Branch out, scientists at Alzheimer’s Research UK conference say. Go after tau, glial activation, lipids, in a systematic way. Understand how these pathways connect to the amyloid hypothesis.
Convened by ARUK to learn from the antibody’s billion-dollar bust, industry and academic leaders declare insufficient CNS target engagement, say peripheral sink did not work, and brainstorm how to move forward.
A few attempts at Alzheimer’s therapy claim hints of promise in early clinical trials, though several did not include placebo controls.
At CTAD, tau-PET data from people in different stages of various neurodegenerative diseases highlighted both commonalities and peculiarities.
Biogen and Genentech rolled out more data from their Phase 1b trials, renewing hope that amyloid removal will work and shoring up dosing for Phase 3.
Scientists at SfN presented innovative ways to slow amyloid accumulation and preserve synapses.
The tau aggregation inhibitor LMTM tanks in second Phase 3 trial for Alzheimer’s. The sponsor now plans to develop the “placebo.”
Patients on solanezumab saw small improvements on multiple secondary endpoints.
Researchers at SfN 2016 proposed dialing up the immune response in Alzheimer’s brains to enhance phagocytosis.
At SfN 2016, researchers debuted new mouse models that may better represent human disease.
Researchers at SfN 2016 touted the advantages of APP knock-ins, but noted they are less useful than overexpression models for studying behavior.
Researchers at SfN 2016 painted a more detailed picture of how misfolded proteins may proliferate, as one cell spreads these “hot potatoes” to the next.
Despite no warning signs in ongoing clinical trials, researchers are searching for safer drugs, and better biomarkers to measure what they do.
In Seeon, researchers reported that blocking the protease may heal dystrophic neurites and repair electrical activity.
At the 2nd Kloster Seeon meeting on BACE proteases, researchers linked BACE substrates to regulation of synaptic activity.