Off-target troubles aside, tau tracers took the cake at the 10th Human Amyloid Imaging conference, held January 13-15 in Miami Beach, Florida. Even as researchers continue to sort out the vagaries of working with investigational tracers, they have started delving into deeper questions than whether neurofibrillary tangles are merely present in the brain. Scientists are asking how patterns of tau deposition relate to Aβ, neurodegeneration, and connectivity in Alzheimer’s disease. Preliminary cross-sectional data hint at a considerable lag between Aβ and tau accumulation in familial AD. New ligands debuted at HAI this year, but whether they will better detect tau deposits than the current batch remains to be seen. Leaders in the field still don’t know how well tau PET will work in other forms of dementia, such as FTD, PSP, and CBD.
Using PET, researchers are trying to match tau spread against structural and functional defects.
Preliminary data suggests a long lag between Aβ and tau deposits as the disease develops.
Attendees grapple with conflicting binding results
AV1451 appears too weak to diagnose non-AD tauopathies.