Epidemiology: is the frequency of dementia changing and why? Are time trends in AD similar to those seen in other related disorders such as stroke or FTD?
Are environmental interventions (optimal CV control, diet, physical activity, etc.) likely to change the frequency and by how much?
What can pathology contribute to our understanding, given that autopsies come very late in the disease course and show mixed pathology in most cases? Lea Grinberg, Brazil/USA
Are amyloid and tau dead horses in sporadic, late onset AD, given the disappointments with interventions that were successful in eliminating amyloid yet without clinical benefit?
How can we improve our animal models which so far have been based primarily on transgenic animals with mutations coming from early onset genetic cases, while late onset sporadic disease is associated with completely different factors?
Is APOE4 a potential treatment target, given that we do not understand its mechanism?
Is neuroinflammation: a useful potential therapeutic target?
How should we allocate resources, given that until now 90% were allocated to amyloid and tau research which has led us nowhere?
The need for multiple targets, outcomes, and approaches Vladimir Hachinski, Canada