Tweaked, Aβ-Antibodies Cross Blood-Brain ‘Border’ (Bye-Bye, Barrier?)
With genetic tinkering to their antibody transport vehicle, Denali scientists aim to temper both ARIA and anemia, while maintaining potency against Aβ.
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With genetic tinkering to their antibody transport vehicle, Denali scientists aim to temper both ARIA and anemia, while maintaining potency against Aβ.
Brain regions that have most recently evolved may be most vulnerable to FTLD.
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 over time.
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.
Dynamic, lipid-rich inclusions of α-synuclein appear toxic, while stable, fibril-rich aggregates seem to protect neurons.
A new strategy, which marries nanobodies or misfolded tau to a ubiquitin ligase RING domain, tags tangles for disposal.
The consortium has cranked out dozens of mouse models of late-onset AD for the research community. Strains carry humanized Aβ and tau, and a growing list of risk variants.
A retrospective study finds that gut damage precedes Parkinson’s disease onset, independent of bacterial infection.
This super-sized isoform resists phosphorylation and aggregation, and occurs in cerebellum and brainstem, regions largely spared from tau pathology.
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