At CTAD, a Phase 2 open-label extension of this anti- Aβ protofibril antibody posted data as expected, and new Phase 3 trials for people with early and preclinical Alzheimer’s were described.
After years of building an online registry, designing selection algorithms, and getting sites up and running, COVID-19 nearly derailed this trial-ready cohort once again. Now, the first participants have reached the final queue.
One of the most coveted achievements AD researchers are striving for these days is to develop a biomarker that could, simply and inexpensively, detect if a person has early Alzheimer's disease...
Remote assessments on a smartphone closely matched tests taken in the clinic. They also may detect slip-ups in learning—an earlier cognitive deficit that arises in preclinical AD.
After missing primary endpoints in Alzheimer’s trials, this p38 MAPKa inhibitor gained some traction in a test in people with DLB.
BANish Aβ? BAN2401 Antibody Makes Its Move in Phase 3 Program BAN2401 Forges AHEAD into Phase 3, Preclinical AD TRC-PAD Funnel Finally Touches Down Learning Troubles Spied by Smartphone Track with Biomarkers In Phase 2 Trial, Neflamapimod Aids Cognition ...
A plasma assay for Alzheimer’s could radically speed up screening for clinical trials; alas, competing assays don’t measure the same thing.
In mouse models of tauopathy, microglia populations are far from binary. Different activation stages emerge at different phases of disease, some marked by viral defense pathways.
New drug application is first for Alzheimer’s disease in the U.S. since 2003, and first based on amyloid hypothesis.
New synaptic profiling and imaging techniques are enabling scientists to zero in on synaptic proteins, including phospho-tau, that make the difference between clinical Alzheimer’s and resilience.
Two cohorts—IDEAS and WHIMS—show Aβ accumulation and brain shrinkage in cognitively normal and impaired elderly who were exposed to levels of air pollution even within current EPA limits.
At CTAD, intranasal insulin trial stumbles, pioglitazone gets a postmortem, a RAGE inhibitor tries to hang on.
Researchers found that bits of tau from the protein’s microtubule-binding region can be detected in the cerebrospinal fluid. These, not phospho-tau or total tau, reflect neurofibrillary tangles in the Alzheimer’s brain.
Confronting unprecedented challenges this past year, scientists found ways to tide their research over and keep clinical trials mostly on track.
Changes in the composition of the cerebrospinal fluid and synapses may reveal novel insights into AD pathology.