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 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.
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.
In mice lacking the recycling protein GGA3, BACE1 trafficking stalls, local Aβ production increases, and axons swell. Does this explain the neuritic dystrophies seen in early AD?
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.
In mice, forebrain neurons with hobbled retromers ooze fragments of tau and several BACE1 substrates into the CSF. Similar proteins are up in CSF from people with MCI and Alzheimer’s disease.
Could this forestall the amyloid cascade and the onset of Alzheimer’s disease?
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.