Bassoon Heralds Spread of Toxic Tau
Knocking down the synaptic scaffolding protein in mice eased neurofibrillary tangles, gliosis, and neurodegeneration.
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Knocking down the synaptic scaffolding protein in mice eased neurofibrillary tangles, gliosis, and neurodegeneration.
Along with previously identified rare variants in TREM2, SORL1, and ABCA7, a massive exome sequencing effort identified variants in ATP8B4 and ABCA1.
Without this mechanosensor, microglia slowly respond to plaques. In mice, a Piezo1 agonist bolstered plaque containment and lowered amyloid burden.
In mice, this glycoprotein fragment accelerated amyloid deposition in cerebral blood vessels; in people, higher levels correlated with faster cognitive decline and greater AD risk.
Phospho-tau and tangles accumulated, microglia bloated with lipids, and the brain atrophied in these mice.
The antibody removed less plaque than expected and did not slow cognitive decline, according to top-line data. Detailed data to come at CTAD.
These unassuming cells keep cerebral vessels supple, forcing CSF through the brain and clearing Aβ. Their abilities wane with age, but can be restored.
Brain-wide transcriptomics identified genes that characterize astrocytes by anatomical region and morphology. Some are risk genes for neurodegeneration.
Once assumed to be high-molecular-weight oligomers, these short, diffusible fibrils share the same structure as their plaque-bound counterparts. Both bind lecanemab.
Scientists now have more options to model late-onset Alzheimer’s disease. APOE, TREM2, and gene combinations better mimic LOAD than do models of familial AD.
The iPSC Neurodegenerative Disease Institute proposes a reference iPSC line to standardize research between labs.
Sans SYK, mice struggle to mobilize disease-associated microglia or reign in amyloid or myelin fragments.
Activating the microglial receptor also left amyloid untouched, despite prompting microglia to surround plaques.
Two different model systems catalogued cell states: DAM-like, antigen-presenting, cytokine-, and interferon-based. More work is needed to pin down function.
While GFAP seems a sensitive biomarker of Aβ plaque removal, NfL might respond more slowly.
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