More than a hundred years after Alois Alzheimer described the disease that bears his name, we still remain empty-handed regarding effective causal therapies. For decades, much of AD research has been concentrating on the processes leading to the generation and the prevention of amyloid beta plaques. Moreover, we have been convinced that mechanisms that trigger familial AD can be directly transferred to sporadic, age-associated forms. Despite the fact that the causality between amyloid beta and amyloid plaques and cognitive deficits in AD is still lacking proof of concept, and furthermore, a whole series of clinical studies ultimately remained ineffective, the amyloid cascade hypothesis still dominates basic research, experimental therapy approaches, and clinical studies.
This meeting aims at bringing together current knowledge on other cellular and molecular processes that contribute to AD pathogenesis - which, in part, have not earned the attention they deserve so far - and at fostering discussion on future perspectives in AD research. Topics to be covered include inflammation, vascular dysfunction, mitochondrial integrity, cell cycle events, lipid metabolism, tau biochemistry, protein misfolding and autophagy.
On behalf of the Scientific Committee I would be glad to welcome you in Hanover!
Christian Behl, Organizer