ApoE4 raises CSF tau more in women than in men, suggesting sex may influence the risk of neurodegeneration, especially in amyloid-positive E4 carriers.
PET scans detect activated glial cells in current and recently retired professional football players up to 21 years after their last concussion.
The neurodegeneration marker appears to track disease severity in AD and MS patients with great sensitivity.
The largest study yet on neurofilament light chain suggests plasma levels rise with disease and correlate with other signs of neurodegeneration.
Levels of a neuronal protein in blood correlated with rate of decline in two U.K. cohorts.
Serial data establishes different trajectories for CSF t-tau and p-tau.
The ligand binds the microglia-specific CSF1 receptor in animal and postmortem studies; human trials are forthcoming.
During deep sleep, people with AD pathology, particularly tau tangles, have less low-frequency slow-wave brain activity, which is important for memory consolidation.
In a research study, one-fifth of healthy people who learned they were at high risk for AD said they might consider physician-assisted death as a future option.
The plasma biomarker neurofilament light was able to distinguish individual mutation carriers from noncarriers three years prior to onset.
Carriers accumulate fewer tangles than noncarriers for a given amount of amyloid, explaining how the gene variant may lower a person’s Alzheimer’s risk.
A simple blood draw may help distinguish garden-variety PD from other, less common parkinsonian disorders early in disease.
The circular transcripts correlate with AD pathology and dementia severity, suggesting potential roles in pathogenesis or as biomarkers.
The modeling approach reinforces the idea that tau pathology propagates through the brain’s physical architecture, including neuronal networks.
The blood-based marker may be far more scalable and cost-effective for tracking the disease than PET imaging and CSF biomarkers.