Confronting unprecedented challenges this past year, scientists found ways to tide their research over and keep clinical trials mostly on track.
Changes in the composition of the cerebrospinal fluid and synapses may reveal novel insights into AD pathology.
Assays will help doctors diagnose Alzheimer’s disease and amnestic mild cognitive impairment in Taiwanese clinics.
At AAT-ADPD, researchers report how they built on prior reports that a person’s blood level of p-tau181 tells if they have Alzheimer’s.
Plaque-busting antibodies reset the time course of amyloid accumulation, but so far provide only hints of a clinical benefit in mild AD. Good news: once gone, plaque stays gone for a while.
A new PET tracer. Plasma glial fibrillary acidic protein. Two new, promising surrogates for astrogliosis are filling in the Alzheimer’s biomarker toolbox. Both reflect Aβ amyloid better than they do tau tangles.
As life expectancy increases in countries such as Nigeria, Brazil, China, and others, so does the number of people with dementia. How to provide modern care for them?
As FTD consortia chase biomarkers, they see plasma NfL and neuronal pentraxin-2—which reflect neurodegeneration—change before symptoms. Trials nudge progranulin and poly-DP. Still needed: more markers of the pathophysiology that unfolds in the brain.
A new trial will compare digital and blood-based biomarkers to amyloid PET scans in order to learn which ones best pick out early plaque accumulation.
At CTAD, tau-PET data from people in different stages of various neurodegenerative diseases highlighted both commonalities and peculiarities.
Longitudinal studies in DS have pegged biomarkers and cognitive measures as potential clinical trial readouts. Hundreds of adults are anticipated to join trial-ready cohorts this year.
Herpes infection upped risk in ApoE4 carriers, damaged brain tissue, and correlated with neurodegeneration markers in the CSF.