano FJ2, Vizuete M2, Davila JC1, Vitorica J.2 and Gutierrez A.1 1Dept. Cell Biology, Genetics and Physiology, Faculty of Sciences, University of Malaga. IBIMA. CIBERNED. Malaga, Spain. 2Dept. Biochemistry and Molecular Biology, Faculty of Pharmacy, University of Seville. IBIS. CIBERNED. Seville, Spain. AIMS: Cognitive decline in Alzheimer's disease (AD) patients has been linked to synaptic damage and neuronal loss. Hyperphosphorylation of tau protein destabilizes microtubules leading to the accumulation of autophagy/vesicular material and the generation of dystrophic neurites, thus contributing to axonal/synaptic dysfunction. In this study, we analyzed the effect of a microtubule-stabilizing compound in the progression of the disease in the hippocampus of APP751SL/PS1M146L transgenic model. METHODS: APP/PS1 mice (3 month-old) were treated with a weekly intraperitoneal injection of 2 mg/kg epothilone-D (Epo-D) for 3 months. Vehicle-injected animals were used as controls. Mice were tested on the Morris water maze, Y-maze and objectrecognition tasks for memory performance. Abeta, AT8, ubiquitin and synaptic markers levels were analyzed by Western-blots. Hippocampal plaque, synaptic and dystrophic loadings were quantified by image analysis after immunohistochemical stainings. RESULTS: Epo-D treated mice exhibited a significant improvement in the memory tests compared to controls. The rescue of cognitive deficits was associated to a significant reduction in the AD-like hippocampal pathology. Levels of Abeta, APP and ubiquitin were significantly reduced in treated animals. This was paralleled by a decrease in the amyloid burden, and more importantly, in the plaque-associated axonal dystrophy pathology. Finally, synaptic levels were significantly restored in treated animals compared to controls. CONCLUSION: Epo-D treatment promotes synaptic and spatial memory recovery, reduces the accumulation of extracellular Abeta and the associated neuritic pathology in the hippocampus of APP/PS1 model. Therefore, microtubule stabilizing drugs could be considered therapeutical candidates to slow down AD progression. Supported by FIS-PI12/01431 and PI15/00796 (AG), FIS-PI12/01439 and PI15/00957(JV), co-financed by FEDER funds from European Union.
