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.
A plasma assay for Alzheimer’s could radically speed up screening for clinical trials; alas, competing assays don’t measure the same thing.
Regulators in the U.S. and Europe have certified a mass-spectrometry-based blood test for amyloid-β. Plasma phospho-tau markers are poised to come next.
After shutting down a Phase 3 program last March, Biogen now says the futility analysis it did was incorrect, and that a new analysis of a larger dataset in fact supports filing for FDA marketing approval next year.
A new single-nucleus RNA-Seq study of 3,900 endothelial cells finds a boost in angiogenesis and antigen presentation genes, drawing attention to the vascular component of AD.
Amyloids of AIMP2 found in Parkinson’s disease may seed α-synuclein aggregation.
Despite overall falling dementia rates in the U.S., black people remain more susceptible than whites.
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.
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?
By pinpointing where tau pathology starts in a person’s brain, researchers better predicted future spread and determined small changes in tangle load.
Phospholipase C-γ2 acts downstream of TREM2 to rev up beneficial inflammation, phagocytosis, and cell survival.