Newswise — When 225 researchers from around the world convened in Miami to exchange the latest on β amyloid positron emission tomography in January, there was a palpable sense of urgency. At the 6th Annual Human Amyloid Imaging (HAI) Conference, the possibility of approval, potentially within months, of the first amyloid-scanning compound for clinical use hung over the room. As scientists openly discussed new research developments on all fronts of this young field, they also wrestled with whether and how to disclose plaque status to people without dementia, how to use amyloid scans in the clinic, and how to reliably read plaque scans.
Scientists presented new data on how genes and age influence plaque deposition, as they start to pinpoint when and where this pathology first crops up in the brain. A growing number of longitudinal studies that follow cognitively normal and mildly impaired people at varying degrees of genetic risk suggest brain amyloid deposition is bad news, though it often takes years before someone shows symptoms of forgetfulness.
But even as longitudinal studies converge, all does not fit. The conference brought to a boil a theme that has been simmering: In many cases, plaque scans don’t match a patient’s clinical Alzheimer’s diagnosis, and more research is needed to find out which of the two is more accurate. This process may shake up the diagnosis of AD and give more prominence to related, understudied forms of dementia. At the conference, researchers agreed that the field urgently needs compounds to trace all defining pathologies, above all, neurofibrillary tangles. The debut of the first tau-only scan data in humans received rapt attention, and two more compounds are in late preclinical stages. A nine-part series http://www.alzforum.org/new/detail.asp?id=3074 by Alzforum reporters covers these points and more.
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