The company has halted all trials of atabecestat.
Engineered nanoparticles snatched extracellular Aβ, ferried it into cells, and switched on autophagy, clearing the peptide from the brains of mice. Would this work as a drug?
Contrary to previous findings, both proteins seem to escape via passive diffusion. This has implications for therapeutic strategies to keep them where they belong.
Aggregates that form inside, or just pass through, oligodendrocytes take on the properties of the virulent strain that gives rise to multiple system atrophy.
ApoE4 raises CSF tau more in women than in men, suggesting sex may influence the risk of neurodegeneration, especially in amyloid-positive E4 carriers.
Exposure to lipid membranes embedded with cholesterol accelerate Aβ fibril formation by up to 20-fold.
A large retrospective study in veterans finds that even brain injuries that cause no loss of consciousness come with a twofold higher risk of developing all-cause dementia.
The two datasets reveal almost identical cognitive decline in prodromal AD, the stage targeted by secondary prevention trials.
Even at below threshold levels, cortical amyloid can drive cognitive decline, tau accumulation.
Two tau PET tracers flag brain areas that accumulate tangles, without background labeling in the choroid plexus. However, pesky off-target binding was seen in the meninges.
The antioxidant ebselen promotes disulfides in SOD1, restores dimerization, and prevents protein misfolding.
Biogen showed results from clinical trials of anti-Aβ and anti-α-synuclein antibodies at the American Academy of Neurology annual meeting.
Researchers take first steps on road to targeting disease-causing APP mutations and amyloid processing.
The drug had no effect on any clinical measure, while there were side effects such as rashes, insomnia, and thoughts of suicide.
In an AD mouse model, a deficit in specialized mediators prevented microglia from tempering inflammation and clearing Aβ. Time to learn about resolvins?
No filters selected