Researchers at SfN 2016 proposed dialing up the immune response in Alzheimer’s brains to enhance phagocytosis.
At SfN 2016, researchers debuted new mouse models that may better represent human disease.
Researchers at SfN 2016 touted the advantages of APP knock-ins, but noted they are less useful than overexpression models for studying behavior.
Astrocytes and Exosomes Implicated in Protein Propagation Knock-In Alzheimer’s Mice Catch on More Broadly in the Field Next-Generation Mouse Models: Tau Knock-ins and Human Chimeras Inflammation Helps Microglia Clear Amyloid from AD Brains Exosomes and ...
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.