Changes in the composition of the cerebrospinal fluid and synapses may reveal novel insights into AD pathology.
Protein levels track with cognitive function and can distinguish Alzheimer’s patients from controls.
What’s with all those head-to-head comparison studies of academic and commercial biomarker tests? Could we not just pick one that works, and be done?
A plasma assay for Alzheimer’s could radically speed up screening for clinical trials; alas, competing assays don’t measure the same thing.
At this year’s AAIC, no sooner had scientists reported that phospho-tau in the CSF might reflect early responses to amyloid, than they reported parallel data for phospho-tau in blood.
At AAIC, researchers touted phospho-tau species, especially p217 and p181. They tick up in CSF as an early response to amyloid accumulation.
In 2,144 Colombian ADAD family members, plasma NfL in gene carriers rises as early as two decades before their symptoms start.
At AAIC, researchers presented baseline data from an ongoing, five-year study asking whether the anti-Aβ antibody crenezumab can forestall cognitive decline in autosomal-dominant Alzheimer’s disease.
Longitudinal data identifies four stages of amyloid plaque buildup, with the earliest deposits appearing in the precuneus and posterior cingulate.
The field is searching for a combination of clinical features and biomarkers that will identify the disease in people with mild cognitive impairment.
In carriers of a PD-causing mutation, PET scans showed serotonin transporter loss before motor symptoms set in.
Fully automated immunoassay could offer cost-effective screening for AD.
A meta-analysis of 47 studies suggests CSF NfL is particularly elevated in a select few, suggesting it could help in differential diagnosis.
In healthy, older adults specific EEG patterns correlated with plaque and tangle burdens.
Using different techniques, contestants vied for the best way to tell which ADNI participants would develop clinical, cognitive, or imaging signs of Alzheimer’s disease.