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.
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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.
A single-nuclei RNA-Seq study found more autophagy and chaperone gene expression in familial AD brain, more intense microglial activation in sporadic.
Using different methods and studying different populations, two studies report similar trajectories of fluid and imaging biomarkers over a 20-year span of AD.
Methylated CAG-repeat RNAs and 14-3-3θ promote TDP-43 aggregation.
In awake fruit flies, neurons pass toxic lipids to glia for storage. When the flies sleep, glia metabolize the fat to reset for a new day.
In more than 52,000 cognitively healthy people, elevated plasma GFAP or NfL more than doubled the risk the person would develop dementia over the next 14 years.
A new, stem-cell-based method generated neural cultures that live long enough to suffer the consequences of TDP-43 dysregulation.
People receiving personalized Type 2 diabetes management were 28 percent less likely to develop dementia, and 15 percent less likely to get Alzheimer's.