The global platform trial for Alzheimer’s due to mutations in APP or presenilin will try to treat or prevent symptoms by deploying a therapeutic antibody that homes in on a piece of tau known to aggregate into neurofibrillary tangles.
The FTD Prevention Initiative merges cohort studies from across the world with a common goal—to execute effective clinical trials for FTD.
The first topline Phase 2 results from an antibody targeting Parkinson’s pathology, Roche’s prasinezumab, were a mixed bag. Next steps are unclear.
Merged Consortia Forge Path to Trials in Frontotemporal Dementia FTD Fluid Markers for Degeneration: Check. For Pathology: Not Yet. Imaging Exposes Hugely Heterogeneous Brain Changes Among FTDs Moving Target: Can Standardized Tests Track Symptoms of FTD? ...
At this year’s ICFTD meeting, researchers reviewed the lay of the land of current and planned trials for FTD, with glimpses of how the newly formed FTD Prevention Initiative seeks to coordinate treatment and prevention trials in the future.
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.
An international group of researchers* have agreed upon recommendations to revise the criteria for postmortem diagnosis of Alzheimer’s disease (AD)...
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?
Subtle memory deficits resolved after volunteers stopped taking the Novartis BACE inhibitor.
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.
At AD/PD 2021, clinicians discussed neurological symptoms and brain tissue damage in older people who died from COVID-19.
By shifting to home nursing and telemedicine, clinical researchers kept inching ahead during lockdowns.
Researchers used PET scans from 4,000 people to link RBFOX1 risk variants to amyloidosis. People with lower RBFOX1 expression in their brains had more amyloid and worse cognition.
Sending low-intensity, gamma frequency electric current through the brain boosted short-term memory, perhaps by increasing cholinergic transmission.