The protease suppresses Aβ in Down’s syndrome organoids.
Post-translational modifications differ from those in AD tau fibrils, and may dictate tau strains.
The creation of long-term memories requires a continual supply of myelin provided by newly formed oligodendrocytes. Alas, the generation of fresh oligodendrocytes diminishes with age, along with memory.
FDA approves adding safety and efficacy data from an Alzheimer’s trial to the drug’s label.
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.
Synapse loss and mitochondrial stress, as seen by separate PET tracers, go hand-in-hand in Alzheimer’s, Parkinson’s, and frontotemporal dementia.
New research presented at the HAI conference also finds links between UCB-J uptake and plaques, tangles, and cognitive decline.
PET Tracer Detects Synapse Loss Across Alzheimer’s Brain Multimodal Imaging of Neurodegenerative Diseases Links Pathology and Cellular Dysfunction Tau PET: The Field Expands Rapidly Can PET Match Up Areas of Protein Deposit With Alzheimer’s Symptoms? How ...
Quite independently of what it does to Aβ or tau, ApoE4 stokes α-synuclein pathology in mouse models. People with Lewy body dementia who carry ApoE4 had more phosphorylated synuclein in their brains, and their cognition declined faster.
Researchers implicate PrP in the toxicity of Aβ, tau, and α-synuclein oligomers in several neurodegenerative diseases.
Compared with people who carry two copies of ApoE3 or ApoE4, ApoE2 homozygotes had an 87 and 99.6 percent lower risk for AD, respectively.
Poor lysosomal function in dopaminergic neurons derived from people with YOPD points to disease origin and potential therapies.
Frequent heading weakened verbal memory in amateur soccer players, and more so in ApoE4 carriers.
A small molecule binds the retromer complex, preventing Aβ accumulation, tau hyperphosphorylation, and their downstream consequences in mice.
Aberrant protein-protein interactions centered on HSP90 may contribute to Alzheimer’s disease. Can an inhibitor set things right?