Poster Presentations

Thursday, March 12 – Friday, March 13 ,2009

TAU, Cytoskeleton and Tauopathies:

INTERACTION BETWEEN TOXIC AMYLOID-BETA OLIGOMERS AND TAU IN THE INDUCTION OF ALZHEIMER PHENOTYPE
J. Brouillette¹, I. Kuperstein², A. Van der Jeugd³, D. Blum¹, R. d'Hooge³, B. De Strooper², L. Buée^1
1INSERM U837, Lille, France, ²Center for Human Genetics, Leuven, Belgium, ³Katholieke Universiteit Leuven, Leuven, Belgium

THE NPC1/P301L-MOUSE
S. Zonnur¹, V. Meske¹, J. Götz², T. Ohm^1
1Institut für Integrative Neuroanatomie, Klinische Zell- und Neurobiologie, Berlin, Germany, ²Brain and Mind Research Institute, Alzheimer's and Parkinson's Disease Laboratory, Sydney, Australia

GENDER-DEPENDENT NEUROGENERATIVE ROLE OF CHRONIC STRESS IN P301L TAU TG MICE
I. Sotiropoulos¹, T. Kimura¹, N. Sahara¹, O.F.X. Almeida², A. Takashima^1
1RIKEN Brain Science Institute, Laboratory for Alzheimer's Disease, Wako, Japan, ²Max Planck Institute of Psychiatry, Neuroadaptations Group, Munich, Germany

HIGH-YIELD PURIFICATION OF FETAL TAU PRESERVING ITS STRUCTURE AND PHOSPHORYLATION PATTERN
M. Handzusova¹, N. Ivanovova¹, P. Novak¹, J. Hanes², M. Novak^1
1Institute of Neuroimmunology, Slovak Academy of Sciences, Bratislava, Slovakia, ²Axon Neuroscience, Vienna, Austria

PHOSPHORYLATION REGULATES THE ASSOCIATION OF TAU WITH MEMBRANES
A. Pooler, D. Hanger
King's College London, Neuroscience, London, United Kingdom

PIN1 INVOLVEMENT IN MODULATION OF TAU PHOSPHORYLATION IN A CELLULAR MODEL OF ALZHEIMER DISEASE
A. Bulbarelli, E. Lonati, E. Cazzaniga, A. Aldeghi, M. Masserini
University of Milano-Bicocca, Department of Experimental Medicine, Monza, Italy

MULTIFACETED FOLDING OF PHF CORE TAU AFTER BINDING TO MONOCLONAL ANTIBODIES: IMPLICATIONS FOR PHF FORMATION
Z. Flachbartova, M. Bartkova, B. Kovacech, A. Kovac, E. Kontsekova, R. Skrabana, M. Novak
Institute of Neuroimmunology, Bratislava, Slovakia

MULTI-SITE PHOSPHORYLATION ASSAYS FOR TAU PROTEIN
M. Ward, E. Schofield, A. Hye, H. Byers
Proteome Sciences plc, London, United Kingdom

MONOCLONAL ANTIBODY DC40 REVEALS THE DIRECT INTERACTION BETWEEN THE PRO-RICH REGION AND THE MICROTUBULE BINDING DOMAIN OF TAU
M. Bartkova, B. Kovacech, R. Skrabana, M. Novak
Institute of Neuroimmunology, Bratislava, Slovakia

HOOK PROTEINS ARE ASSOCIATED WITH TAU PATHOLOGY OF ALZHEIMER`S DISEASE AND MODULATE INTRACELLULAR TRANSPORT
L. Herrmann, T. Arendt, M. Holzer
University of Leipzig, Paul Flechsig Institute of Brain Research, Leipzig, Germany

SECRETAGOGIN AND NEUROPROTECTION (TAU) IN ALZHEIMER´S DISEASE; HUMAN AND TRANSGENIC MOUSE (P301L) STUDIES
J. Attems¹, M. Heikenwalder², M. Grosinger-Quass¹, A. Aguzzi², L. Wagner³, R. Nitsch⁴, F. Lintner¹, K. Jellinger^5
1Otto Wagner Hospital, Institute for Pathology, Vienna, Austria, ²University Hospital of Zurich, Institute for Neuropathology, Zurich, Switzerland, ³Medical University of Vienna, Department of Medicine III, Vienna, Austria, ⁴University Hospital of Zurich, Division of Psychiatry Research, Zurich, Switzerland, ⁵Institute for Clinical Neurobiology, Vienna, Austria

THE UNFOLDED PROTEIN RESPONSE IS ACTIVATED IN PRETANGLE NEURONS IN ALZHEIMER'S DISEASE HIPPOCAMPUS
J. Hoozemans¹, E. van Haastert¹, D. Nijholt², A. Rozemuller¹, P. Eikelenboom³, W. Scheper^2
1VU University Medical Center, Department of Pathology, Amsterdam, Netherlands, ²Academic Medical Center, Neurogenetics Laboratory, Amsterdam, Netherlands, ³VU University Medical Center, Department of Psychiatry, Amsterdam, Netherlands

(DE)PHOSPHORYLATION OF TAU - AN IN VITRO NMR STUDY
I. Landrieu¹, L. Amniai¹, P. Barbier², J. Louis³, J. Goris³, V. Peyrot², V. Janssens³, G. Lippens^1
1CNRS UMR 8576, Villeneuve d'Ascq, France, ²Université de Marseille/Faculté de Pharmacie, Marseille, France, ³Katholieke Universiteit Leuven, Leuven, Belgium

DISSOCIATION OF SYNAPTIC DYSFUNCTION AND BEHAVIOR IN A TAUOPATHY MOUSE MODEL (PRP-MAPT) OF ALZHEIMER'S DISEASE
R. Crozier, N. Breysse, R. Hosszu, M. Bowlby, J. Bard
Wyeth Research, Neuroscience, Princeton, United States

ENDOGENOUSLY OVERPRODUCED Aβ CAUSES CELL DEATH  IN NGF-DEPRIVED HIPPOCAMPAL NEURONS VIA EARLY TAU HYPERPHOSPHORYLATION
G. Amadoro¹, V. Corsetti¹, M. Ciotti¹, F. Florenzano¹, S. Capsoni², G. Amato², P. Calissano^1
1CNR, Department of Neurobiology and Molecular Medicine, Rome, Italy, ²European Brain Research Institute, Rome, Italy

APOLIPOPROTEIN E DEFICIENCY ENHANCES TAU HYPERPHOSPHORYLATION IN P301L MUTANT HUMAN TAU MICE
F. Gloeckner, V. Meske, T.-G. Ohm
Center for Anatomy, Charité, Institute of Integrative Neuroanatomy, Berlin, Germany

RELATIONSHIP BETWEEN TAU PHOSPHORYLATION STATUS AND AGITATION AND AGGRESSION IN ALZHEIMER'S DISEASE
S. Guadagna, R. J. Williams, P. T. Francis
King's College London, London, United Kingdom

EFFECTS OF HSP90 INHIBITORS ON TAU HYPERPHOSPHORYLATION IN NEURONS
C. Volbracht¹, R.M. Bailey², J. Lewis^2
1H. Lundbeck A/S, Molecular Neurobiology, Valby, Denmark, ²Mayo Clinic College of Medicine, Department of Neuroscience, Jacksonville, United States

REGULATION OF TAU SPLICING BY FACTORS LOCATED ON CHROMOSOME 21
A. Andreadis¹, L. Gao¹, S.-W. Tse¹, S. Stamm^2
1University of Massachusetts Medical School, Cell Biology, Worcester, United States, ²University of Kentucky, Biochemistry, Lexington, United States

STRUCTURAL POLYMORPHISM OF 441-RESIDUE TAU AT SINGLE RESIDUE RESOLUTION
M. Mukrasch¹, S. Bibow¹, J. Korukottu¹, S. Jeganathan², J. Biernat², C. Griesinger¹, E. Mandelkow², M. Zweckstetter^3
1Max Planck Institute for Biophysical Chemistry, Göttingen, Germany, ²Max Planck Unit for Structural Molecular Biology, Hamburg, Germany, ³Max Planck Institute for Biophysical Chemistry, NMR-based Structural Biology, Göttingen, Germany

TAU PHOSPHORYLATION AND NEURONAL APOPTOSIS INDUCED BY THE BLOCKADE OF PP2A INVOLVE GSK3β
L. Martin, A. Magnaudeix, M. Crochetet, C. Wilson, F. Terro
Faculté de médecine, Limoges, France

PP2A ACTIVATES THE ANTI-APOPTOTIC FUNCTION OF BCL-2, WHILE THE DEPHOSPHORYLATION OF TAU BY PP2A FACILITATES APOPTOSIS
X.-A. Liu
Tongji Medical College, Hua-Zhong University of Science and Technology, Pathophysiology Department, Wuhan, China

PROTEASOME INHIBITION INDUCED RE-LOCALIZATION AND AGGREGATION OF TDP-43 IN NEURONAL CELLS
J. van Eersel¹, Y.D. Ke¹, M. Bi¹, J. Kril², J. Götz¹, L.M. Ittner^1
1University of Sydney, Brain & Mind Research Institute, Sydney, Australia, ²University of Sydney, Department of Pathology, Sydney, Australia

MICROTUBULE-STABILIZING EFFECT OF NOTCH ACTIVATION IN PRIMARY CORTICAL NEURONS
G. Ferrari-Toninelli, S.A. Bonini, P. Bettinsoli, D. Uberti, M. Memo
University of Brescia, Department of Biomedical Sciences and Biotechnologies, Brescia, Italy

AUTOPHOSPHORYLATION OF JNK3: POTENTIAL ROLES IN TAU PHOSPHORYLATION AND DYNAMICS
S. Braithwaite, J. Moore, V. Anand, B. Ludwig, S. Nawoschik, P. Reinhart, W. Hirst, J. Dunlop
Wyeth Research, Neuroscience, Princeton, United States

MODELING TAUOPATHIES USING PORE-FORMING AGENT POLY-APS FOR EFFECTIVE INTRANEURONAL DELIVERY OF EXOGENOUS TAU PROTEIN
A. Mietelska-Porowska¹, D. Koss², M. Baksalerska-Pazera¹, B. Platt², R. Scott², G. Niewiadomska^1
1Nencki Institute of Experimental Biology PAS, Warsaw, Poland, ²Institute of Medical Sciences, University of Aberdeen, Aberdeen, United Kingdom

ASSOCIATION OF CORTICOBASAL DEGENERATION AND HUNTINGTON'S DISEASE: CAN TAU AGGREGATES PROTECT HUNTINGTIN TOXICITY?
D. Caparros-Lefebvre¹, O. Kerdraon², D. Devos³, C.-M. Dhaenens², D. Blum², A. Delacourte², C.-A. Maurage², L. Buee², B. Sablonniere^2
1Centre Hospitalier, Valenciennes, France, ²Inserm, U837, Lille, France, ³CHR, Lille, France

EARLY ONSET FAMILIAL ALZHEIMER-TYPE DEMENTIA ASSOCIATED WITH NEUROFIBRILLARY DEGENERATION AND SUBCORTICAL GLIAL TAU PATHOLOGY
O. Kalev, G. Kovacs, H. Budka
Institute of Neurology/Medical University Vienna, Vienna, Austria

HUMAN TRUNCATED TAU PROTEIN INDUCES MITOCHONDRIAL DAMAGE AND OXIDATIVE STRESS IN A RODENT MODEL OF TAUOPATHY
M. Cente, P. Filipcik, M. Novak
Institute of Neuroimmunology, Bratislava, Slovakia

PREVENTION OF NON-NATIVE DISULPHIDE BRIDGES FORMATION IN TAU PROTEIN WITHOUT THE USE OF REDUCING AGENT
G. Krajciova¹, R. Skrabana¹, J. Kucerak¹, A. Opattova¹, P. Filipcik², M. Novak^1
1Institute of Neuroimmunology, Neuroscience, Bratislava, Slovakia, ²Axon Neuroscience, Vienna, Austria

NEURONAL ELAV PROTEINS AS A NEW TARGET FOR BETA-AMYLOID: IMPLICATIONS FOR ALZHEIMER'S DISEASE
M. Amadio, S. Govoni, A. Pascale
University of Pavia, Exptl. and Appl. Pharmacology Department, Pavia, Italy