Subgroup analysis addresses APOE4 randomization imbalance, claims treatment with this anti-Aβ protofibril antibody slowed cognitive decline.
The effect is small and stable, but consistent across several drugs. Researchers at CTAD debated whether it might be manageable by adjusting dosing.
Bump in the Road or Disaster? BACE Inhibitors Worsen Cognition Second Look at BAN2401 Data Still Positive, Despite Snafu Blood Tests for Amyloid Step Out at CTAD It’s Official: Tau PET Sees Tangles, and Staging Tangles Predicts Decline Amyloid PET Aids ...
Much like tau, Aβ, and α-synuclein, pathological TDP-43 spreads through the mouse brain, following the trail of neuronal connections and corrupting healthy protein along the way.
Alzheimer’s Researchers Seek Advice on How to Include African-Americans Do African-Americans Have More, or Different, Alzheimer’s Disease? Too Little Data to Tell Is Alzheimer’s more common, or different, in black Americans? Or do cerebrovascular risk ...
At a workshop on engaging more black Americans in ADRD research, new CSF findings stood out against a general dearth of data on Alzheimer’s disease in underrepresented minorities.
Despite having a higher incidence of Alzheimer’s or a related dementia, relatively few black people participate in research studies or drug trials. How to achieve full representation?
In AD brain, scientists see a genome-wide histone acetylation pattern replete with peaks near familiar AD genes such as APP, presenilin, tau, complement receptor, and more.
Clusters of neurons harboring somatic mutations in 56 genes linked to neurodegenerative diseases may be commonplace in the human brain.
X-ray crystallography yields high-resolution structure.
An antibody that binds fibrin blocks neuro-inflammatory signaling while allowing normal clotting.
Analysis of MRI brain volume data identifies multiple AD and FTD/ALS disease subtypes with distinct patterns of degeneration over time.
The most detailed look yet at hippocampal wiring may guide future functional studies and disease research.
Neuromuscular junctions between human stem cell-derived motor neurons and skeletal muscle fibers faltered when cells came from an ALS patient.
A small molecule that protects neurons fends off a short region of Aβ from a specific pocket on the LilrB2 receptor.