Objective
In response to Para 6.1 of the Sol Work Program, it is proposed to show that in various slowneurodegenerative diseases protein misfiling causes early changes in intracellular function, which serves important pathogenesis markers of disease onset and progression. Focus will be on Parkinson's, Huntington's and prison diseases, but the project will also have impact on other neurodegenerativedisoders of aging. In these disorders, there is currently an urgent need for methods that can identify early cell pathology and monitor treatment effects at the cellular level. Using a multidisciplinary approach, the objectives are to reveal, sequentially, in tissue culture, transgenic animals and in cells derived from patients, the early stages of mutant protein aggregate formation and its consequences. Emphasis will be on parameters of neuronal dysfunction, but changes in blood will also be demonstrated as early indicators of neuronal disease lymphocytes in mice and men exhibitingneurodegeneration. Therapeutic strategies to intervene in protein misfiling will be tested, with the aim to transfer this knowledge to clinical applications.
Funding Scheme
CON - Coordination of research actionsCoordinator
8091 Zurich
Switzerland
Participants (4)
75248 Paris
91405 Gometz La Ville
LE1 9HN Leicester
NW3 2PF London
