It has been more than two decades since genes causing familial Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, motor neuron disease and other neurodegenerative disorders were identified. While numerous molecular and cellular events contributing to these devastating illnesses have been revealed, key pathological events and feasible targets for therapeutic intervention still elude us. Increasing evidence supports that mechanisms underlying neuronal demise may be shared amongst multiple neurodegenerative disorders. For example, compromised mitochondria function, although prominent in Parkinson’s disease, is also shared in Alzheimer’s and amyotrophic lateral sclerosis. Emerging evidence also indicates a negative influence of neurotoxic stress upon the epigenetic, and that the restoration of the epigenome can be beneficial for cognition. Recent insights into the relationship between genome integrity and the aging brain have emphasized the role of DNA damage and repair in neuronal function. Particularly intriguing is the recent observations that protein misfolding can have either beneficial or detrimental effects and that misfolded proteins implicated in several neurodegenerative disease can propagate themselves. New tools for the study of neurodegenerative disorders include the use of human neurons derived from induced plu**otent stem cells (iPSCs) in addition to advances in the field of biomarkers and functional imaging.
In this meeting, we aim to address emerging areas in neurodegenerative disease research that may reveal novel mechanisms and targets for therapeutic intervention. We will bring experts in studying various degenerative diseases using diverse approaches together to provide reviews of up and coming areas in these fields and inspire new insights and approaches to the battle against neurodegenerative disease. Opportunities for interdisciplinary interactions will be significantly enhanced by the concurrent meeting on Neurogenesis, which will share two plenary sessions with this meeting.
