In some patients, the blood Aβ42/40 test fell too close to the cutoff for specialists to confidently diagnose AD. Comorbidities, drugs also complicate results. Two CSF tests are FDA-approved.
Mirroring earlier results, a larger study finds that high levels of this tau fragment in CSF tracked with neurofibrillary tangles, but not amyloid plaques.
In some patients, the blood Aβ42/40 test fell too close to the cutoff for specialists to confidently diagnose AD. Comorbidities, drugs also complicate results. Two CSF tests are FDA-approved.
CSF monocytes increasingly crank out the chemokine CXCL16, while T cells up its receptor, CXCR6. The same cross-talk unfolded among microglia and T cells around plaques.
In a small pilot study, tailoring lifestyle changes to the individual boosted cognition, with an effect size three times that seen in the Finger trial.
In the Graduate trials, the anti-amyloid antibody gantenerumab cleared only half as much plaque as it had done in earlier studies. Is formulation or dosing to blame?
In a head-to-head comparison, donanemab banished four times as much plaque in the first six months as aducanumab did, partly due to its faster titration.
Adding to our collection of APP, Presenilin, Tau, and Trem2 mutations, the new dataset curates neurologic and non-neurologic information, ranging from clinical to molecular.