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.
Functional connections between two brain regions are the strongest indicator that pathologic, accumulated tau will spread from one to another.
When observed over an eight-year period, people with the highest plasma concentrations were more likely to die than people with lower levels.
New study finds no uptick in herpes viruses in AD. If herpes plays a role, it says, then probably it acts as an early trigger of pathology.
Aβ oligomers latch onto adrenergic receptors, mobilizing a kinase that phosphorylates tau. Blocking adrenergic signaling wards off memory problems in amyloidosis mice.
These oily microglia resemble the foamy macrophages seen in atherosclerotic plaques. They correlate with aging, inflammation, and neurodegenerative disease.
Single-nucleus transcriptomics of postmortem AD brain and mouse models of amyloidosis hammers home the species-specific responses of microglia to Aβ pathology.
Three studies found no link between vascular disease and cerebral amyloidosis.
Positive allosteric modulators improve learning and memory in mouse models of AD and epilepsy.