Lecanemab Sweeps Up Toxic Aβ Protofibrils, Catches Eyes of Trialists
In a comparison with aducanumab and gantenerumab, lecanemab mopped up protofibrils most efficiently; the antibody has been chosen for DIAN-TU and AHEAD 3-45 trials.
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In a comparison with aducanumab and gantenerumab, lecanemab mopped up protofibrils most efficiently; the antibody has been chosen for DIAN-TU and AHEAD 3-45 trials.
The huge collaborative effort unearthed 42 new risk loci and confirmed 33 others. The hits reinforce known disease pathways and predict progression.
Reactive astrocytes spell trouble for synapses, while microglial transform from protective to destructive as disease progresses.
Neurons with TMEM106B aggregates lose nuclear TDP-43 in ALS models. In tauopathy models, they accumulate no p-tau.
Trontinemab swooped into the brain and removed amyloid efficiently, while causing few cases of ARIA. One person with cerebrovascular pathology died.
Scientists at AAIC said ARIA-E resembles inflammation related to cerebral amyloid angiopathy. The prime suspect? The complement cascade.
These are the first deaths reported from clinical use of lecanemab. One was APOE4 homozygote; both developed severe ARIA-E and seizures.
ARIA rates have been the same or lower than in the Phase 3 trial. About 9,000 people are being treated in the U.S., half as many in Japan. EMA reverses course, recommending approval.
As immunotherapies enter care, scientists explore when to stop them, how amyloid removal relates to cognitive benefit, and whether fluid markers will track both plaque and tangles responses.
In Madrid, researchers touted the benefits of plasma prescreening and showed baseline data on these early AD populations. Meanwhile, remternetug has begun Phase 3.
Lilly’s Phase 2 trial of its O-GlcNAcase inhibitor ceperognastat failed to meet clinical endpoints. The drug’s adverse events suggest potential off-target effects.
Bepranemab results bolster hopes for antibodies targeting tau’s middle section. Whether tangle clearance will improve clinical outcomes remains unclear.
By starting at a low dose and upping it stepwise for four months, scientists nearly halved the risk of ARIA while preserving plaque clearance.
To some, the findings suggest that non-AD pathologies, driven by other comorbidities, might contribute to cognitive decline in these populations.
Vendors of plasma p-tau217-based tests are filing with U.S. and European regulators for approval of fully automated, in vitro diagnostics.
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