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AD risk scores based on gene expression in microglia associate with having amyloid plaques, and a microglial genomic atlas displays how variants influence gene expression. Polygenic variation in neurons sways cognition.
Found in one Swedish family, this mutation speeds up plaque deposition by way of two different mechanisms, leading to disease onset as young as age 40.
Single-nuclei expression analysis identified different cell clusters from people who carried autosomal-dominant Alzheimer’s mutations or risk variants for late-onset AD. Also, microglia RNA-Seq goes big.
Scientists are testing passive and active immunotherapies that take down pyroglutamate Aβ, and a combo Aβ/tau vaccine.
In an open-label Phase 2 study, fluid biomarkers suggested the anti-sortilin antibody restored lysosomal function and reduced neuroinflammation in people with symptomatic FTD. Tantalizingly, participants worsened less than historical controls.
In the wake of the controversial thumbs-up for Aduhelm, the U.S. federal government is probing not only aducanumab’s price and approval history, but also the FDA’s accelerated approval pathway in general.
Scientists worry about trial recruitment and retention, and discuss whether upcoming trials should allow aducanumab as a background therapy.
Patients taken off the drug continue to outperform those who were never on it, and decline slows even more once treatment resumes. Cognition and plasma Aβ changes are consistent with disease-modifying effect.
While payers public and private are deliberating whether or not to cover this first-in-class drug, the health economics group ICER re-affirms its original conclusion that aducanumab is overpriced.
Biogen sponsors an observational study on the drug’s effects; no word yet on the FDA-required Phase 4 trial. Meanwhile, researchers suggest other ways to test efficacy.
Initial results from the first trial of an antisense oligonucleotide against tau in Alzheimer’s are in. BIIB080 appears safe and curbed total tau and phospho-tau 181 levels in the CSF. Clinical outcomes were not assessed.
Data from a Phase 2 trial also suggested that when amyloid dropped in treated brain, plasma p-tau217 followed suit. Using a CAMD progression model, Lilly claims the biomarker responses correlated with slower decline.
At AAIC, leading Alzheimer’s clinicians plug gaps in the FDA label. They urge exclusion of people with cerebrovascular risk, and an MRI monitoring bonanza. Meanwhile, clinical rollout starts slow, with major hospitals declining to administer.
Aducanumab: Will Appropriate-Use Recommendations Speed Uptake? On Donanemab, Plaques Plummet. Off Donanemab, They Stay Away Antisense Therapy Stifles CSF Tau in Mild Alzheimer’s Disease Seeking Real-World Data on Whether Aducanumab Works Will Insurance Co
Senescent astrocytes spew HMGB1, a harbinger of cell death. Blocking this release prevented cell senescence, reduced neurofibrillary tangles, and improved memory in mice.
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