At a topical meeting in Leuven, Belgium, a coherent picture began to emerge for how these membraneless organelles function in health and disease.
Researchers at AD/PD 2017 presented new data on an antibody and small molecules targeting amyloid.
A broadening drug development pipeline now contains Phase 1 or 2 drugs on targets unrelated to Aβ or tau.
A trial of an α-synuclein antibody is making use of the technology to follow subtle changes in the day-to-day function of participants.
Even without this important sidekick at hand, scientists are forging ahead with efficacy trials of their first attempts at disease-modification in Parkinson’s
Three anti-tau antibodies are in Phase 1 or 2, while an O-GlcNAcase inhibitor got the green light to start testing.
Manufacturers of a therapy system called neuroAD, which combines transcranial magnetic stimulation with cognitive training, are applying for FDA marketing clearance.
Overexpressing miR-132 dampened AD pathology in young mice, and appeared to nourish the birth of new hippocampal neurons in older animals.
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.