Short Aβ Fibrils Easily Isolated from Alzheimer's Brain Fluid
Once assumed to be high-molecular-weight oligomers, these short, diffusible fibrils share the same structure as their plaque-bound counterparts. Both bind lecanemab.
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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.
While the familial Swedish AD mutation spurred synaptic growth, BACE inhibition, or APP deletion, had the opposite effect.
Without the trafficking protein Numb, tau accumulated in retinal ganglion cells and motor neurons, accelerating hind limb paralysis.
TANK-binding kinase 1 gets wrapped up in poly-GA aggregates translated from C9ORF72. TDP-43 aggregation ensues.
USP11 spurs tau acetylation and aggregation. In women, one copy escapes X-inactivation.
ADNI4 will run from 2022 to 2027 and recruit 500 new participants, at least half of whom will be from underrepresented racial and ethnic groups.
Data from two large international familial cohorts predict disease onset, helping researchers select the best participants for secondary prevention trials.
Middle-aged people who strode 8,000+ steps a day were less likely to have a range of conditions, including diabetes and hypertension.
Blocking glycolysis triggers microglia to crank up lipid metabolism, boosting ATP production and improving phagocytosis. In Alzheimer’s disease, the opposite happens.