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.
DIAN, Roche, Lilly disclose that neither gantenerumab nor solanezumab slowed cognitive decline in the first-pass comparison of drug and placebo groups. Analyses are ongoing; dose may have been too low.
Researchers implicate PrP in the toxicity of Aβ, tau, and α-synuclein oligomers in several neurodegenerative diseases.
Middle-aged WTC responders have cognitive problems, which correlate not only with their PTSD symptoms and exposure to toxic dust, but also with biomarkers of amyloid and tau.
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.
Single-nucleus transcriptomics of postmortem AD brain and mouse models of amyloidosis hammers home the species-specific responses of microglia to Aβ pathology.
With experiments and careers on hold, scientists working from home are turning to virtual lab meetings and journal clubs to keep up morale.
New study finds no uptick in herpes viruses in AD. If herpes plays a role, it says, then probably it acts as an early trigger of pathology.
In Alzheimer’s brain, granulovacuolar bodies in neurons harbor activated necrosomes. They correlate with tau pathology and neuron loss, raising new questions about how neurons die in this disease.
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?
Aβ oligomers latch onto adrenergic receptors, mobilizing a kinase that phosphorylates tau. Blocking adrenergic signaling wards off memory problems in amyloidosis mice.
Functional connections between two brain regions are the strongest indicator that pathologic, accumulated tau will spread from one to another.
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 cells are primed to attack. Their targets include Epstein-Barr virus peptides.
Two studies reveal new aspects of the neurovascular physiology that regulate the flow of oxygenated blood into the brain’s arterioles and capillaries in response to neuronal stimulation.