Alzheimer’s Proteomics Treasure Trove?
Analysis of brain tissue from Alzheimer’s patients offers a glimpse of proteomic changes in the disease.
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Analysis of brain tissue from Alzheimer’s patients offers a glimpse of proteomic changes in the disease.
At AAIC, researchers debuted a method that detects changes in plasma Aβ42 in people with brain amyloid. If confirmed, a widely available screening test for presymptomatic AD could follow.
Researchers at AAIC reinforced the idea that tau pathology drives cognitive decline, although amyloid plaques were implicated in semantic memory deficits.
Researchers at AAIC described different correlates of CSF and PET measures of Aβ and tau.
AAIC presentations identified early imaging changes in aging and AD, and reinforced the idea that CSF markers change little over the short term.
Researchers at AAIC presented several imaging measures that may help explain the phenomenon of preserved cognition in the face of AD pathology.
Tau in the plasma rises after traumatic brain injury, with cognitive decline, and progression to mild cognitive impairment.
Alzheimer’s science has undergone a paradigm shift toward the disease’s silent phase. For trials, this means change at every level: new participants, new screening tools, new outcome measurements. What’s the progress?
Clinical validation is showing automated Elecsys, Lumipulse assays to be reliable and predictive. The story on blood tests has turned from non-starter to intensely promising for broad-based screening.
Certified reference material by which companies can calibrate assays is now available worldwide.
An infrared spectral signature of amyloid β-sheets predicted AD conversion years before diagnosis.
High vascular risk scores and Aβ burden independently associate with cognitive decline, but combined, they speed things up.
Investors pledge new money for research into biomarkers that yield marketable tests.
Sensitive cognitive tests detect deficits in preclinical Alzheimer’s even before an amyloid scan reads positive. And CSF Aβ42 drops a decade before that—pushing research ever farther into the preclinical phase.
Where does TREM2-dependent microglial activity fit into the staging diagram of Alzheimer’s disease?