Held in Boston’s Park Plaza Hotel, this year’s CTAD conference filled its chosen venue to fire regulation capacity. The space bustled with scientists heading to talks, posters, and various private meetings in rooms up and down the hallways. Despite a notable absence of success stories for large trials, a sense of optimism pervaded the scene, which stands in marked contrast to a public perception of all-failure-all-the-time in Alzheimer disease trials. True, verubecestat data was flat-out negative in mild to moderate AD and some scientists began to fret about a possible class effect, but on the other hand, several anti-Aβ antibodies posted evidence of removing amyloid plaque reasonably safely from the human brain, and all breaks were off on prep work for multiple large-scale prevention trials in the preclinical phase of this long disease. CTAD news ran the gamut from creative approaches to developing drugs (think young men’s plasma fraction) to creative approaches to measuring subtle cognitive change (think burst mobile tests and digital pen), to on-the-spot ApoE genotyping (think cube). Learn the latest with our 13-part news series.
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 budding 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.
This open conference is rapidly becoming the place to present and debate new data on the underlying mechanisms of all neurodegenerative diseases. Read the latest on APP processing, APP receptors, tau synthesis and degradation. Find the cutting edge on the role of microglia in protecting and exacerbating disease, and the promise of human proteomics for tracking disease progression at a systems level.
Confused about protein liquid-liquid phase transitions? You are not alone. Researchers working in this emerging field gathered in Leuven in early May to make sense of the latest data linking protein droplets to biological function and disease. Read Tom Fagan’s report, and come away with a clearer sense of membraneless organelles, and their disassembly and transport back into the nucleus, where they belong. Be ready for wild ideas about low-complexity domains as internal chaperones and plant drought protection mechanisms, echoing what’s going on with these neurodegenerative disease proteins.
Held in the historic Austrian capital, the 13th AD/PD conference reflected a rapidly growing field. The meeting jammed science into five parallel sessions, with 545 talks running from early morning till late evening and some 1,200 posters vying for attention. There were no show-stopping announcements, but researchers noted biomarker advances on both the PET and CSF front, as well as a flourishing variety of basic science talks on tau, TREM2, epigenetics, and other topics. On the clinical side, one company touted a successful Phase 3 trial for transcranial magnetic stimulation to treat Alzheimer’s, but potential disease-modifying therapies for both AD and PD remain in development.