Cell lines can serve as sensors for strains found in different human tauopathies.
Researchers at SfN 2016 painted a more detailed picture of how misfolded proteins may proliferate, as one cell spreads these “hot potatoes” to the next.
Diminishing Alzheimer’s pathology in mice appears to be as easy as shining a light in their eyes. Could it work in people?
Less aquaporin-4 in astrocytes surrounding blood vessels suggests impaired clearance of Aβ in people with AD.
In a PD mouse model, microbes pump out short-chain fatty acids that worsen synuclein aggregation and motor problems. Intestinal flora from people appears to do the same.
Enhancing glutamate transport partially restores neural function in mice.
PET scans detect activated glial cells in current and recently retired professional football players up to 21 years after their last concussion.
Friends and colleagues grapple with the loss of this young investigator.
Insulin delivered directly to the brain does nothing to Aβ in an AD mouse model, complicating the relationship between diabetes and Alzheimer’s.
Evidence from a nationally representative sample suggests a 12-year drop in age-specific risk of dementia.
Eli Lilly has given up on regulatory submission for mild AD, but leaves door open to seeking approval for earlier disease stages if three ongoing studies succeed.
Strains injected into mouse brain seed tau aggregation at different rates and in different regions of the brain.
Using a new, quantitative MRI method, researchers find accelerated myelin deterioration in preclinical Alzheimer’s disease.
This new inhibitor, which only works once phosphorylated by GSK3, reduced amyloid load and prevented cognitive deficits in an AD mouse model.
At least one phosphate tag may quell Aβ excitotoxicity.