A genetic polymorphism in the human prion protein that shielded cannibalistic tribe members from the disease kuru could help researchers understand the structural biology of Creutzfeldt-Jacob disease.
Microglia internalize pathogenic forms of tau more robustly when anti-tau antibodies adorn the protein.
Could filling these cavities with a small molecule be therapeutic?
Alzheimer’s experts gathered in Las Vegas to chart a path for combination trials on repurposed drugs.
Researchers tie oligomers with different structures to distinct temporal, spatial, and cognitive effects in living brains.
Proper form and function of the brain’s immune cells depend on a diverse mix of “good” bacteria in the mouse intestine.
Levels of a neuronal protein in blood correlated with rate of decline in two U.K. cohorts.
A new study reports that Aβ disturbs sleep patterns that help cement memories.
However, once a person has ALS, diabetes does not affect how long they survive.
A new crystal structure shows a unique shape of Aβ in the arms of solanezumab. Exactly how this and other antibodies in the clinical pipeline grip Aβ could explain some differences in trial results.
Cellular, animal, and human studies suggest that the AD risk gene PICALM escorts Aβ through the blood-brain barrier.
In separate studies, researchers propose that high CSF ferritin and D-serine could become biomarkers to predict declining cognition in Alzheimer’s disease.
They overexpress Activin, allowing neurons to regrow axons in the central nervous system.
The motor neurons most sensitive to ALS require a microRNA cluster to survive, lest PTEN activates apoptosis.
The signature fall of cerebrospinal fluid concentrations of Aβ that herald Alzheimer’s may be preceded by a brief boost.
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