Longitudinal ADNI data tie higher sTREM2 in CSF to slower cognitive decline, reinforcing the idea that TREM2 activity protects the brain from AD pathology.
The pattern varied from person to person, depending on the site of injury, in contrast to the stereotyped distribution of tau tangles seen in Alzheimer’s disease.
What’s with all those head-to-head comparison studies of academic and commercial biomarker tests? Could we not just pick one that works, and be done?
Protein levels track with cognitive function and can distinguish Alzheimer’s patients from controls.
Changes in the composition of the cerebrospinal fluid and synapses may reveal novel insights into AD pathology.
A plasma assay for Alzheimer’s could radically speed up screening for clinical trials; alas, competing assays don’t measure the same thing.