A Biochemical Society Focused Meeting

Proceedings (invited speakers) will be published in .

Abstract deadline: 5 November 2009.

Online abstract submission is now closed. If you wish to submit an abstract please contact the Conference Office. Late abstracts will not appear in the programme book.

Oral communication slots are available at this meeting. All attendees, particularly researchers in the early stages of their career, are invited to submit a poster abstract for consideration as an oral communication.

Student Travel Grants are available for this meeting.

ASN NEURO kindly sponsored a poster prize of £250 for the best posters displayed at the meeting. The prize was awarded to Tara Caffrey (University of Oxford, UK).

The Alzheimer's Society kindly sponsored a £250 prize for the best oral communication - selected from abstracts - presented at the meeting. The prize was awarded to Kunie Ando (Free University of Brussels, Belgium).
 

Meeting Background

Alzheimer’s Disease (AD), is a progressive, increasingly common neurodegenerative condition without an available treatment. This is mainly due to our limited understanding of the pathogenic mechanisms that underlie this condition. It is characterized by two pathological hallmarks: the neuritic plaques made up of amyloid beta protein and the neurofibrillary tangles made up hyper-phosphorylated Tau protein. Familial forms of AD have invariably pointed to abnormalities in the amyloid peptide and as a result much of the research activity in this field has focused on understanding the mechanisms that underlie amyloid mediated toxicity and possible therapeutics. More recently however, the contribution of the intraneuonal tangles and related  tangle pathology has been recognized, as it has been shown that aberrant Tau regulation and function is sufficient to cause more than one type of neurodegenerative disease. In addition, the putative relationship between the amyloid and Tau pathologies have attracted considerable attention. It is now believed that in AD, amyloid pathology precedes Tau pathology and that Tau mediated toxicity may ultimately give rise to neuronal dysfunction and loss which manifests in the clinical symptoms of dementia. However, the precise role of Tau in the pathology of the various behaviourally and neuropathologically distinct tauopathies, the mechanisms of Tau toxicity and the potential functional interaction of Tau and amyloid in AD remain elusive. Nevertheless, novel observations regarding the various aspects of Tau-misregulation-dependent pathogenesis are emerging from various cellular, vertebrate and invertebrate animal models including rodents, C. elegans and Drosophila and supported by emerging human data.

We have organized a Focused Meeting bringing together scientists working on tauopathies utilizing divergent approaches and models. The small residential setting of the meeting will be conducive to formal and informal discussions and delegates will have the opportunity to exchange ideas with fellow scientists working on various aspects of tauopathies in a range of systems and models. Our confirmed speakers include Professor Jesus Avila, Professor Jean-Pierre Brion, Professor Luc Buee, Professor Frank LeFarla, Professor Khalid Iqbal, Professor Eckhard Mandelkow, Professor Eva Mandelkow Dr. Amrit Mudher, Dr. Makis Skoulakis and Professor Maria Spillantini.

Topics to include:

The biochemistry and processing of Tau in physiological and pathological conditions. 

Pathololgical mechanisms including axonal transport disruption, filament formation, synaptic dysfunction and others.

Tau and b interactions.