Using mass spectrometry to detect teensy amounts of phospho-tau species in plasma, researchers reported that p-tau-217 and p-tau-181 picked out people with Aβ pathology. Differences between groups appear to be huge. An MS-based test for plasma Aβ42 corresponded to brain amyloid, and is going in for regulatory approval.
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.
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.
Researchers at an international frontotemporal dementia congress reported progress in finding markers that track disease, but no luck thus far with diagnostic markers.
Rather than changing one by one, many biomarkers—including cognition, tau PET, hippocampal atrophy, and CSF p-tau—shift together, around the time of symptom onset in young adults with familial AD.
Amyloid and tau PET are helping scientists pinpoint the underlying cause of specific AD symptoms. Perhaps imaging of certain brain regions will help predict an individual’s progression.
Two papers report that phosphorylated tau in the blood distinguishes people with AD from healthy controls and from people with frontotemporal and vascular dementias.
Brain imaging and cognitive tests may be the gold standards for tracking AD progression, but clinical trials using these procedures are expensive, risky, and time-consuming...