What went down in London town during the AAIC meeting? Whether you were there or could not go this year, Alzforum reporters captured the highlights. Read about a promising plasma Aβ assay that flags people who have brain amyloid plaques, raising hope for faster, cheaper, less-invasive screens for therapy studies. Witness a bidding push for primary prevention trials, as well as an official call to be ambitious on modifiable risk factors. New variants of microglial genes emerged, as did basic science proposing that the AD brain is filled with a “cloud” of different Aβ strains.
At AAIC, researchers debuted a method that detects changes in plasma Aβ42 in people with brain amyloid. If confirmed, a widely available screening test for presymptomatic AD could follow.
Interim data from IDEAS study find that amyloid PET has a greater effect in real-world practice than in research settings. Nearly half of people diagnosed with AD did not have the disease.
At AAIC 2017, researchers presented new approaches to find genetic variants linked to AD risk and to understand their contributions to disease.
In London, researchers claimed that a monomer is the minimal structure required for tau strains. On the other hand, the sky seems the limit for the number of Aβ strains that form in an individual brain.
Researchers will enroll young adults who carry familial AD mutations in the first trial of a mechanism-based, investigational drug to try to prevent amyloid from depositing in the brain.
Scientists at AAIC described a large, multidomain intervention trial in the United States to test if lifestyle changes can stave off cognitive decline. YMCAs nationwide are in on the project; similar trials are in the works in other countries.
Report details ways to improve care of people who have dementia, argues for societies to implement ambitious prevention strategies, but offers only reduction of hypertension as a plausible intervention.
Researchers at AAIC described different correlates of CSF and PET measures of Aβ and tau.
Researchers at AAIC reinforced the idea that tau pathology drives cognitive decline, although amyloid plaques were implicated in semantic memory deficits.