Protein levels track with cognitive function and can distinguish Alzheimer’s patients from controls.
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?
A plasma assay for Alzheimer’s could radically speed up screening for clinical trials; alas, competing assays don’t measure the same thing.
At this year’s AAIC, no sooner had scientists reported that phospho-tau in the CSF might reflect early responses to amyloid, than they reported parallel data for phospho-tau in blood.
At AAIC, researchers touted phospho-tau species, especially p217 and p181. They tick up in CSF as an early response to amyloid accumulation.
Using a collection of isogenic iPSC-derived neurons harboring different familial AD mutations, researchers found that, across the board, the mutations meddled with endosomes via elevated β-CTF.
The phenotype of ApoE4 astrocytes and microglia resembles that of these cells in Alzheimer’s brain. Could defects in lipid metabolism and the extracellular matrix bring on the disease?