Investors pledge new money for research into biomarkers that yield marketable tests.
In an unselected cohort, amyloid-PET scans changed clinical diagnoses and treatment plans for a quarter of participants.
High vascular risk scores and Aβ burden independently associate with cognitive decline, but combined, they speed things up.
ApoE4 raises CSF tau more in women than in men, suggesting sex may influence the risk of neurodegeneration, especially in amyloid-positive E4 carriers.
For the first time, NIA-AA proposal bases diagnosis in living people solely on biomarkers for plaques and tangles.
An infrared spectral signature of amyloid β-sheets predicted AD conversion years before diagnosis.
At AAT-AD/PD, scientists showed that correlated amyloid patches are an even earlier marker than brain-wide positivity, while others puzzled over why tau signals are lower in older people.
A comparison of these large data sets shows that while the two forms of Alzheimer’s disease have separate triggers, they follow the same course and are much more similar than different.
Scientists at the AAT-AD/PD conference debuted new detection methods for this biomarker, which they say distinguished healthy controls from MCI and AD.
Injecting 13C-labeled leucine intravenously, researchers tracked tau turnover in the human brain and cerebrospinal fluid for the first time.
What goes up can come down—rising tides of VILIP-1, neurogranin, and SNAP-25 ebb after onset of AD symptoms.
In three independent cohorts, cognitively healthy people had a higher amyloid burden as they approached the age at which their parents developed late-onset AD.
Longitudinal neuroimaging of DIAN participants reveals that in most regions of the brain affected by AD pathology, Aβ accumulates first, then metabolism slows, then the brain shrinks.
In people with an autosomal-dominant AD mutation, Aβ and tau start accumulating long before the estimated onset of symptoms.
A Japanese company enters the arena with a plasma Aβ test that rivals CSF for detecting brain amyloid.