Reconceptualizing the BBB: Is It Time to Swap ‘Barrier’ for ‘Border'?
Given the adaptive nature of the interface between the blood and brain, some scientists propose viewing it much like an actively managed border crossing, rather than a wall.
NEWS
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.
Human Evolution Offers Clues to Frontotemporal Dementia
Study shows links among rapidly evolving genes, selective vulnerability, and genes that are mis-spliced when TDP-43 fails to function.
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.
Single-Cell Methylomes Offer Clues to Aging
In mouse brain, mRNA methylation distinguishes cell subtypes and changes with age. One standout: APP. It loses its methyls over time.
Oligodendrocytes Pump Out Aβ42, Worsening Plaques and Synaptotoxicity
Three new papers report these myelin-producing cells contribute up to a third of plaque Aβ in transgenic mice.
CSF Proteins Spot Alzheimer’s Mutation Carriers Decades Before Symptoms
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.
New Alzheimer’s Gene? Cytochrome P450 Protein Linked to Tangles
In a tau PET GWAS, a SNP linked to higher expression of the oxidizing enzyme was associated with more cortical tangles.
SPOTLIGHT
Tweaked, Aβ-Antibodies Cross Blood Brain 'Border' (Bye Bye, Barrier?)
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 and vascular inflammation, without compromising engagement with Aβ plaques. In a related review, scientists propose rethinking the blood-brain barrier as more a bustling border crossing than a static wall. Read the two-part series.
Oligodendrocytes Pump Out Aβ42, Worsening Plaques and Synaptotoxicity
Three independent studies report that these cells contribute up to a third of plaque in mouse models of amyloidosis. What’s more, suppressing oligodendrocyte Aβ production curbed neuronal hyperactivity. In human brain, too, oligodendrocytes express all the necessary genes to make Aβ peptides, hinting that the cells may play a hitherto unrecognized role in Alzheimer’s pathogenesis.
Glial Cell Communities Conspire to Drive Alzheimer’s Disease
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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