Recruitment, recruitment, recruitment: Registries get creative in how they promote research engagement and fill prevention trials.
Who doesn’t dread hours of testing at a clinic? Innovation needed! Learn about frequent “burst” testing via mobile app, and a digital pen that captures more information than the old paper-and-pencil test.
In people who carry a repeat expansion in the C9ORF72 gene, gray and white matter are smaller and subtle impairments in cognition appear decades before symptom onset.
Clinical validation is showing automated Elecsys, Lumipulse assays to be reliable and predictive. The story on blood tests has turned from non-starter to intensely promising for broad-based screening.
10th CTAD: Finally, Alzheimer’s Field Is Serious About Prevention Trials At CTAD, Tau PET Emerges as Favored Outcome Biomarker for Trials Automated CSF Tests: Check. Blood Tests: In the Works Cognitive Testing Is Getting Faster and Better Don’t Be an ...
Tau’s apparent lockstep with cognitive decline dominated the PET conversation. Piramal flaunted data, and Merck/Cerveau are close behind. A first stab at imaging synapses in the hippocampus drew notice, too.
Two complementary studies find that ApoE4 has little influence on plaques once they are present.
Alzheimer’s science has undergone a paradigm shift toward the disease’s silent phase. For trials, this means change at every level: new participants, new screening tools, new outcome measurements. What’s the progress?
By injecting tau-enriched extracts derived from AD brains into transgenic mice, researchers dissect how Aβ plaques fuel tau pathology.
Slow vital capacity, a measure of respiratory function, predicted the rate of disease progression in ALS patients, suggesting the test could be used as a primary endpoint in clinical trials.
Small molecules that stabilize G-quadruplexes cut C9ORF72 RNA and protein deposits in half.
A segment of tau forms a tight molecular zipper that promotes fibrillogenesis. Zipper inhibitors blocked aggregation of full-length tau in cells.
Plaque fibrils differ markedly from person to person, yet commonalities exist among people with clinical subtypes of the disease.
A case study describes amyloidosis in a 39-year-old homozygous for a TREM2 mutation, but experts question the interpretation.
TIA1 bolsters tau toxicity, leading to synaptic malfunctions, cognitive impairment, and early death in transgenic animals.
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