6545 RESULTS
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Transcriptomics pinpoints an expansion of pro-inflammatory microglia in people who carried the R47H-TREM2 variant. A similar cadre of microglia arose in female tauopathy mice carrying a single copy of the AD risk variant.
The same 24 proteins that are downregulated in an Alzheimer’s proteomic study are turned up in young APOE4 carriers. Two proteins, the kinases Yes1 and Fyn1, are targets of the drug dasatinib, which is being tested as an anti-aging senolytic in AD.
While Phase 3 trials of subcutaneous gantenerumab continue, scientists say delivering the antibody to the brain via the transferrin receptor might be twice as efficient.
In a mouse model of amyloidosis, microglia carried Aβ aggregates into grafted wild-type tissue. The immune cells played a key part in the subsequent growth of plaques in the graft.
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.
At CTAD, scientists discussed whether a cognitive benefit on semorinemab was real, even as gosuranemab might have made people a bit worse. Other scientists are building an ambitious tau platform, including combination trials.
Data shown at CTAD suggests the Aβ42/40 ratio falls in the blood before it does in the CSF, offering perhaps the earliest glimpse at the pathophysiology of Alzheimer's. Measuring that change prospectively might be a tall order.
At CTAD, all eyes were on the anti-amyloid antibody donanemab, which is before the FDA. Scientists showed how Phase 3 is enrolling, and how plasma tau enables wholly remote inclusion of people with plaques and tangles.
Aduhelm Lowers Tau; Registry to Track Real-World Performance Donanemab Phase 3 Puts Plasma p-Tau, Remote Assessments to the Test Plasma Aβ—First Sign of AD, But Tough to Measure Prospectively? More Tau Antibodies Bid Adieu; Semorinemab Keeps Foot in Door
While a death causes jitters, new blood phospho-tau data from Phase 3 trials strengthen the antibody’s claim to disease modification, and post-market studies seek evidence of benefit.
The new gene JADE1 encodes an adaptor protein that sits in tangles and nonetheless appears neuroprotective. The study also turned up three AD and two PSP genes, suggesting PART overlaps with these conditions.
In cell culture and mouse models, verubecestat rallied tumor-promoting macrophages to eat glioma cells, slowing tumor growth.
In Alzheimer's mice without the AD risk gene Abi3, fewer microglia crowd around amyloid plaques. Cultured microglia without Abi3 appear stuck in a torpor, even though their phagocytosis mostly works.
In mouse models, a sluggish thalamic reticular nucleus shortens slow-wave sleep. In one model, activating this brain area lengthened the mice's slumber while also reducing their plaque loads.
At a recent conference, researchers presented more evidence tying the APOE4 allele to disrupted lipid metabolism. They linked this problem to Aβ production.
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