Vascular troubles preceded amyloid deposition and other disease markers in a new Alzheimer’s progression model based on ADNI data.
The use of gene expression profiling to characterize Alzheimer disease pathology has, unsurprisingly, focused on...
The results of the AD2000 study of donepezil (Aricept) in Alzheimer's—published in the June 26 Lancet—made a big splash in the media pond. While confirming previous...
Fungal cells cropped up in multiple brain regions of all AD brains examined, but how they got there and what they are doing remains mysterious.
P25 overexpression in APP transgenic mice is one of perhaps many artifacts of APP overexpression, APP, researchers charge. Do APP/PS1 transgenic mouse phenotypes need re-evaluation?
A veteran of the Battle of the Bulge, Terry trained legions of neuropathologists at Einstein and UCSD. He described paired helical filaments and linked synapse loss to cognitive decline.
A Japanese company enters the arena with a plasma Aβ test that rivals CSF for detecting brain amyloid.
A chemist at the University of Cambridge, Dobson developed equations that described the kinetics of protein aggregation in diseases such as Alzheimer’s.
Herpes viruses that are commonly found in human brain promote rapid Aβ fibrillization and deposition in AD model systems.
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.
Scientists have turned their attention toward testing therapies in early-stage patients who have underlying brain pathology but little to no functional impairment...
A new mass spectrometry analysis provides the most thorough catalog yet of modifications to tau.
Wild-type mice exposed to blood from Alzheimer’s amyloidosis mice developed plaques, tau phosphorylation, neuroinflammation, and synaptic deficits.
After veru- and atabecestat, now a third β-secretase inhibitor, by Eli Lilly and AstraZeneca, is being pulled from ongoing Phase 3 trials of symptomatic Alzheimer’s disease.
Viral surfaces attract proteins from the extracellular environment of the person they infect. This corona of host proteins makes the virus more or less infective—and promotes amyloid fibrils.