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.
Certified reference material by which companies can calibrate assays is now available worldwide.
PET scans indicate no more AD pathology in PD-MCI than healthy controls, suggesting their cognitive decline results from other factors.
In people who carry a repeat expansion in the C9ORF72 gene, gray and white matter are smaller and subtle impairments in cognition appear decades before symptom onset.
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.
Tau’s apparent lockstep with cognitive decline dominated the PET conversation. Piramal flaunted data, and Merck/Cerveau are close behind. A first stab at imaging synapses in the hippocampus drew notice, too.
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?
Slow vital capacity, a measure of respiratory function, predicted the rate of disease progression in ALS patients, suggesting the test could be used as a primary endpoint in clinical trials.
The neurodegeneration marker appears to track disease severity in AD and MS patients with great sensitivity.
A longitudinal study identified regions in the default mode network as among the first to accumulate Aβ.