Alzheimer’s disease is characterized by diminishing memory and thinking skills, affecting as many as 8 million Europeans, most over the age of 60. The causes of Alzheimer’s disease are still largely unknown, though they are likely a combination of genetic, environmental and other factors.
As part of ongoing research to better understand the complexities of the human brain, European‐funded FP7‐HEALTH AgedBrainSYSBIO consortium (on systems biology, synapse and ageing) is embarking on efforts to unravel molecular mechanisms involved in brain functioning both in normal conditions and during ageing.
We expect that this meeting will generate novel interactions between leading groups in the field. Because of the increasing interest in ageing‐related diseases such as neuropathologies, we expect the symposium to gather up to 150 participants. This symposium will bring together clinicians, biologists, bioinformaticians, statisticians, who will present the latest advances in the field of neuroscience, taking advantage of state‐of‐the‐art approaches provided by omics‐biotechnologies, supercomputers, neuroimaging, amongst others.
The meeting will survey recent discoveries in the field of normal and pathological brain ageing: from systems biology to the clinic.
The Keynote lecture will summarise clinical insights on normal and pathological ageing
Session I: Synapses and ageing ‐ Mechanisms governing establishment, functioning and plasticity of synapses are essential to development of adapted behaviour. Alterations in the synaptic molecular machinery are involved in diverse age‐related cognitive disorders, including Alzheimer's disease, which increasingly appears as a synaptopathy. This session will illustrate recent advances, through diverse approaches including cellular imaging, electrophysiology, genomics, and genetics in deciphering the molecular processes involved in normal and pathological synaptic function, and particularly in Alzheimer's disease.
Session II: Systems Biology session ‐ Alzheimer's Disease is a complex pathology. Both its aetiology and the development of symptoms involve a large number of molecular partners. Genetic analyses have revealed that the large number of genes carrying an accrued risk actually encode for proteins being part of a limited number of biochemical pathways. Interactions between the molecular partners is therefore key to understand the disease and propose new treatments. The session will present the different interweaved approaches used to approach this issued, including proteomics, analysis of interaction networks and mathematical modelling.
Session III: Pluripotent stem cell based models ‐ To showcase how AD patho‐mechanisms can be deciphered in vitro, how classical human genetics‐ GWAS (genome wide association studies) is used to identify LOAD‐associated genes and how these candidate genes can be further studied using an iPSC‐based approach to differentiate these patient iPS cell lines into function interneurons. Data pertaining to the transcriptomes and associated pathways are then incorporated into databases which can be interrogated.
Alzheimer’s disease, systems biology, synapse, ageing, ageing‐related diseases, neuropathologies, omics‐biotechnologies, neuroimaging