Studies in mice and humans show that sleep suppresses extracellular tau and slows its spread.
In familial Alzheimer’s disease, rise in NfL in the blood precedes disease onset by 16 years.
Stakeholders have until February 11 to comment on draft FDA guidance for biomarker qualification.
During deep sleep, people with AD pathology, particularly tau tangles, have less low-frequency slow-wave brain activity, which is important for memory consolidation.
The largest study so far to compare brain scans and CSF among African-Americans and Caucasians finds differences, but participant numbers remain small.
The ligand binds the microglia-specific CSF1 receptor in animal and postmortem studies; human trials are forthcoming.
This past year, therapeutic antibodies massively reduced brain amyloid, blood tests came into their own, and systems-based approaches transformed the study of gene expression, glial cells, and selective vulnerability.
An ultrasensitive assay picked up elevated concentrations of N-terminal tau fragments in the blood of people with AD.
Case study in early onset AD finds PET ligand tracks regional tau burden.
In patients across a range of neurodegenerative diseases, NfL ramps up in the cerebrospinal fluid. Levels are higher in those with worse disease.
FDG PET revealed the formation of a new functional brain network. It explains clinical improvements noted previously.
In sporadic and familial forms of AD, progranulin climbs in the cerebrospinal fluid as disease progresses, perhaps reflecting microglial activation.
Researchers are applying the proposed 2018 NIA-AA diagnostic criteria to three large, standing cohorts. How did the research framework perform?
People with a lot of neurofilament light protein in their spinal fluid are more likely to develop mild cognitive impairment in the next four years.
Large IDEAS data set establishes that PET scans are valuable in clinical practice. Other studies suggest CSF biomarker ratios perform nearly as well.