New Assay, New Cohorts—Plasma p-Tau181 Looks Even Better 217—The Best Phospho-Tau Marker for Alzheimer’s? In DIAN-TU, Gantenerumab Brings Down Tau. By a Lot. Open Extension Planned Confused About the DIAN-TU Trial Data? Experts Discuss Active Tau Vaccine: ...
The AAT-AD/PD conference hosted a virtual conversation about what the trial’s disappointing cognitive and tantalizing biomarker data might mean. Hidden between thank you’s and pledges to stay committed were substantive points of debate and context.
Data shown at AAT-AD/PD explain why the DIAN-TU trial missed its primary endpoint. But gantenerumab strongly reduced plaques, tau, phospho-tau, and slowed NfL. This result prompted an open-label extension, sustaining hope for efficacy.
P-tau217 appears sooner than p-tau181 in the brain, and it distinguishes AD from controls and other dementias even more cleanly.
At AAT-ADPD, researchers report how they built on prior reports that a person’s blood level of p-tau181 tells if they have Alzheimer’s.
A trial of nearly 20,000 participants found no benefit over five years.
Two papers report that phosphorylated tau in the blood distinguishes people with AD from healthy controls and from people with frontotemporal and vascular dementias.
From caregivers going it alone to understaffed nursing homes on lockdown, people with neurodegenerative disease and their caregivers are feeling enormous strain from the novel coronavirus. They are adapting to the new normal with technology.
Most observational cohorts are on pause, and many clinical trials have stopped dosing. The long-term effects on the integrity of AD studies are unclear.
With experiments and careers on hold, scientists working from home are turning to virtual lab meetings and journal clubs to keep up morale.
United Kingdom’s DRI pivots to fight COVID-19. The facility could test 10,000 samples per day.
Under diabetic conditions, SERP1 binds secretase subunit, cranking up cleavage of APP but not Notch. The finding offers a mechanistic link between diabetes and Alzheimer’s.
The slowdown of proteasomes stymied TDP-43’s entry into the nucleus and promoted its aggregation in the cytoplasm.
In a conditional mouse knockout, lack of neuronal BIN1 slowed excitatory signaling, leading to spatial memory problems. Could this play a role in Alzheimer’s?
In the human brain, alpha waves fell out of sync, while delta-theta waves swelled in concert with amyloid plaques, neurofibrillary tangles. Alpha modulation correlated with cognitive decline.