TREM1 Muddles Myeloid Cell Metabolism and Memory in Old Mice
In peripheral macrophages and microglia, the receptor disrupts glucose metabolism. TREM1-deficient amyloidosis mice also had healthier neurons, better memories.
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In peripheral macrophages and microglia, the receptor disrupts glucose metabolism. TREM1-deficient amyloidosis mice also had healthier neurons, better memories.
In a multiple sclerosis model, activated microglia reverse electron transport (RET) in their mitochondria, creating oxidative stress. Blocking RET eased pathology.
Fast Plaque Clearance with Little ARIA? So Teases Trontinemab at AD/PD 2024 TauRx Parses Subgroups to Make the Case for Methylene Blue Derivative, Again Therapeutic Contenders Target Hard-to-Reach Pockets of Tau Mouse Models and Markers for Cerebral Amylo
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.
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