Repeat Expansion Mutations More Common Than Thought
A whole-genome sequencing study estimated that people are two to three times more likely to be affected by these mutations than predicted by epidemiology.
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A whole-genome sequencing study estimated that people are two to three times more likely to be affected by these mutations than predicted by epidemiology.
In mice with prion disease, microglia shifted from gobbling up misfolded protein to engulfing flagging neurons. This change coincided with symptom onset.
Scientists are honing transferrin receptors to whisk bulky, anti-Aβ antibodies throughout the brain without setting off ARIA and anemia. By halving the effector function of their antibody transport vehicle, Denali researchers blunted red blood cell loss a
The adaptive nature of the interface between blood and brain led some scientists to envision it more like an actively managed border crossing, not a wall.
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.