Chimeric Protein Dephosphorylates Tau, Improves Memory
In tauopathy mice, a peptide construct recruited protein phosphatase 1 to tau. Dephosphorylation lowered total tau, restoring synaptic density and memory.
In tauopathy mice, a peptide construct recruited protein phosphatase 1 to tau. Dephosphorylation lowered total tau, restoring synaptic density and memory.
In mouse brain, mRNA methylation distinguishes cell subtypes and changes with age. One standout: APP. It loses its methyls with age.
Three new papers report these myelin-producing cells contribute up to a third of plaque Aβ in transgenic mice.
A CSF proteomics study in ADAD mutation carriers identified 137 potential markers. They span the AD continuum. For 12 of them, their concentrations change prior to those of classic AD biomarkers.
In a tau PET GWAS, a SNP linked to higher expression of the oxidizing enzyme was associated with more cortical tangles.
Plaques rev up neural oscillations, while tangles turn them down, ultimately leading to sluggish synapses. The slowdown foreshadows symptoms.
Transcriptomes of more than 400 postmortem brains reveal microglia and astrocyte subtypes that collaborate to precipitate pathologic changes.
XWAS from three research groups identified a dozen genetic loci that may help explain sex differences in AD.
Where in the amyloid cascade does inflammation fit? Everywhere, according to a new snRNA-Seq study of more than 400 postmortem brains. The authors identified one microglial subtype that promotes plaques, another that promotes tangles, and an astrocyte subtype that contributes to cognitive decline. Intriguingly, in brains with plaques but few tangles, a different set of glial subtypes predominated. The data add to the evidence that AD has a cellular phase.
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