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GeneExpression Systems & Appasani Research Conferences (ARCEI.ORG)
Jointly Presents

Inaugural
European Neurodegenerative Diseases-2010 Meeting
On
‘Biology to Drugs & Therapeutics’

September 20-21, 2010
Oriel College
University of Oxford, Oxford, United Kingdom

“A Unique Theme to Combine Neurobiology, Memory & Diseases”

Meeting Venue: Oriel College-Oxford University:   
When the quarrel between Henry II and Philip Augustus in 1167 made it impossible for English students to attend the University of Paris, the opportunity for developing a similar institution arose at Oxford. Dominican friars established their main house of study there on arrival in England in 1221 and were followed in 1224 by the Franciscans. Divinity was constituted as a superior faculty and students were admitted who already possessed an arts degree.

Oriel College founded in 1326 by King Edward II, this is the fifth oldest college at Oxford University and intended to help students who were already graduates to obtain a further degree. Past 684 years Oriel continued to maintain its intellectual standards, and admitted women for the first time in 1985. Oriel’s notable alumni include Sir Walter Raleigh, Thomas Harriot, Cecil Rhodes, Cardinal Newman, and two Nobel Laureates: Sir Alexander Todd (Chemistry), and James Meade (Economics).

Oriel always a place for higher learning, and authorities in various fields meet hear and share knowledge. Attend this meeting and be part of the rich heritage of education…….

Expected Maximum Capacity:
Target Audience 100
Total Speaker Presentations: 30
Total Poster Presentations: 15
Total Exhibit Booths: 15


Topics or Highlights of the Meeting:
Neurodevelopment & Mechanisms
Sensory & Motor Systems
Cognition & Behavior
Disorders of Nervous System
Drug Development



Focus of the Theme Meeting:

Brain diseases, in particular neurodegenerative diseases, represent a growing public health concern. Understanding the biology of neuronal cells (neurons) and their communication with neighboring cells at synapses is crucial in order to know the defects and pathophysiology of brain disorders. To discover and develop innovative drug compounds for these central nervous system diseases it is essential to gather intellectual minds from academia, biotech and pharmaceutical industries to have a forum. Such forum will enhance knowledge and dissipate of data and ideas which will ultimately bring more scientific and business collaborations.

The conference will bring together experts and young researchers with diverse backgrounds in molecular and cellular neurobiology, biochemistry, electrophysiology, behavior, cognition, perception, and disease biology, and the first conference discussing new developments in this highly interdisciplinary area of brain research. The conference should be interesting for graduate students, postdoctoral fellows, professors from academia and scientists, directors and executives from industry, as well as for anyone interested in brain functions and their associated diseases. Authorities in the filed will be invited as key speakers. Few speakers will be also selected from the applicants, based on the submitted abstracts. Dedicated time will be allowed for presentation of posters and viewing the exhibits and to know the available cutting-edge reagents, services in the field.

AGENDA/SPEAKERS

Monday, September 20, 2010
7:00 – 8:30 A.M: Registration Open
7:30 – 8:45 A.M: Continental breakfast
8:00 - 9:00 A.M: Technology Session I
10.00 AM – 6.00 PM Scientific Sessions

Tuesday, September 21, 2010
7:00 – 8:30 A.M: Registration Open
7:30 – 8:45 A.M: Continental breakfast
8:00 - 9:00 A.M: Technology Session I
10.00 AM – 6.00 PM Scientific Sessions


Scientific Committee:

Krishnarao Appasani, Ph.D., MBA
Founder & CEO
GeneExpression Systems, Inc, Waltham, MA, USA

Ioannis Ragoussis,PhD.
Head of Genomics
Wellcome Trust Centre for Human Genetics
University of Oxford, Oxford, UK

Keynote Speakers:

Anthony Monaco, MD, PhD
Pro-Vice-Chancellor & Professor of Human Genetics
University of Oxford-Wellcome Trust Ctr. for Human Genetics
Oxford, United Kingdom

Title: Genetic basis of neurological and psychiatric disorders

John Collinge, MD., FRS. 
Professor and Head
Dept. of Neurodegenerative Disease
UCL Institute of Neurology &
National Hospital for Neurology and Neurosurgery
London, United Kingdom

Title: Prion propagation and its wider implications in neurodegeneration
Joan Fallon, Ph.D.    Industry Keynote Speaker
Chief Executive Officer
Curemark LLC
Rye, NY USA
Title: Autism: Biology and drugs

Other Speakers:

Mart Saarma, PhD.                           
Academy Professor &
Director of the Institute of Biotechnology
University of Helsinki, Helsinki, Finland
Title: Biology and therapeutic potential of he new CDNF/MANF family of neurotrophic factors

Dr. Fred W. Van Leeuwen   
Professor of Neuroscience
Maastricht University Faculty of Health, Medicine and Life Sciences
Maastricht, The Netherlands
Title: Misframed proteins and protein quality control in Alzheimer’s and Parkinson’s disease

Giovanna Mallucci, MD., PhD.       
Professor at the MRC Toxicology Unit
University of Leicester
Leicester, UK
Title: TBA

Zoltán Molnár, MD., DPhil.                          
Professor of Developmental Neuroscience
Dept. of Physiology, Anatomy and Genetics
University of Oxford, Oxford, UK
Title: TBA

Per Svenningsson, MD., PhD.                   
Group leader
Dept.of Physiology and Pharmacology
Karolinska Institutet, Stockholm, Sweden
Title: TBA

Simon E. Fisher, D.Phil.                              
Royal Society Research Fellow &
Reader in Molecular Neuroscience
Wellcome Trust Centre for Human Genetics
University of Oxford, Headington, UK
Title: Functional genomic dissection of speech and language disorders

Inna Slutsky, PhD.                           
Professor of Physiology and Pharmacology
Sackler School of Medicine
Tel Aviv University, Tel Aviv, Israel
Title: Role of amyloid-beta in synaptic function of hippocampal neurons

Dr. Frederic Checler                       
Investigator
Institut de Pharmacologie Moléculaire et Cellulaire
UMR6097, Valbonne, France
Title: Parkin is a transcriptional repressor of p53

Clare E. Mackay, PhD.                     
Senior Research Fellow of Psychiatry
John Radcliffe Hospital & University of Oxford,
Headington, Oxford, UK
Title: Imaging risk for Alzheimer’s disease; the effect of age and APOE genotype on brain function

Gero Miesenböck, MD.
Waynflete Professor of Physiology
University of Oxford, Oxford, UK
Title: TBA

Liliana Minichiello, PhD.                             
Reader in Neuroscience and Molecular Biology
Deputy Director for the Centre for Neuroregeneration
University of Edinburgh, Edinburgh, Scotland
Title: Signaling pathways in LTP and learning

Stéphane Palfi, MD., PhD.   Sponsored by Oxford Biomedica, PLC
Principal Investigator & Professor
Henri Mondor Hospital & University of Paris 12
Créteil, France
Title:
ProSavin® a Gene Therapy for Parkinson's Disease

Anne Bertolotti, Ph.D.
Group Leader of Neurobiology
MRC Laboratory of Molecular Biology
Hills Road, Cambridge, UK
Title: TBA

 

Jan Grimm, PhD.                  
Chief Scientific Officer
Neurimmune Therapeutics AG
Schlieren, Switzerland
Title: Antibody therapy of neurodegenerative diseases

 

Kenneth J. Rhodes, Ph.D.              
Vice President, Discovery Neurobiology
Biogen Idec., Cambridge, MA, USA
Title: Repairing the Nervous System: Opportunities in Pain and MS

Dr. Susanne Aileen Funke                         
Institute of Structural Biology and Biophysics
Forschungszentrum Juelich GmbH
Julich, Germany
Title:Oral treatment with the Amyloid-β oligomer precipitating substance D3 improves pathology of Alzheimer’s transgenic mice

Dr. Marcello D'Amelio                                             
European Centre for Brain Research
Santa Lucia Foundation
Rome, 00143, Italy
Title: Non-apoptotic caspase-3 activity triggers synaptic degeneration in a mouse model of Alzheimer ’s disease

Martin R. Turner, MBBS, PhD.                  
Lady Edith Wolfson Clinician Scientist
Oxford University-John Radcliffe Hospital, Oxford, UK
Title: Biomarkers In Amyotrophic Lateral Sclerosis

 

Dr. Giuseppe Sciamanna                
European Center for Brain Research
Santa Lucia Foundation, Rome, taly
Title: Corticostriatal plasticity in transgenic animal models of DYT1 dystonia

Richard Wade-Martins, M.A., DPhil.                                  
Principal Investigator & University Lecturer
University of Oxford, Oxford, UK
Title: Molecular mechanisms of Parkinson's disease and gene therapy studies

Rebecca Pruss, PhD.                      
Chief Scientific Officer
Trophos, S.A, Marseille, France
Title: Where’s the target? Drug discovery strategies for neurodegenerative diseases

Jackie de Belleroche, PhD.,  DSc., FRCPath.     
Professor of Neuroscience at the Centre for Neuroscience
Imperial College London & Hammersmith Hospital
London, UK
Title: Amyotrophic Lateral Sclerosis: elucidating disease mechanisms

 

Exhibitors are welcome to reserve their booth space early!

Please contact if you are interested in speaking in the scientific or Technology workshops of this meeting.

GeneExpression Systems, Inc.
P.O. Box 540170
Waltham, MA 02454 USA
Tel: (781) 891-8181
Fax: (781) 891-8234
E-mail: Genexpsys@expressgenes.com
www.expressgenes.com

Poster Abstract Submission by July 20, 2010

All Abstracts


Title: Imaging risk for Alzheimer’s disease; the effect of age and
APOE genotype on brain function

Clare E. Mackay, PhD., Senior Research Fellow, University Dept of Psychiatry
Functional Magnetic Resonance Imaging Center (FMRIB), University of Oxford, John Radcliffe Hospital, Headington, Oxford, UK

Older age and carrying the APOE e4 gene are the best established risk factors for Alzheimer's Disease. Using functional magnetic resonance imaging (fMRI) we recently demonstrated that young healthy carriers of APOE e4 have increased brain activation compared to non-carriers in the same structures that show AD pathology decades later in life. We went on to investigate the differential effects of APOE genotype on brain aging and found clear differences, supporting the hypothesis that APOE e4 carriers have ‘accelerated aging’ compared to non-carriers. I will describe these studies and discuss the relevance of imaging at risk groups for understanding neurodegenerative disease.

Parkin is a transcriptional repressor of p53
Dr. Frederic Checler, Institut de Pharmacologie Moléculaire et Cellulaire
UMR6097, CNRS/UNSA, Valbonne, France
Frédéric Checler et Cristine Alves da Costa
IPMC et IN2M, UMR6097 CNRS/UNSA, Valbonne, France

Parkinson’s disease (PD) is characterized by exacerbated apoptosis. Several proteins responsible for genetic cases of PD control p53-dependent cell death. We recently showed that parkin, a protein responsible for most of autosomal recessive PD cases acts as a transcriptional regulator of the oncogene p531. We established that parkin physically interacts with p53 promoter and that such interaction is abolished by pathogenic mutations. Therefore, a novel parkin-mediated transcriptional function links p53 to familial PD.
1- Alves da Costa, C. et al. (2009). Nat. Cell. Biol. 11, 1370-1375

Functional genomic dissection of speech and language disorders
Simon E. Fisher, D.Phil.,
Royal Society Research Fellow, Reader in Molecular Neuroscience, Wellcome Trust Centre for Human Genetics, University of Oxford, Headington, UK

People who carry rare mutations in the FOXP2 gene have problems mastering the complex sequences of mouth movements needed for speech, along with deficits in many aspects of expressive and receptive language. The gene encodes a highly conserved transcription factor that appears to help regulate development and/or function of neuronal subpopulations in a wide range of non-speaking vertebrates. I will describe how FOXP2 can be used as a unique window into key neurogenetic pathways, through complementary approaches involving diverse model systems. For example, we have shown that FOXP2 point mutations implicated in human speech deficits cause impaired motor-skill learning and abnormal synaptic plasticity in mutant mice. Moreover, our functional genomic analyses of human neuronal cell models identified the CNTNAP2 gene as a direct downstream target regulated by FOXP2. Intriguingly, CNTNAP2 is itself implicated in common cases of language impairment. Overall, this work demonstrates how we can begin to bridge gaps between molecules, neurons and the brain to provide new understandings of aetiological pathways underlying human neurodevelopmental disorders.

Misframed proteins and protein quality control in Alzheimer’s and Parkinson’s disease
Dr. Fred W. Van Leeuwen, Maastricht University-Faculty of Health, Medicine and Life Sciences
Department of Neuroscience, Maastricht, The Netherlands

Sporadic forms of Alzheimer’s (AD) and Parkinson’s disease (PD) are the most frequent

types. They share a common feature: the accumulation of insoluble protein deposits. We focus on the significance of the ubiquitin-proteasome system (UPS) and the possible consequences of the accumulation of aberrant proteins for protein homeostasis. In AD, but not in PD we have found evidence for the occurrence and functional relevance of misframed proteins such as UBB+1.  UBB+1 is the result of the inaccurate conversion of monotonic sequences in the genome and its subsequent translation (“Molecular Misreading”, Science 279, 242-247, 1998) and inhibits the proteasome. I will discuss the relation between Aβ-plaque formation and UBB+1.

Oral treatment with the Amyloid-β oligomer precipitating substance D3 improves pathology of Alzheimer’s transgenic mice
Susanne Aileen Funke1, Thomas van Groen2, Inga Kadish2, Dirk Bartnik3; Luitgard Nagel-Steger3, Olexandr Brener3, Lei Wang1, Pia Zißmann3, Eva Birkmann1,3, Dieter Willbold1,3

1) ISB-3, Forschungszentrum Jülich, 52425 Jülich, Germany
2) Dep. Cell Biology and Dept. Neurobiology, University of Alabama, Birmingham, A.L. 35294-0006, USA
3) Institut für Physikalische Biologie, Heinrich Heine Universität Düsseldorf,  40225 Düsseldorf, Germany

Today, only palliative therapies for Alzheimer’s disease (AD) are available. The present study reports on in vitro and in vivo properties of the Aβ targeting d-enantiomeric amino acid peptide "D3". We show that next to plaque load and inflammation reduction, oral application of the peptide improved the cognitive performance of AD transgenic mice. In addition, we provide in vitro data elucidating a novel potential mechanism underlying the observed in vivo activity of D3.
Additionally, in a second part of the talk we will shortly report on an ultra-sensitive assay for the detection of Aβ aggregates in body fluids. 

Non-apoptotic caspase-3 activity triggers synaptic degeneration in a mouse model of Alzheimer ’s disease
Dr. Marcello D'Amelio, Assist. Prof. in Human Physiology,Medical School University Campus-Biomedico, Santa Lucia Foundation at European Centre for Brain Research , Rome, Italy

Synaptic loss in brain regions mediating memory is the major pathological correlate of cognitive decline in early stages of AD; yet, the molecular mechanisms underlying synaptic failure are largely unknown. I report a non-apoptotic baseline caspase-3 activity in hippocampal dendritic spines, and an enhancement of this activity at the onset of memory decline in the APPswe mouse model of AD. Caspase-3 increase leads to alterations of glutamatergic synaptic transmission and plasticity, and correlate with spine degeneration and a deficit in hippocampal-dependent memory. Importantly, pharmacological inhibition of caspase-3 activity in Tg2576 mice restores synaptic GluR1 levels, glutamatergic synaptic transmission, spine size, and improves memory function. These findings point to enhanced synaptic caspase-3 activation as a novel AD biomarker indicating possible avenues for selective pharmacological therapy during early stages of AD.

Biomarkers In Amyotrophic Lateral Sclerosis
Martin R. Turner, MBBS, MA, PhD, MRCP., MRC/MNDA Lady Edith Wolfson Clinician Scientist, Honorary Consultant Neurologist, Richard & Joan Doll Fellow, Green Templeton College, Oxford University-John Radcliffe Hospital, Oxford, UK

Amyotrophic lateral sclerosis (ALS) is a rapidly progressive degenerative disorder of cerebral motor cortex, corticospinal tract, brainstem and spinal anterior horn cell motor neurons. There is an established clinicopathological overlap with frontotemporal dementia and an emerging theme of aberrant RNA processing. The need for biomarkers in ALS is most urgently within therapeutic monitoring where survival is the primary endpoint in most clinical trials, but also as part of the diagnostic pathway to reduce the current average delay of one year from symptom onset. This presentation will discuss promising biomarker candidates emerging from MRI and biofluids (CSF and blood).

ProSavin® a Gene Therapy for Parkinson's Disease
Stéphane Palfi, MD., PhD., Principal Investigator & Professor, Henri Mondor Hospital and University of Paris 12, Faculty of Medicine, Paris, France

Abstract: Oral dopaminergic treatments have remained the primary standard of care for Parkinson’s disease (PD). Although highly efficacious in the early stages of disease they are associated with debilitating long term side effects that seriously impact on the quality of life and restrict the longevity of such treatment. We have developed a lentiviral vector (ProSavin®) derived from the equine infectious anaemia virus expressing the three key dopamine biosynthetic enzymes. ProSavin studies have demonstrated dopamine replacement and significant long term efficacy in a severe non human primate model following injection into the putamen. A phase I/II clinical trial to evaluate the safety and efficacy in late stage PD patients was initiated in France. A summary of the translation of ProSavin® from the bench to the clinic will be presented

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