Fast Plaque Clearance with Little ARIA? So Teases Trontinemab at AD/PD 2024
In a small dose-finding study, Roche’s new brain-shuttle-based anti-amyloid antibody mopped up nearly all plaques in three months, without triggering edema.
In a small dose-finding study, Roche’s new brain-shuttle-based anti-amyloid antibody mopped up nearly all plaques in three months, without triggering edema.
In APOE4/4 microglia, Aβ triggers an uptick of a triglyceride synthesis enzyme. The cells then accumulate lipid droplets and release something neurotoxic.
Lamivudine slightly improved markers of astrogliosis and amyloid pathology. The drug suppresses activity of retrotransposons that are under-methylated in AD.
All endpoints were missed. Company to consider withdrawing the drug, as discussed during FDA Advisory Committee meeting.
Modeling physiological dipeptide repeat expression and partial loss of normal C9ORF72 protein, new knock-in mice show a TGF-β1-driven collagen response in their spinal neurons.
In snoozing mice, silencing neurons dampened ion waves in the interstitial fluid and slowed the flow of solutes. Activating neurons powered CSF flow through the brain.
Mitochondrial activation waned in brain cells a year before mice developed plaques. Inhibiting the kinase GSK3β partially restored the organelles.
A new immunoassay detects N-terminal fragments of tau. They predict tangle accumulation, cortical atrophy, and cognitive decline.
The port city of Lisbon, the launch point of many a voyage of exploration, seemed a fitting site to host the 18th International Conference on Alzheimer’s and Parkinson’s Diseases and related neurological disorders. Disease-modifying therapies for amyloid plaques now approved, researchers are searching for similar treatments for tau, synuclein, and other potential drivers of neurodegeneration. With more than 4,700 attendees navigating 600+ presentations during five days, often spread across six parallel sessions, the conference was bustling, yet imbued with a sense of discovery. Speakers discussed new small-molecule and antibody therapies, combination approaches, new plasma biomarkers for tau and TDP43, and a good smattering of basic biology, from cellular resilience to microglial diversity. Follow along with Alzforum’s conference coverage.
Epigenetics keeps retrotransposons under wraps; alas, tau can unleash these restraints, allowing these jumping genes to flare in tauopathies. A pilot study targeting the HIV drug lamivudine at retrotransposons in mild cognitive impairment was safe and nudged some neurodegeneration and neuroinflammation markers. Meanwhile, long-read sequencing found that people with AD had less methylated, i.e., perhaps more active, retrotransposons than controls.
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