Aduhelm Lowers Tau; Registry to Track Real-World Performance
While a death causes jitters, new blood phospho-tau data from Phase 3 trials strengthen the antibody’s claim to disease modification, and post-market studies seek evidence of benefit.
611 RESULTS
Sort By:
While a death causes jitters, new blood phospho-tau data from Phase 3 trials strengthen the antibody’s claim to disease modification, and post-market studies seek evidence of benefit.
A new study reports that activated microglia soak up glucose, and may be responsible for the elevated FDG PET signal seen in early Alzheimer's disease. Mouse microglia used 28 times more FDG than did neurons.
In a collaborative tour de force, scientists for the first time compared eight Aβ assays in the same plasma samples. Mass-spectrometry assays more accurately picked up brain amyloid than did most immunoassays, but one fully automated immunoassay was on par.
Therapies targeting key neurodegenerative disease proteins, or biomarkers, are failing. Can Mendelian randomization test cherished assumptions?
The sandwich immunoassay recognizes small soluble oligomers in both cerebrospinal fluid and plasma with high sensitivity and specificity.
Amyloid Time: Because amyloid burden grows at a constant rate after having crossed a tipping point, scientists were able to predict when a person’s symptoms will begin, using only his or her age and one PET scan.
In an aging cohort, weak LC signal intensity on MRI correlated with plaques, tangles, and memory problems.
North Carolina and South Texas centers to focus on risk factors and diversity.
Network analysis of human PET brain imaging data suggests amyloid plaques set the stage for microglial activation that, in turn, drives tangle spread through the brain.
Markers of neuronal injury rose in plasma within a few months of severe COVID-19, then fell back to normal by six months. Some cases with brain symptoms had lower Aβ and higher tau in their blood.
Decades before tangles become rampant, the biomarker p-tau231 rises in both CSF and plasma. More surprising: neuroinflammation markers do, too.
Among old people with high total tau levels in plasma, cognition slid far less in those who are active than in their inactive peers. Could blood tests motivate at-risk people to exercise?
In carriers of the allele, cognition falters a bit earlier than in noncarriers. Brain amyloid, structure, and metabolism changed, as previously seen in sporadic and familial AD, but only some of the fluid markers did.
Compared to amyloid PET and cortical thickness, tau PET better foretold waning cognition across the Alzheimer's disease spectrum, from cognitively normal to dementia. Age, but not sex or APOE status, hastened deterioration over two years.
A set of 19 plasma proteins identified clinical Alzheimer’s cases with 97 percent accuracy, and it distinguished mild versus severe dementia. The panel was tested in two small cohorts.