Alarmed by crushing screen failure rates of the first prodromal Alzheimer’s trials, EPAD and GAP are chasing new ways to reach people who don’t know they really should be in a secondary prevention trial.
This past year, the Global Alzheimer’s Platform and the European Prevention of Alzheimer’s Dementia have moved quickly, and jointly, to pave the way toward more, faster, cheaper trials. Will they be better, too?
At AAIC, researchers suggested splitting out the markers in a new staging scheme. Called ATN, it aims to clarify underlying causes of atypical dementias and suspected non-Alzheimer’s pathology (SNAP).
Antibodies that cling specifically to human APP revealed differences in expression patterns of the protein in mouse models of Alzheimer’s disease.
Scientists pool samples and creatively mine the genomes of thousands of patients to find coding and non-coding variants that associate with the disease.
Using PET tracers, researchers have linked the presence of tau tangles to neurodegeneration in preclinical and clinical AD, and fingered Aβ as the instigator of tau toxicity.
Take a three-dimensional tour of the plaques and tangles of mouse and human brains as they develop Alzheimer’s disease-related pathology.
In First Phase 3 Trial, the Tau Drug LMTM Did Not Work. Period. Staging of Alzheimer’s, the Second: Neurodegeneration Does Not Equal Tauopathy Coming to a Center Near You: GAP and EPAD to Revamp Alzheimer’s Trials Access: How to Bring People in ‘From the ...
Claims of a positive effect in a small subgroup of patients are statistically meaningless, experts say.
Antisense oligonucleotides can flip expression of tau from the three-repeat to the four-repeat form. These ASOs triggered tau aggregation and behavioral problems.
Imaging study correlated four patterns of neurodegeneration that map to two neural networks with certain behavioral symptoms.
Four researchers received awards totaling $350,000 for their contributions to Alzheimer’s research.
Researchers may soon add another imaging agent to their tool kit—one that tracks synapse loss.
At Keystone, researchers also linked the receptor to microglial homeostasis and migration, and resolved lingering questions about TREM2’s role in plaque clearance.
A PET study comparing amyloid, tau, and volumetric imaging in preclinical AD identifies a region where local tangles correlate with brain-wide amyloid.
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