Monday, 23 June 2014
Cineworld: The O2, London, SE10 0DX, UK
Currently, there are many biomarkers for diagnosis of Alzheimer’s disease. However most of them do not provide consistent results. This event will discuss current research aimed at obtaining reliable biomarkers which could be used to diagnose Alzheimer’s disease at very early stage and also to provide objective and reliable measures of disease progress.
The deadline for abstract submissions for oral presentation is March 10th 2014.
Abstracts for poster presentation only can be submitted up to two weeks before the event. You can download the instructions for authors at www.euroscicon.com/AbstractsForOralAndPosterPresentation.pdf
Why have we failed to cure AD
Professor Amos Korczyn, Professor Emeritus, Tel-Aviv University Medical School, Israel
Attempts to find cure for Alzheimer’s disease (AD) have failed so far, in spite of enormous investments, intellectual and financial. It is unlikely that attacking a downstream phenomenon, like apoptosis or beta-amyloid, can cure AD, or prevent its progression. Senile dementia is the result of a combination of several processes. Epidemiological studies have identified many risk factors, some genetic but most environmental and therefore modifiable. Therefore a concerted action to fight the dementia epidemic must be made by aggressive action against its risk factors, and this battle must begin in midlife, not in old age.
The biomarkers assessment in a Memory Clinic : is there any added value
Professor Adrian Ivanoiu, MD, PhD, neurologist, Saint Luc University Hospital & Institute of Neuroscience, Catholic University of Louvain, Brussels, Belgium
Patients with mild cognitive impairment consulting a Memory Clinic are at risk of developing Alzheimer disease (AD), although it remains difficult to make an accurate prediction only on the basis of the cognitive examination. For a more precise diagnosis biological markers for AD have been developed and consist in a biological analysis of the cerebrospinal fluid and brain imaging by MRI and PET. They witness either an abnormally high deposition of βamyloid peptide in the brain or an early neuronal and synaptic damage related to neurodegeneration. Although many biomarkers are now available the method lacks of standardization and validation particularly in unselected clinical populations.
Cerebrospinal fluid Presenilin-1: a potential new biomarker for Alzheimer’s disease
Dr Javier Sáez-Valero, Professor and Group Leader, Instituto de Neurociencias de Alicante, Universidad Miguel Hernández-CSIC, & Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Spain
Presenilin-1 (PS1) is the active component of the γ-secretase complex, and its presence in cerebrospinal fluid (CSF) has not been measured to date. Recently we have demonstrated that PS1 is present in CSF as 100–150-kDa hetero-complexes containing both the N- and C-terminal fragments of the protein, as well other γ-secretase components, but differ from active γ-secretase membrane-complexes. Particularly, the levels of the highly stable PS1 complexes are increased in CSF samples from Alzheimer’s disease (AD) cases, suggesting potential value as a biomarker for AD. Estimation of PS1 CSF levels may be useful to challenge the disease-modifying effects of newer Alzheimer’s therapy.
Investigation of novel functional and metabolic MRI biomarkers for the preclinical assessment of taupathology in AD
Dr Niall Colgan, Research Associate, UCL Centre for Advanced Biomedical Imaging, London UK
A key neuropathological hallmark of Alzheimers Disease(AD) is the presence of intracellular neurofibrillary tangles(NFTs) of hyperphosphorylated Tau protein. There is a need for greater understanding of the relationship between tau burden and non-invasive imaging data for improved diagnosis and therapeutic assessment of this devastating disease. In this work, a mouse model of tauopathy was used to investigate how elevated tau expression affects the clinically implementable MRI parameters: i) cerebral blood flow (CBF) using arterial spin labelling (ASL) ii) amide proton transfer(APT) using chemical exchange saturation transfer (CEST) iii) brain glucose metabolism using glucoCEST iv) the diffusion properties of tissue water using diffusion tensor imaging (DTI) v) brain morphology using high resolution 3D structural imaging with tensor based morphometry (TBM). This is the first application of ASL, CEST and DTI to the tauopathy as well as glucoCEST to investigate neurodegenerative disease.
Eye movement biomarkers in Alzheimer’s disease
Dr Olivier Coubard, The Neuropsychological Laboratory, Paris, France