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.
At an expert meeting convened by Alzheimer’s Research UK, scientists from Eli Lilly shared Aβ biomarker data from the Expedition 3 trial with colleagues in academia and pharma. Reading the trial’s tea leaves together, the group felt that solanezumab entering the brain from the blood might have brought Aβ along for the ride, confounding CSF biomarker measurements. To boot, the trial appears to have enrolled participants with more brain amyloid than its predecessors. Given the weakness of the biomarker results, scientists, despite a day of deliberation, were left with merely a gut feeling that the hint of a cognitive benefit in the trial was probably real, if too small. A lively brainstorm session of where AD translational research should go next concluded the day. Read Gabrielle Strobel’s two-part story.
If the setback of the Expedition 3 study of solanezumab set their mood in the beginning, attendees at the 2016 Clinical Trials on Alzheimer’s Disease conference soon bucked up and voiced renewed determination to tackle this illness. Many took positive secondary outcomes and trends in this Phase 3 trial as a sign that this or more potent anti-amyloid drugs given earlier will make a bigger dent in the disease process. Short of major surprises, the meeting reaffirmed the sense that AD will only be slowed by deploying potent drugs at the right target (probably more than one), with the right dose, and certainly at the right time.
When more than 30,000 registrants gathered at the San Diego Convention Center for the Society for Neuroscience annual meeting November 12-16, they exchanged their latest data on the basic science on Alzheimer’s disease. Topics ran the gamut from protein propagation and inflammation to the hunt for plasma biomarkers and potential therapeutics. Alzforum reporter Madolyn Rogers brings you highlights.
Since the first Kloster Seeon meeting on β-secretases in 2013, a handful of BACE inhibitors have entered clinical trials and researchers have learned more about what these proteases do in development and adulthood. What’s the status of the field in the fall of 2016? Check out our coverage of the 2nd Kloster Seeon meeting. Highlights include conditional BACE1 knockouts, updates on non-APP substrates cleaved by BACE, news about BACE’s role in dystrophic neurites, assays to measure off-target effects and—finally—the arrival of BACE1-selective inhibitors.