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.
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.
Researchers envision p-tau-based blood tests for Alzheimer’s disease within a few years, but maybe not a stand-alone test.
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?
In the negative Phase 2 trial of prasinezumab, populations with more rapid decline benefited; this informed the design of a new Phase 2b study.
Two mouse models presented at AD/PD may hand scientists more translationally relevant tools to explore LOAD pathophysiology and treatment. The tricks: targeted replacement and knocking in multiple GWAS variants.
Both shy and funny, Allsop was a pioneer of modern Alzheimer's research.
Data from Phase 3 trials of elenbecestat show no harm to cognition, leaving open a chance that the drugs could be used safely in the future.
New research implicates IL-6 signaling and even Aβ42 itself as BACE targets, complicating efforts to resurrect BACE inhibitors at a low dose.
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.
In therapy-like paradigm, suppressing ApoE4 in astrocytes toned down tauopathy. This assuaged microglia, neurodegeneration, and revived nest-building.
Sending low-intensity, gamma frequency electric current through the brain boosted short-term memory, perhaps by increasing cholinergic transmission.
In cell culture, neurons with the strongest expression of cell-cycle proteins survived best in the presence of Aβ oligomers.
Disruption of the membraneless organelles may explain toxicity of tau aggregates.