Amyloid Alone—Any Amyloid—Raises P-Tau in Mice
Cerebrospinal fluid p-tau217 and -181 rose in tandem with amyloid deposition in the brain, regardless of whether the plaques contained Aβ or amyloid formed by a different protein.
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Cerebrospinal fluid p-tau217 and -181 rose in tandem with amyloid deposition in the brain, regardless of whether the plaques contained Aβ or amyloid formed by a different protein.
People with subjective or mild cognitive impairment are less likely to get dementia if their CSF Aβ38 levels are high. Should γ-secretase modulators be revived?
Tau PET holds a slight edge over the plasma marker in people who already have mild cognitive impairment.
At CTAD, scientists presented an electronic version of the CDR, plus new digital tests. Will smartphone apps pick up mild cognitive impairment and even preclinical cognitive change?
AI-powered apps catch changes in how a person speaks that may reveal cognitive decline in frontotemporal dementia and early Alzheimer’s. Can smartphones deliver biomarkers for trial enrollment and diagnosis?
Data shown at CTAD suggests the Aβ42/40 ratio falls in the blood before it does in the CSF, offering perhaps the earliest glimpse at the pathophysiology of Alzheimer's. Measuring that change prospectively might be a tall order.
At CTAD, all eyes were on the anti-amyloid antibody donanemab, which is before the FDA. Scientists showed how Phase 3 is enrolling, and how plasma tau enables wholly remote inclusion of people with plaques and tangles.
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.