Robert D. Terry, 93, Co-Founder of U.S. Alzheimer’s Research
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.
6400 RESULTS
Sort By:
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.
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.
Machine learning analysis of 912 PET scans says neurofibrillary tangles spread through the AD brain in one of four distinct patterns.
A chemist at the University of Cambridge, Dobson developed equations that described the kinetics of protein aggregation in diseases such as Alzheimer’s.
A panel of experts concludes the evidence for this scary prospect is weak, but recommends neurosurgeons use separate neurosurgical instruments for young and old patients. The experts called for further studies.
Droplets of triglycerides accumulate in microglia exposed to Aβ fibrils. These cells barely ate Aβ, and released molecules that damage neurons.
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.
The L1CAM cell adhesion marker is a widely adopted marker of neuron-derived extracellular vesicles. Except it cannot be found in those teeny packets, claims a new study.
The APOE3-Jacksonville variant generates a protein whose greater lipid-hauling capacity renders it less prone to self-aggregate. This boosted phospholipid trafficking and reduced the number of plaques and downstream damage.