As the brain ages, what protects it from cognitive decline? A two-day conference focused on reserve and resilience.
Showcasing forays into the biology of tau, researchers at AD/PD reported news on tau’s transcriptional regulation, its bungling of synaptic vesicles, its sway over the epigenome, and even flashed an atomic structure.
The receptor responds to brain insults such as oligomeric Aβ and cellular debris by jolting microglia into clean-up mode, according to researchers at AD/PD 2017.
In tauopathy mice, ApoE4 hastened neuroinflammation and neurodegeneration. No amyloid involved. (Tip: Think A1 astrocytes.)
In the field’s march toward automated testing, scientists for the first time used biomarker cutoffs determined in one cohort to predict amyloid accumulation in a second. It worked.
Emerging data on new tau ligands raise hope of more signal, less noise, and help with a broad range of tauopathies. Read news culled from the AD/PD and HAI 2017 meetings.
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.