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?
Middle-aged WTC responders have cognitive problems, which correlate not only with their PTSD symptoms and exposure to toxic dust, but also with biomarkers of amyloid and tau.