Amyloid in ADDavid Knopman, USA Capsule: Are βA and tau wrong treatment targets in sporadic, late onset AD, given the disappointments with human anti-amyloid studies, although they were successful in eliminating amyloid, significant clinical benefit were not seen? Since βA deposition is very prevalent in aging and is not necessarily associated with dementia, how do we know that it is a worthwhile therapeutic target? Could other biomarkers, such as synaptic loss or neurodegeneration add specificity?
15:30-15:40
Discussion
15:40-16:05
To futility or not – when and how should futility analysis be applied?Rema Raman, USA Capsule: AD treatment exploratory studies are excessively costly and long. Should the studies always be continued till the planned end? Is discontinuation always justified and ethical when treatment seems non-effective during the study?
16:05-16:15
Discussion
16:15-16:40
Neuropathology of dementiaLea Grinberg, Brazil/USA Capsule: What can pathology contribute to our understanding, given that autopsies come very late in the disease course and show mixed pathology in most cases?
16:40-16:50
Discussion
16:50-19:35
ALZHEIMER’S ASSOCIATION SATELLITE III
HALL A
Chair:
Peter Whitehouse, USA
16:50-16:55
Introduction Peter Whitehouse, USA
16:55-17:20
Is APOE4 a potential treatment target, given that we do not understand its mechanism?Daniel M. Michaelson, Israel Capsule: It is now almost 30 years since the identification of APOE polymorphism as important genetic determinant of AD, yet the underlying mechanism is still unknown and it is not even clear whether APOE4 is toxic or just less protective than APOE3. And, should APOE4 related dementia be designated as a separate disease?
17:20-17:35
Discussion
17:35-18:00
Is neuroinflammation a useful potential therapeutic target?Michael Heneka, Germany Capsule: Examination by pathologists demonstrate the existence of inflammation in the brain of patients with dementia and this is supported by imaging, genetic, and neurochemical studies. However, attempts to ameliorate the condition of patients have largely failed. Does that mean that the inflammatory processes are just epiphenomena, or perhaps have different roles in early and late stages of the disease? Could it be that inflammation has both beneficial and toxic effects?
18:00-18:15
Discussion
18:15-18:40
Fear and loathing in AD trialsLon Schneider, USA Capsule: The cases of Aducanumab, albumin/IVIG exchange, and oligomannurarate show the difficulties in preforming and interpreting data. What is the way forward? Are the targets wrong or are the other methods used mistaken? Failure of design, methods, execution or analysis?
18:40-18:55
Discussion
18:55-19:20
The need for multiple targets, outcomes, and approachesVladimir Hachinski, Canada Capsule: The typical patient with Alzheimer’s Disease harbor 8 pathologies, hence we need to target more than one mechanism.Cognition, motion and emotion are closely inter-related and should be considered for a composite outcome measure that would increase the likelihood of a positive result. The high risk dementia prevention strategy that prevails, needs to be complemented by population level strategies, where most of the gains can be made in the near future.
