Is GWAS likely to contribute significantly to Alzheimer’s disease (AD) patients care?
Capsule: Genome-wide association studies (GWAS) looking at genetic variants in different individuals may identify variants associated with disease. These cross-national investigations have been applied widely to AD, identifying several “disease-specific” alterations. Is the huge and expensive investment likely to help in patient care?
16:10-16:15
Introduction and Pre-Debate Voting
16:15-16:35
Yes:John Hardy, UK
16:35-16:55
No: Amos Korczyn, Israel
16:55-17:00
Rebuttals, Discussion and Post-Debate Voting
17:00-20:30
ALZHEIMER’S ASSOCIATION SATELLITE I: OVERCOMING THE IMPASSE IN DEMENTIA PREVENTION AND TREATMENT
HALL A
Chair:
Zaven Khachaturian, USA
17:00-17:05
Opening remarks Zaven Khachaturian, USA
17:05-17:20
Introduction from the Alzheimer’s Association (AA) Heather Snyder, USA
Capsule: The AA leads the way to end AD and all other dementia — by accelerating global research, driving risk reduction and early detection, and maximizing quality care and support. The AA fosters and facilitates advances in scientific discussion through publications, conferences and collaborations, including our partnership with CONy to support the CONy Dementia Satellite.
17:20-17:50
The complex realityAmos Korczyn, Israel
Capsule: The overwhelming failure of the attempts to prevent or cure Alzheimer’s disease (AD) should lead us to rethink the problem. Is AD a real disease or is it a syndrome? Can we use genetic early onset AD as a template for the sporadic disease? What is the role of comorbidities in older people with dementia? Since AD is a multifactorial disorder can we expect to find a “silver bullet” that will cure AD? Is the idea of “the sooner the better” really valid?
17:50-18:05
Discussion
18:05-18:35
Why use a biological definition of AD?Bart De Strooper, UK
Capsule: Traditional definition of AD consisted clinical features and pathological hallmarks of both amyloid-β and tau. This is because the clinical manifestations are not very specific. The development of biomarkers, particularly PET-scans, showed that many older individuals carry amyloid deposits yet without cognitive symptoms. Do we have enough data to be certain that they will definitely develop dementia?
18:35-18:50
Discussion
18:50-19:20
Non pharmacological interventionsMiia Kivipelto, Sweden
Capsule: Are environmental interventions (optimal CV control, diet, physical activity, etc.) likely to change the frequency of dementia and by how much? Have any of these factors been shown to prevent the occurrence of dementia or do they merely delay the onset, and if so, by how much? What is the number needed to treat (NNT) in order to prevent one case? These are standard questions for drug treatment and should be also relevant for non-pharmacological interventions.
19:20-19:35
Discussion
19:35-20:00
Animal models of ADAndrea Tenner, USA
Capsule: Is the employment of young, genetically modified rodents without comorbidities likely to lead us to find a cure for sporadic AD? Several treatments were beneficial in those animal models yet failed in humans. Are the models misleading us? How can we improve?
