Drop of Hope? No Cognitive Worsening on BACE Inhibitor
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.
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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.
In therapy-like paradigm, suppressing ApoE4 in astrocytes toned down tauopathy. This assuaged microglia, neurodegeneration, and revived nest-building.
After news on “new data” they won’t see, three committee members argue against approval.
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.
New data presented at the AD/PD conference offer the first evidence that a brain-shuttle strategy can work in people; the lecanemab and aducanumab antibody programs offer small updates.
The field is shifting from targeting tau’s tips to its mid-region, especially where tau binds microtubules. Several new candidates are in the clinic; whether the strategy will work remains to be seen.
The Phase 2 trial provides the strongest evidence yet that removing most amyloid from the brain bolsters cognition, although the benefit is small.
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.
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.
In early stage trials, light and sound promoted neuronal communication, calmed immune cells, and slowed brain atrophy, but cognitive benefit remains unclear.
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