An epigenetic approach towards the recovery of neuronal network plasticity and cognitive function in neurodegenerative disease
Disorders such as Huntington?s (HD) or Alzheimer?s disease (AD) cause a huge emotional and economical burden to our societies and an effective therapy is not yet available. A number of studies and most recent data from members of this consortium suggest that epigenetic factors regulating gene-expression, such as histone-acetyltransferases (HATs) and histone-deacetylases (HDACs), may play a central role in the pathogenesis of AD and HD and that targeting those mechanisms could be a promising therapeutic avenue. Our hypothesis, which is supported by published and preliminary data is that abnormal histone regulation via HATs and HDACs could cause neurodegeneration and cognitive dysfunction by modifying several sets of genes implicated in neuronal functioning. Our plan is to combine all levels of the chain to explore and exploit this possibility. To this end we have assembled a consortium with a unique combination of expertise. Within the 3-year period EPITHERAPY will define the epigenetic signature of AD and HD pathogenesis. We will identify those HATs and HDACs that are most promising drug targets for the treatment of AD and HD. This knowledge will enable the development of novel epigenetic drugs that could help to treat patients suffering form neurodegeneration and dementia. The collaborative effort and synergy that will result from this project will be extremely valuable to complete the objectives and will help to develop effective therapies for neurodegenerative diseases.
animal models, behavioural studies, genetics, neuropathology, therapy, Alzheimer's Disease, Huntington's disease, epigenetics, histone deacetylases, histone acetylases, gene expression
2009 - 2012
Andre Fischer (Coordinator)