Off-target troubles aside, tau tracers took the cake at the 10th Human Amyloid Imaging conference, held January 13 to 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.
You thought Alzheimer’s was complicated? Or Parkinson’s? Try dementia with Lewy bodies, the common disease occupying the territory between those two poles. DLB is heterogeneous and often overlooked. Yet the International Dementia with Lewy Bodies Conference held earlier this month in Fort Lauderdale, Florida, showcased a field coming into its own. For four days, four hundred researchers, patients, care partners, and other stakeholders traded new insights. Because this conference last convened about a decade ago, there was much to learn. Over the din of disease classification debates that perennially accompany spectrum diseases, the meeting reflected a field trying to build on a broadly accepted consensus diagnosis, its unifying foundation. Pharmaceutical companies are dipping in their toes, GWAS are ramping up, and prodromal biomarker cohorts are forming. Farthest ahead is Japan—the only country that has annual DLB conferences, an approved medication, and arguably the best diagnostic scan standardized across centers.
At the International Symposium on ALS/MND in Orlando, Florida, scientists, neurologists, and people with ALS were excited to hear about clinical progress to treat motor-neuron disease. Attendees pondered the preliminary, but positive, results of gene therapy trials in spinal muscular atrophy—results that may open the door for similar gene therapy in ALS. They heard news of completed and ongoing trials of edaravone, a drug that may slow ALS in certain people, and about therapeutics that relieve distressing problems with speech and swallowing. Basic science also made a showing. A better understanding of how pathogenic proteins travel from cell to cell emerged, and researchers debuted new genetic variants to explain some inherited ALS risk.
At the 8th Clinical Trials on Alzheimer’s conference held November 5-7 in Barcelona, 900 attendees traded results on trials from the closely watched Aβ antibodies aducanumab and gantenerumab to a long list of lesser-known therapeutic candidates. The most pressing issue discussed at this meeting was how to design trials to be able to see a drug effect in early AD, while the tools are still evolving. The field has learned much about the importance of rigorous dose-finding, exposure, and target engagement, but new frontiers have cropped up. How best to identify the right patient population, knowing how fast a given early-stage person is likely to progress, and measuring subtle improvement in barely impaired people have become the challenges of the day. To meet them, tools development is actively ongoing even as a larger clinical trials infrastructure is forming across both sides of the Atlantic.
Some 29,000 registrants descended on McCormick Place, the largest convention center in the United States, for the Society for Neuroscience annual meeting, held October 17-21 near downtown Chicago. Among the 18 symposia, 31 minisymposia, 98 nanosymposia, 650 poster sessions, and numerous special lectures was a shrinking but still lively fraction of Alzheimer’s science. Alzforum reporters Madolyn Rogers and Tom Fagan ferreted it out.
At the 10th Brain Research Conference: RNA Metabolism in Neurological Disease, a satellite of the Society for Neuroscience annual meeting, attendees learned about a parade of mice modeling different aspects of ALS and FTD that result from expansions in the C9ORF72 gene. Knockouts lose control of their immune systems, while transgenics overexpressing the repeat-heavy human gene ranged from normal to having movement and cognitive abnormalities. The results suggest the repeats cause toxicity, but scientists have plenty more to do to understand what the mice are telling them.