In Familial Alzheimer’s, β-Synuclein Rises in Blood a Decade Before Onset
In ADAD mutation carriers, blood β-synuclein crept up after their amyloid-PET scans had turned positive, but before axons degenerated. Does it reflect crumbling synapses?
In ADAD mutation carriers, blood β-synuclein crept up after their amyloid-PET scans had turned positive, but before axons degenerated. Does it reflect crumbling synapses?
Cryo-EM identifies a similar protein fold in these ependymal cell inclusions as in parenchymal TMEM106b fibrils.
By utilizing advances in parallel imaging, scientists cut the time needed for diagnostic MRI scans from 18 to 6.5 minutes, without a noticeable loss in quality.
Early stage trials hint that new therapeutics could take down APP, boost ApoE2, or fix inflammatory and metabolic dysfunction in AD.
Vendors of plasma p-tau217-based tests are filing with U.S. and European regulators for approval of fully automated, in vitro diagnostics.
The findings suggest that non-AD pathologies, driven by other comorbidities, might contribute to cognitive decline in these populations.
The commercial software icobrain aria sharpened radiologists’ detection of ARIA-E and ARIA-H. The FDA approved the technology for clinical use November 7.
In Madrid, researchers touted the benefits of plasma prescreening and showed baseline data on these early AD populations. Meanwhile, remternetug has begun Phase 3.
This week, more news from CTAD. Alzheimerologists learned that, after years of trying to fold more underrepresented groups into trials, they were indeed reaching and screening more non-white people, but so many of them do not have brain amyloid that their enrollment percentage is still low. On the up side: tools keep improving. MRI is speeding up, AI can help spot ARIA, and p-tau blood tests are heading toward certification as in vitro diagnostics. And while two anti-amyloid antibodies are a nice start, researchers are trialing many more ways to fight AD.
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