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.
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.
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.
In tauopathy mice, ApoE4 hastened neuroinflammation and neurodegeneration. No amyloid involved. (Tip: Think A1 astrocytes.)
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.
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.
Overexpressing miR-132 dampened AD pathology in young mice, and appeared to nourish the birth of new hippocampal neurons in older animals.
Manufacturers of a therapy system called neuroAD, which combines transcranial magnetic stimulation with cognitive training, are applying for FDA marketing clearance.
Three anti-tau antibodies are in Phase 1 or 2, while the first O-GlcNAcase inhibitor got the green light to start testing.